Carbohydrate Metabolism
Carbohydrates
Dietary Carbohydrates
Glucose
Lipid Metabolism
Energy Metabolism
Glycolysis
Starch
Carbohydrate Sequence
Insulin
Liver
Gluconeogenesis
Fructose
Lactic Acid
Sucrose
Phosphoglucomutase
Phosphofructokinase-1
Pentose Phosphate Pathway
Citric Acid Cycle
Phosphofructokinases
Glucose Tolerance Test
Molecular Sequence Data
Carbon Isotopes
Galactose
Thermoproteus
Oxidation-Reduction
Plant Tubers
beta-Fructofuranosidase
Gene Expression Profiling
Pyruvate Kinase
Metabolic Networks and Pathways
Fructosediphosphates
Fatty Acids, Nonesterified
Oxygen Consumption
Fatty Acids
Carbon
Fermentation
Carbon Dioxide
Dietary Fats
Plant Leaves
Gene Expression Regulation, Plant
Metabolism
Pyruvic Acid
Photosynthesis
Glucagon
Phosphorylases
Lipids
Mannose
Glycerol
Fructose-Bisphosphate Aldolase
Fructose-Bisphosphatase
Oligosaccharides
Nitrogen
Glycerol Kinase
Contraceptives, Oral, Sequential
Antigens, Tumor-Associated, Carbohydrate
Glucosyltransferases
Amino Acid Sequence
Body Weight
Muscle, Skeletal
Oligonucleotide Array Sequence Analysis
Lectins
Models, Biological
Insulin Resistance
Plant Proteins
Acetates
Amino Acids
Metabolome
Culture Media
Magnetic Resonance Spectroscopy
Solanum tuberosum
Maltose
Carbon Radioisotopes
Obesity
Enzymes
Ketone Bodies
RNA, Messenger
Rats, Inbred Strains
Hexokinase
Glycogen Synthase
beta-Amylase
Transcriptome
Mutation
Glucose-1-Phosphate Adenylyltransferase
Glucokinase
Gene Expression Regulation, Bacterial
Glucose-6-Phosphate Isomerase
Dietary Proteins
Homeostasis
Ethynodiol Diacetate
Glycosylation
Monosaccharides
Cholesterol
Base Sequence
Plant Roots
Glucose-6-Phosphate
RNA, Plant
Glycoproteins
Eriobotrya
Norgestrel
Hydrogen-Ion Concentration
Adenosine Triphosphate
Chromatography, High Pressure Liquid
Phosphogluconate Dehydrogenase
Phenotype
Growth Hormone
Adipose Tissue
Plant Stems
Species Specificity
Signal Transduction
Stress, Physiological
Phosphotransferases
Vitis
Electrophoresis, Gel, Two-Dimensional
Gene Expression Regulation
Seeds
Alcohol Oxidoreductases
Transcription Factors
Cells, Cultured
Biotransformation
Adaptation, Physiological
Pyruvate Dehydrogenase Complex
Diet, Carbohydrate-Restricted
Cell Wall
Arabidopsis
Propionates
Transcription, Genetic
Cluster Analysis
Rats, Sprague-Dawley
Diabetes Mellitus, Type 2
Exercise
Gene Expression Regulation, Fungal
Contraceptives, Oral, Combined
Hypoglycemia
Biological Transport
Microsomes, Liver
Phosphofructokinase-2
Sequence Analysis, DNA
Anaerobiosis
Physical Endurance
Oxygen
Cytochrome P-450 Enzyme System
Gene Expression
Substrate Specificity
Rats, Wistar
Plant Lectins
Protein Binding
Gene Expression Regulation, Enzymologic
Malate Dehydrogenase
Glycopeptides
Swine
Pregnancy
Microarray Analysis
Reverse Transcriptase Polymerase Chain Reaction
Isocitrate Dehydrogenase
Diabetes Mellitus
Metagenome
Mitochondria
Saccharomyces cerevisiae
Bacteria
Proteins
Role of glutamine in human carbohydrate metabolism in kidney and other tissues. (1/3923)
Glutamine is the most abundant amino acid in the human body and is involved in more metabolic processes than any other amino acid. Until recently, the understanding of many aspects of glutamine metabolism was based on animal and in vitro data. However, recent studies using isotopic and balance techniques have greatly advanced the understanding of glutamine metabolism in humans and its role in glucose metabolism in the kidney and other tissues. There is now evidence that in postabsorptive humans, glutamine is an important glucose precursor and makes a significant contribution to the addition of new carbon to the glucose carbon pool. The importance of alanine for gluconeogenesis, viewed in terms of the addition of new carbons, is less than previously assumed. It appears that glutamine is predominantly a renal gluconeogenic substrate, whereas alanine gluconeogenesis is essentially confined to the liver. As shown recently, renal gluconeogenesis contributes 20 to 25% to whole-body glucose production. Moreover, glutamine has been shown not only to stimulate net muscle glycogen storage but also to stimulate gluconeogenesis in normal humans. Finally, in humans with type II diabetes, conversion of glutamine to glucose is increased (more so than that of alanine). The available evidence on the hormonal regulation of glutamine gluconeogenesis in kidney and liver and its alterations under pathological conditions are discussed. (+info)Relationship between glycosyl hydrolase inventory and growth physiology of the hyperthermophile Pyrococcus furiosus on carbohydrate-based media. (2/3923)
Utilization of a range of carbohydrates for growth by the hyperthermophile Pyrococcus furiosus was investigated by examining the spectrum of glycosyl hydrolases produced by this microorganism and the thermal labilities of various saccharides. Previously, P. furiosus had been found to grow in batch cultures on several alpha-linked carbohydrates and cellobiose but not on glucose or other beta-linked sugars. Although P. furiosus was not able to grow on any nonglucan carbohydrate or any form of cellulose in this study (growth on oat spelt arabinoxylan was attributed to glucan contamination of this substrate), significant growth at 98 degrees C occurred on beta-1,3- and beta-1,3-beta-1,4-linked glucans. Oligosaccharides generated by digestion with a recombinant laminarinase derived from P. furiosus were the compounds that were most effective in stimulating growth of the microorganism. In several cases, periodic addition of beta-glucan substrates to fed-batch cultures limited adverse thermochemical modifications of the carbohydrates (i.e., Maillard reactions and caramelization) and led to significant increases (as much as two- to threefold) in the cell yields. While glucose had only a marginally positive effect on growth in batch culture, the final cell densities nearly tripled when glucose was added by the fed-batch procedure. Nonenzymatic browning reactions were found to be significant at 98 degrees C for saccharides with degrees of polymerization (DP) ranging from 1 to 6; glucose was the most labile compound on a mass basis and the least labile compound on a molar basis. This suggests that for DP of 2 or greater protection of the nonreducing monosaccharide component may be a factor in substrate availability. For P. furiosus, carbohydrate utilization patterns were found to reflect the distribution of the glycosyl hydrolases which are known to be produced by this microorganism. (+info)Glucose kinetics during prolonged exercise in highly trained human subjects: effect of glucose ingestion. (3/3923)
1. The objectives of this study were (1) to investigate whether glucose ingestion during prolonged exercise reduces whole body muscle glycogen oxidation, (2) to determine the extent to which glucose disappearing from the plasma is oxidized during exercise with and without carbohydrate ingestion and (3) to obtain an estimate of gluconeogenesis. 2. After an overnight fast, six well-trained cyclists exercised on three occasions for 120 min on a bicycle ergometer at 50 % maximum velocity of O2 uptake and ingested either water (Fast), or a 4 % glucose solution (Lo-Glu) or a 22 % glucose solution (Hi-Glu) during exercise. 3. Dual tracer infusion of [U-13C]-glucose and [6,6-2H2]-glucose was given to measure the rate of appearance (Ra) of glucose, muscle glycogen oxidation, glucose carbon recycling, metabolic clearance rate (MCR) and non-oxidative disposal of glucose. 4. Glucose ingestion markedly increased total Ra especially with Hi-Glu. After 120 min Ra and rate of disappearance (Rd) of glucose were 51-52 micromol kg-1 min-1 during Fast, 73-74 micromol kg-1 min-1 during Lo-Glu and 117-119 micromol kg-1 min-1 during Hi-Glu. The percentage of Rd oxidized was between 96 and 100 % in all trials. 5. Glycogen oxidation during exercise was not reduced by glucose ingestion. The vast majority of glucose disappearing from the plasma is oxidized and MCR increased markedly with glucose ingestion. Glucose carbon recycling was minimal suggesting that gluconeogenesis in these conditions is negligible. (+info)Conversion of brain-specific complex type sugar chains by N-acetyl-beta-D-hexosaminidase B. (4/3923)
The N-linked sugar chains, GlcNAcbeta1-2Manalpha1-6(GlcNAcbeta1-4)(Manalpha1++ +-3)Manbeta1-4GlcNAcb eta1-4(Fucalpha1-6)GlcNAc (BA-1) and GlcNAcbeta1-2Manalpha1-6(GlcNAcbeta1-4)(GlcNAcbeta1 -2Manalpha1-3)Manb eta1-4GlcNAcbeta1-4(Fucalpha1-6)GlcNAc (BA-2), were recently found to be linked to membrane proteins of mouse brain in a development-dependent manner [S. Nakakita, S. Natsuka, K. Ikenaka, and S. Hase, J. Biochem. 123, 1164-1168 (1998)]. The GlcNAc residue linked to the Manalpha1-3 branch of BA-2 is lacking in BA-1 and the removal of this GlcNAc residue is not part of the usual biosynthetic pathway for N-linked sugar chains, suggesting the existence of an N-acetyl-beta-D-hexosaminidase. Using pyridylaminated BA-2 (BA-2-PA) as a substrate the activity of this enzyme was found in all four subcellular fractions obtained. The activity was much greater in the cerebrum than in the cerebellum. To further identify the N-acetyl-beta-D-hexosaminidase, BA-1 and BA-2 in brain tissues of Hex gene-disrupted mutant mice were detected and quantified. PA-sugar chains were liberated from the cerebrum and cerebellum of the mutant mice by hydrazinolysis-N-acetylation followed by pyridylamination. PA-sugar chains were separated by anion-exchange HPLC, size-fractionation, and reversed-phase HPLC. Each peak was quantified by measuring the peaks at the elution positions of authentic BA-1-PA and BA-2-PA. BA-2-PA was detected in all the PA-sugar chain fractions prepared from Hexa, Hexb, and both Hexa and Hexb (double knockout) gene-disrupted mice, but BA-1 was not found in the fractions from Hexb gene-disrupted and double knockout mice. These results indicate that N-acetyl-beta-D-hexosaminidase B encoded by the Hexb gene hydrolyzed BA-2 to BA-1. (+info)Sugar- and nitrogen-dependent regulation of an Amanita muscaria phenylalanine ammonium lyase gene. (5/3923)
The cDNA of a key enzyme of secondary metabolism, phenylalanine ammonium lyase, was identified for an ectomycorrhizal fungus by differential screening of a mycorrhizal library. The gene was highly expressed in hyphae grown at low external monosaccharide concentrations, but its expression was 30-fold reduced at elevated concentrations. Gene repression was regulated by hexokinase. (+info)Characterisation of recombinant glycosylation variants of insulin-like growth factor binding protein-3. (6/3923)
There are three potential N-glycosylation sites in the non-conserved central region of the insulin-like growth factor binding protein-3 (IGFBP-3) sequence (N89AS, N109AS, N172FS). IGFBP-3 exists as two glycoforms which reduce to a single form on enzymatic deglycosylation. To determine the functional significance of the carbohydrate chains, the N-glycosylation sites were mutated singly and in combinations by substituting Asn residues with Ala. Each recombinant glycoform was detected by radioimmunoassay, indicating that glycosylation is not essential for secretion in Chinese hamster ovary cells. Ligand blotting of the conditioned media using [125I]IGF-I indicated that all seven mutants are active. On the basis of the number and molecular masses of the bands detected for each glycoform, there is approximately 4, 4.5 and 5 kDa of carbohydrate on Asn89, Asn109 and Asn172 respectively, with variable occupancy of Asn172. Ternary complex formation by the glycovariants in the presence of ALS and excess IGF-I was not significantly different from that of fully glycosylated recombinant human (rh)IGFBP-3 [Ka (fully glycosylated)=12.5+/-4.1 l/nmol; mean Ka (all mutants)=22.1+/-3.0 l/nmol]. In contrast, Asn to Asp substitutions decreased acid-labile subunit (ALS) binding activity. Cell-surface association experiments indicate that glycosylation may influence the partitioning of IGFBP-3 between the extracellular milieu and the cell surface. Therefore, while the carbohydrate units appear to be non-essential to ALS or IGF binding, they may modulate other biological activities of IGFBP-3. (+info)Prevalence of undiagnosed diabetes and abnormalities of carbohydrate metabolism in a U.S. Army population. (7/3923)
OBJECTIVE: The Third National Health and Nutrition Examination Survey (NHANES III) reported that 4.3-6.3% of adult Americans have undiagnosed diabetes. 15.6% have impaired glucose tolerance, and 10.1% have impaired fasting glucose. By design, NHANES III excluded people in the U.S. military. The purpose of this study was to determine the prevalence of undiagnosed diabetes, impaired glucose tolerance, and impaired fasting glucose among U.S. Army soldiers. RESEARCH DESIGN AND METHODS: A 2-h, 75-g oral glucose tolerance test was performed on a prospective, consecutive sample of 625 asymptomatic soldiers presenting to a U.S. Army medical clinic for physical examinations. Age of subjects was 32 +/- 9 years (mean +/- SD), and 81.0% of subjects were male. BMI was 26.2 +/- 3.7 kg/m2. Race/ethnicity categories included Caucasian (54.4%), African-American (24.4%), Hispanic (17.4%), and other (3.7%). A family history of diabetes was reported by 25.4% of the subjects, and the number of exercise sessions per week was 4.0 +/- 1.5. RESULTS: The prevalence of undiagnosed diabetes was 3 of 625 (0.5%) (95% CI, 0.1-1.4): impaired glucose tolerance, 11 of 598 (1.8%) (0.9-3.3); and impaired fasting glucose 6 of 585 (1.0%) (0.4-2.2). CONCLUSIONS: In this low-diabetes risk U.S. Army population, the prevalence of undiagnosed diabetes, impaired glucose tolerance, and impaired fasting glucose were 0.5, 1.8, and 1.0%, respectively. The prevalence rates found in this study are approximately one-tenth of those found in NHANES III. (+info)Outer membranes of gram-negative bacteria. XIX. Isolation from Pseudomonas aeruginosa PAO1 and use in reconstitution and definition of the permeability barrier. (8/3923)
A method for separating the outer and inner membranes of Pseudomonas aeruginosa PAO1 in the absence of added ethylenediaminetetraacetic acid was devised. The method yields two outer membrane fractions which show the same protein pattern on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, but differ substantially in their relative contents of phospholipids. One of these outer membrane fractions and the inner membrane fraction are less than 4% cross-contaminated, as judged by the content of typical inner and outer membrane markers. The outer membrane contains four major protein bands with apparent molecular weights of 37,000, 35,000, 21,000 and 17,000. Vesicles reconstituted from lipopolysaccharide and phospholipids were impermeable to all saccharides included in the vesicles during vesicle formation. When the vesicles contained outer membrane proteins, they fully retained only those saccharides of greater than 9,000 molecular weight, suggesting that the exclusion limit of the outer membrane of P. aeruginosa for saccharides is substantially larger than the figure (500 to 600 daltons) obtained for certain enteric bacteria. The advantages and potential disadvantages of having an outer membrane with a higher exclusion limit for hydrophilic substances are discussed. (+info)Starvation is a condition where an individual's body does not receive enough nutrients to maintain proper bodily functions and growth. It can be caused by a lack of access to food, poverty, poor nutrition, or other factors that prevent the intake of sufficient calories and essential nutrients. Starvation can lead to severe health consequences, including weight loss, weakness, fatigue, and even death.
Types of Starvation:
There are several types of starvation, each with different causes and effects. These include:
1. Acute starvation: This occurs when an individual suddenly stops eating or has a limited access to food for a short period of time.
2. Chronic starvation: This occurs when an individual consistently does not consume enough calories and nutrients over a longer period of time, leading to gradual weight loss and other health problems.
3. Malnutrition starvation: This occurs when an individual's diet is deficient in essential nutrients, leading to malnutrition and other health problems.
4. Marasmus: This is a severe form of starvation that occurs in children, characterized by extreme weight loss, weakness, and wasting of muscles and organs.
5. Kwashiorkor: This is a form of malnutrition caused by a diet lacking in protein, leading to edema, diarrhea, and other health problems.
Effects of Starvation on the Body:
Starvation can have severe effects on the body, including:
1. Weight loss: Starvation causes weight loss, which can lead to a decrease in muscle mass and a loss of essential nutrients.
2. Fatigue: Starvation can cause fatigue, weakness, and a lack of energy, making it difficult to perform daily activities.
3. Weakened immune system: Starvation can weaken the immune system, making an individual more susceptible to illnesses and infections.
4. Nutrient deficiencies: Starvation can lead to a deficiency of essential nutrients, including vitamins and minerals, which can cause a range of health problems.
5. Increased risk of disease: Starvation can increase the risk of diseases such as tuberculosis, pellagra, and other infections.
6. Mental health issues: Starvation can lead to mental health issues such as depression, anxiety, and irritability.
7. Reproductive problems: Starvation can cause reproductive problems, including infertility and miscarriage.
8. Hair loss: Starvation can cause hair loss, which can be a sign of malnutrition.
9. Skin problems: Starvation can cause skin problems, such as dryness, irritation, and infections.
10. Increased risk of death: Starvation can lead to increased risk of death, especially in children and the elderly.
It is important to note that these effects can be reversed with proper nutrition and care. If you or someone you know is experiencing starvation, it is essential to seek medical attention immediately.
Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.
There are several ways to measure body weight, including:
1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.
It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.
There are several factors that can contribute to the development of insulin resistance, including:
1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.
There are several ways to diagnose insulin resistance, including:
1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.
There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:
1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.
Medications that may be used to treat insulin resistance include:
1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.
It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.
There are several different types of obesity, including:
1. Central obesity: This type of obesity is characterized by excess fat around the waistline, which can increase the risk of health problems such as type 2 diabetes and cardiovascular disease.
2. Peripheral obesity: This type of obesity is characterized by excess fat in the hips, thighs, and arms.
3. Visceral obesity: This type of obesity is characterized by excess fat around the internal organs in the abdominal cavity.
4. Mixed obesity: This type of obesity is characterized by both central and peripheral obesity.
Obesity can be caused by a variety of factors, including genetics, lack of physical activity, poor diet, sleep deprivation, and certain medications. Treatment for obesity typically involves a combination of lifestyle changes, such as increased physical activity and a healthy diet, and in some cases, medication or surgery may be necessary to achieve weight loss.
Preventing obesity is important for overall health and well-being, and can be achieved through a variety of strategies, including:
1. Eating a healthy, balanced diet that is low in added sugars, saturated fats, and refined carbohydrates.
2. Engaging in regular physical activity, such as walking, jogging, or swimming.
3. Getting enough sleep each night.
4. Managing stress levels through relaxation techniques, such as meditation or deep breathing.
5. Avoiding excessive alcohol consumption and quitting smoking.
6. Monitoring weight and body mass index (BMI) on a regular basis to identify any changes or potential health risks.
7. Seeking professional help from a healthcare provider or registered dietitian for personalized guidance on weight management and healthy lifestyle choices.
There are several possible causes of hyperglycemia, including:
1. Diabetes: This is a chronic condition where the body either does not produce enough insulin or cannot use insulin effectively.
2. Insulin resistance: This occurs when the body's cells become less responsive to insulin, leading to high blood sugar levels.
3. Pancreatitis: This is inflammation of the pancreas, which can lead to high blood sugar levels.
4. Cushing's syndrome: This is a rare hormonal disorder that can cause high blood sugar levels.
5. Medications: Certain medications, such as steroids and some types of antidepressants, can raise blood sugar levels.
6. Stress: Stress can cause the release of hormones such as cortisol and adrenaline, which can raise blood sugar levels.
7. Infections: Certain infections, such as pneumonia or urinary tract infections, can cause high blood sugar levels.
8. Trauma: Traumatic injuries can cause high blood sugar levels due to the release of stress hormones.
9. Surgery: Some types of surgery, such as heart bypass surgery, can cause high blood sugar levels.
10. Pregnancy: High blood sugar levels can occur during pregnancy, especially in women who have a history of gestational diabetes.
Hyperglycemia can cause a range of symptoms, including:
1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Headaches
5. Cuts or bruises that are slow to heal
6. Tingling or numbness in the hands and feet
7. Dry, itchy skin
8. Flu-like symptoms, such as weakness, dizziness, and stomach pain
9. Recurring skin, gum, or bladder infections
10. Sexual dysfunction in men and women
If left untreated, hyperglycemia can lead to serious complications, including:
1. Diabetic ketoacidosis (DKA): A life-threatening condition that occurs when the body produces high levels of ketones, which are acidic substances that can cause confusion, nausea, and vomiting.
2. Hypoglycemia: Low blood sugar levels that can cause dizziness, confusion, and even loss of consciousness.
3. Nerve damage: High blood sugar levels over an extended period can damage the nerves, leading to numbness, tingling, and pain in the hands and feet.
4. Kidney damage: The kidneys may become overworked and damaged if they are unable to filter out the excess glucose in the blood.
5. Eye damage: High blood sugar levels can cause damage to the blood vessels in the eyes, leading to vision loss and blindness.
6. Cardiovascular disease: Hyperglycemia can increase the risk of cardiovascular disease, including heart attacks, strokes, and peripheral artery disease.
7. Cognitive impairment: Hyperglycemia has been linked to cognitive impairment and an increased risk of dementia.
It is essential to manage hyperglycemia by making lifestyle changes, such as following a healthy diet, regular exercise, and taking medication if prescribed by a healthcare professional. Monitoring blood sugar levels regularly can help identify the signs of hyperglycemia and prevent long-term complications.
Type 2 diabetes can be managed through a combination of diet, exercise, and medication. In some cases, lifestyle changes may be enough to control blood sugar levels, while in other cases, medication or insulin therapy may be necessary. Regular monitoring of blood sugar levels and follow-up with a healthcare provider are important for managing the condition and preventing complications.
Common symptoms of type 2 diabetes include:
* Increased thirst and urination
* Fatigue
* Blurred vision
* Cuts or bruises that are slow to heal
* Tingling or numbness in the hands and feet
* Recurring skin, gum, or bladder infections
If left untreated, type 2 diabetes can lead to a range of complications, including:
* Heart disease and stroke
* Kidney damage and failure
* Nerve damage and pain
* Eye damage and blindness
* Foot damage and amputation
The exact cause of type 2 diabetes is not known, but it is believed to be linked to a combination of genetic and lifestyle factors, such as:
* Obesity and excess body weight
* Lack of physical activity
* Poor diet and nutrition
* Age and family history
* Certain ethnicities (e.g., African American, Hispanic/Latino, Native American)
* History of gestational diabetes or delivering a baby over 9 lbs.
There is no cure for type 2 diabetes, but it can be managed and controlled through a combination of lifestyle changes and medication. With proper treatment and self-care, people with type 2 diabetes can lead long, healthy lives.
In extreme cases, hypoglycemia can lead to seizures, loss of consciousness, and even coma. It is important to recognize the symptoms of hypoglycemia early on and seek medical attention if they persist or worsen over time. Treatment typically involves raising blood sugar levels through the consumption of quick-acting carbohydrates such as glucose tablets, fruit juice, or hard candy.
If left untreated, hypoglycemia can have serious consequences, including long-term damage to the brain, heart, and other organs. It is important for individuals with diabetes to monitor their blood sugar levels regularly and work with their healthcare provider to manage their condition effectively.
There are several types of diabetes mellitus, including:
1. Type 1 DM: This is an autoimmune condition in which the body's immune system attacks and destroys the cells in the pancreas that produce insulin, resulting in a complete deficiency of insulin production. It typically develops in childhood or adolescence, and patients with this condition require lifelong insulin therapy.
2. Type 2 DM: This is the most common form of diabetes, accounting for around 90% of all cases. It is caused by a combination of insulin resistance (where the body's cells do not respond properly to insulin) and impaired insulin secretion. It is often associated with obesity, physical inactivity, and a diet high in sugar and unhealthy fats.
3. Gestational DM: This type of diabetes develops during pregnancy, usually in the second or third trimester. Hormonal changes and insulin resistance can cause blood sugar levels to rise, putting both the mother and baby at risk.
4. LADA (Latent Autoimmune Diabetes in Adults): This is a form of type 1 DM that develops in adults, typically after the age of 30. It shares features with both type 1 and type 2 DM.
5. MODY (Maturity-Onset Diabetes of the Young): This is a rare form of diabetes caused by genetic mutations that affect insulin production. It typically develops in young adulthood and can be managed with lifestyle changes and/or medication.
The symptoms of diabetes mellitus can vary depending on the severity of the condition, but may include:
1. Increased thirst and urination
2. Fatigue
3. Blurred vision
4. Cuts or bruises that are slow to heal
5. Tingling or numbness in hands and feet
6. Recurring skin, gum, or bladder infections
7. Flu-like symptoms such as weakness, dizziness, and stomach pain
8. Dark, velvety skin patches (acanthosis nigricans)
9. Yellowish color of the skin and eyes (jaundice)
10. Delayed healing of cuts and wounds
If left untreated, diabetes mellitus can lead to a range of complications, including:
1. Heart disease and stroke
2. Kidney damage and failure
3. Nerve damage (neuropathy)
4. Eye damage (retinopathy)
5. Foot damage (neuropathic ulcers)
6. Cognitive impairment and dementia
7. Increased risk of infections and other diseases, such as pneumonia, gum disease, and urinary tract infections.
It is important to note that not all individuals with diabetes will experience these complications, and that proper management of the condition can greatly reduce the risk of developing these complications.
Examples of inborn errors of metabolism include:
1. Phenylketonuria (PKU): A disorder that affects the body's ability to break down the amino acid phenylalanine, leading to a buildup of this substance in the blood and brain.
2. Hypothyroidism: A condition in which the thyroid gland does not produce enough thyroid hormones, leading to developmental delays, intellectual disability, and other health problems.
3. Maple syrup urine disease (MSUD): A disorder that affects the body's ability to break down certain amino acids, leading to a buildup of these substances in the blood and urine.
4. Glycogen storage diseases: A group of disorders that affect the body's ability to store and use glycogen, a form of carbohydrate energy.
5. Mucopolysaccharidoses (MPS): A group of disorders that affect the body's ability to produce and break down certain sugars, leading to a buildup of these substances in the body.
6. Citrullinemia: A disorder that affects the body's ability to break down the amino acid citrulline, leading to a buildup of this substance in the blood and urine.
7. Homocystinuria: A disorder that affects the body's ability to break down certain amino acids, leading to a buildup of these substances in the blood and urine.
8. Tyrosinemia: A disorder that affects the body's ability to break down the amino acid tyrosine, leading to a buildup of this substance in the blood and liver.
Inborn errors of metabolism can be diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood and urine tests. Treatment for these disorders varies depending on the specific condition and may include dietary changes, medication, and other therapies. Early detection and treatment can help manage symptoms and prevent complications.
Examples of inborn errors of carbohydrate metabolism include:
1. Phosphofructokinase (PFK) deficiency: This is a rare genetic disorder that affects the body's ability to break down glucose-6-phosphate, a type of sugar. Symptoms can include seizures, developmental delays, and metabolic acidosis.
2. Galactosemia: This is a group of genetic disorders that affect the body's ability to process galactose, a type of sugar found in milk and other dairy products. Untreated, galactosemia can lead to serious health problems, including liver disease, kidney damage, and cognitive impairment.
3. Glycogen storage disease type II (GSDII): This is a rare genetic disorder that affects the body's ability to store and use glycogen, a complex carbohydrate found in the liver and muscles. Symptoms can include low blood sugar, fatigue, and muscle weakness.
4. Pompe disease: This is a rare genetic disorder that affects the body's ability to break down glycogen. Symptoms can include muscle weakness, breathing problems, and heart problems.
5. Mucopolysaccharidoses (MPS): These are a group of genetic disorders that affect the body's ability to break down sugar molecules. Symptoms can include joint stiffness, developmental delays, and heart problems.
Inborn errors of carbohydrate metabolism can be diagnosed through blood tests, urine tests, and other diagnostic procedures. Treatment depends on the specific disorder and may involve a combination of dietary changes, medication, and other therapies.
There are several different types of weight gain, including:
1. Clinical obesity: This is defined as a BMI of 30 or higher, and is typically associated with a range of serious health problems, such as heart disease, type 2 diabetes, and certain types of cancer.
2. Central obesity: This refers to excess fat around the waistline, which can increase the risk of health problems such as heart disease and type 2 diabetes.
3. Muscle gain: This occurs when an individual gains weight due to an increase in muscle mass, rather than fat. This type of weight gain is generally considered healthy and can improve overall fitness and athletic performance.
4. Fat gain: This occurs when an individual gains weight due to an increase in body fat, rather than muscle or bone density. Fat gain can increase the risk of health problems such as heart disease and type 2 diabetes.
Weight gain can be measured using a variety of methods, including:
1. Body mass index (BMI): This is a widely used measure of weight gain that compares an individual's weight to their height. A BMI of 18.5-24.9 is considered normal, while a BMI of 25-29.9 is considered overweight, and a BMI of 30 or higher is considered obese.
2. Waist circumference: This measures the distance around an individual's waistline and can be used to assess central obesity.
3. Skinfold measurements: These involve measuring the thickness of fat at specific points on the body, such as the abdomen or thighs.
4. Dual-energy X-ray absorptiometry (DXA): This is a non-invasive test that uses X-rays to measure bone density and body composition.
5. Bioelectrical impedance analysis (BIA): This is a non-invasive test that uses electrical impulses to measure body fat percentage and other physiological parameters.
Causes of weight gain:
1. Poor diet: Consuming high amounts of processed foods, sugar, and saturated fats can lead to weight gain.
2. Lack of physical activity: Engaging in regular exercise can help burn calories and maintain a healthy weight.
3. Genetics: An individual's genetic makeup can affect their metabolism and body composition, making them more prone to weight gain.
4. Hormonal imbalances: Imbalances in hormones such as insulin, thyroid, and cortisol can contribute to weight gain.
5. Medications: Certain medications, such as steroids and antidepressants, can cause weight gain as a side effect.
6. Sleep deprivation: Lack of sleep can disrupt hormones that regulate appetite and metabolism, leading to weight gain.
7. Stress: Chronic stress can lead to emotional eating and weight gain.
8. Age: Metabolism slows down with age, making it more difficult to maintain a healthy weight.
9. Medical conditions: Certain medical conditions such as hypothyroidism, Cushing's syndrome, and polycystic ovary syndrome (PCOS) can also contribute to weight gain.
Treatment options for obesity:
1. Lifestyle modifications: A combination of diet, exercise, and stress management techniques can help individuals achieve and maintain a healthy weight.
2. Medications: Prescription medications such as orlistat, phentermine-topiramate, and liraglutide can aid in weight loss.
3. Bariatric surgery: Surgical procedures such as gastric bypass surgery and sleeve gastrectomy can be effective for severe obesity.
4. Behavioral therapy: Cognitive-behavioral therapy (CBT) and other forms of counseling can help individuals develop healthy eating habits and improve their physical activity levels.
5. Meal replacement plans: Meal replacement plans such as Medifast can provide individuals with a structured diet that is high in protein, fiber, and vitamins, and low in calories and sugar.
6. Weight loss supplements: Supplements such as green tea extract, garcinia cambogia, and forskolin can help boost weight loss efforts.
7. Portion control: Using smaller plates and measuring cups can help individuals regulate their portion sizes and maintain a healthy weight.
8. Mindful eating: Paying attention to hunger and fullness cues, eating slowly, and savoring food can help individuals develop healthy eating habits.
9. Physical activity: Engaging in regular physical activity such as walking, running, swimming, or cycling can help individuals burn calories and maintain a healthy weight.
It's important to note that there is no one-size-fits-all approach to treating obesity, and the most effective treatment plan will depend on the individual's specific needs and circumstances. Consulting with a healthcare professional such as a registered dietitian or a physician can help individuals develop a personalized treatment plan that is safe and effective.
In hyperinsulinism, the body produces too much insulin, leading to a range of symptoms including:
1. Hypoglycemia (low blood sugar): Excessive insulin can cause blood sugar levels to drop too low, leading to hypoglycemic symptoms such as shakiness, dizziness, confusion, and rapid heartbeat.
2. Weight gain: Hyperinsulinism can lead to weight gain due to the body's inability to effectively use glucose for energy production.
3. Fatigue: Excessive insulin can cause fatigue, as the body's cells are not able to effectively use glucose for energy production.
4. Mood changes: Hyperinsulinism can lead to mood changes such as irritability, anxiety, and depression.
5. Polycystic ovary syndrome (PCOS): Women with PCOS are at a higher risk of developing hyperinsulinism due to insulin resistance.
6. Gestational diabetes: Hyperinsulinism can occur during pregnancy, leading to gestational diabetes.
7. Acanthosis nigricans: A condition characterized by dark, velvety patches on the skin, often found in the armpits, neck, and groin area.
8. Cancer: Hyperinsulinism has been linked to an increased risk of certain types of cancer, such as breast, colon, and pancreatic cancer.
9. Cardiovascular disease: Excessive insulin can increase the risk of cardiovascular disease, including high blood pressure, heart disease, and stroke.
10. Cognitive impairment: Hyperinsulinism has been linked to cognitive impairment and an increased risk of dementia.
There are several causes of hyperinsulinism, including:
1. Insulin-producing tumors: Tumors that produce excessive amounts of insulin can lead to hyperinsulinism.
2. Familial hyperinsulinism: A genetic disorder that affects the regulation of insulin secretion and action.
3. Pancreatic beta-cell dysfunction: Dysfunction in the pancreatic beta cells, which produce insulin, can lead to hyperinsulinism.
4. Medications: Certain medications such as steroids and certain psychiatric drugs can cause hyperinsulinism.
5. Pituitary tumors: Tumors in the pituitary gland can lead to excessive secretion of growth hormone, which can stimulate insulin production.
6. Maternal diabetes during pregnancy: Women with diabetes during pregnancy may experience hyperinsulinism due to increased insulin resistance and higher insulin levels.
7. Gestational diabetes: High blood sugar during pregnancy can lead to hyperinsulinism.
8. Polycystic ovary syndrome (PCOS): Women with PCOS may experience hyperinsulinism due to insulin resistance and high insulin levels.
9. Cushing's syndrome: An endocrine disorder caused by excessive cortisol production can lead to hyperinsulinism.
10. Other medical conditions: Certain medical conditions such as thyroid disorders, adrenal gland disorders, and pituitary gland disorders can also cause hyperinsulinism.
It's important to note that some individuals with hyperinsulinism may not experience any symptoms, while others may experience a range of symptoms, including:
1. Weight gain
2. Fatigue
3. Headaches
4. Numbness or tingling in the hands and feet
5. Memory loss and difficulty concentrating
6. Mood changes, such as anxiety and depression
7. Skin problems, such as acne and thinning skin
8. Increased risk of heart disease and stroke
9. Growth retardation in children
10. Increased risk of developing type 2 diabetes
If you suspect that you or your child may have hyperinsulinism, it's important to consult with a healthcare professional for proper diagnosis and treatment. A doctor may perform a physical examination, take a medical history, and order blood tests to determine if hyperinsulinism is present and what may be causing it. Treatment options for hyperinsulinism will depend on the underlying cause of the condition. In some cases, medications such as metformin or other anti-diabetic drugs may be prescribed to help regulate blood sugar levels and reduce insulin production. In other cases, surgery or lifestyle changes may be necessary. With proper diagnosis and treatment, it is possible to manage hyperinsulinism and prevent or manage related health complications.
Types of Experimental Diabetes Mellitus include:
1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.
Experimental Diabetes Mellitus has several applications in research, including:
1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.
In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.
Carbohydrate metabolism
Inborn errors of carbohydrate metabolism
Acetolactic acid
2-dehydro-3-deoxyglucarate aldolase
Gluconeogenesis
Galactarate dehydratase
Glucosaminate ammonia-lyase
Willis A. Wood
4-deoxy-L-threo-5-hexosulose-uronate ketol-isomerase
Meso-tartrate dehydrogenase
Jane Anne Russell
Fructan
2-dehydro-3-deoxy-6-phosphogalactonate aldolase
Thomas ap Rees
Cell wall
Glutaminolysis
Acid alpha-glucosidase
Development of the endocrine system
Alpha,alpha-trehalose-phosphate synthase (GDP-forming)
Fructose
William Cumming Rose
Hexose oxidase
Polioencephalomalacia
Fungus
Galactogen
Rollin Turner Woodyatt
Polysaccharide
Ribose 5-phosphate
Mike Berridge
Carl Ferdinand Cori
GANC
Methanogenesis
Metabolism
Food web
Diseases of poverty
Sodium-potassium pump
Galectin-9
Cunninghamella echinulata
Sympathoadrenal system
Diagenesis
Triphenyl phosphate
Methylene cyclopropyl acetic acid
N-glycosyltransferase
Sammy Boussiba
Bifidobacterium longum
Enzyme inhibitor
Short-beaked echidna
Kestose
Oxalyl-CoA decarboxylase
Prostate cancer
Physiological effects in space
Bacteroides thetaiotaomicron
Crimidine
John M. Opitz
Löffler's medium
Index of biochemistry articles
Beta-Hydroxybutyric acid
Dental health diets for dogs
Elizabeth F. Neufeld
Perivitellin-2
Carbohydrate Metabolism Disorders: MedlinePlus
Effects of combined treatment with rosiglitazone and intermediate-acting insulin on carbohydrate metabolism in patients with...
The case for low carbohydrate diets in diabetes management | Nutrition & Metabolism | Full Text
STW 02 Carbohydrate metabolism - akury
Details for:
Regulation of carbohydrate metabolism /
› WHO HQ Library catalog
INVESTIGATION OF THE LEVEL OF MONOSACCHARIDES IN SALIVA OF PATIENTS WITH IMPAIRED CARBOHYDRATE METABOLISM. | Georgian Med News...
The influence of skeletal muscle cell volume on carbohydrate metabolism in contracting skeletal muscle
Long-term and daily use of molecular hydrogen induces reprogramming of liver metabolism in rats by modulating NADP/NADPH redox...
Impact of increased growth hormone secretion on carbohydrate metabolism in adolescents with diabetes. - Radcliffe Department of...
Fructose 1,6-Diphosphatase Deficiency Medication
Figure 7 - Novel Enterobacter Lineage as Leading Cause of Nosocomial Outbreak Involving Carbapenemase-Producing Strains -...
Effects of somatostatin-25 and urotensin II on lipid and carbohydrate metabolism of coho salmon, Oncorhynchus kisutch<...
Modulation of the Activity of Enzymes Involved in Carbohydrate Metabolism during Flower Development of Grapevine ( Vitis...
Gene-centric view of carbohydrate metabolism in quintessential herbivorous fishes from the Red Sea - KAUST PORTAL FOR...
Cct3 MGI Mouse Gene Detail - MGI:104708 - chaperonin containing Tcp1, subunit 3 (gamma)
References - US SPR | CDC
Comparative genome analysis of Streptococcus infantarius subsp. infantariusCJ18, an African fermented camel milk isolate with...
KEGG PATHWAY: rn00030
Recombinant Human SDHA protein (Tagged) (ab226268) | Abcam
Cell Metabolism & Metabolic Control - course unit details - BSc Molecular Biology with a Modern Language - course details (2023...
Analysis of 1321 Eubacterium rectale genomes from metagenomes uncovers complex phylogeographic population structure and...
Endocrinology Research | Cincinnati Children's
Metabolic Problems: MedlinePlus
NHANES 2007-2008:
Standard Biochemistry Profile Data Documentation, Codebook, and Frequencies
Sol Genomics Network
Is there a link between lactose and body odor? | HowStuffWorks
Agricultural Research Institute - Staff
Nos publications en 2010-2011
Glucose9
- Normally your enzymes break carbohydrates down into glucose (a type of sugar). (medlineplus.gov)
- Compliance with these lifestyle modifications is less than satisfactory, however, and a high carbohydrate diet raises postprandial plasma glucose and insulin secretion, thereby increasing risk of CVD, hypertension, dyslipidemia, obesity and diabetes. (biomedcentral.com)
- In addition to glucose, carbohydrate metabolism also includes the metabolism of fructose and galactose, among others. (akuryprodukte.de)
- Objective - investigate glucose , fructose , and galactose levels in saliva of patients with impaired carbohydrate metabolism and establish a relationship with blood plasma parameters . (bvsalud.org)
- long-term regulation of glucose utilisation, enzyme-level control of glycolysis and gluconeogenesis, links to fatty acid metabolism, glycogen turnover, sugar interconversions and the citric acid cycle. (manchester.ac.uk)
- Glucose measurements are used in the diagnosis and treatment of pancreatic islet cell carcinoma and of carbohydrate metabolism disorders, including diabetes mellitus, neonatal hypoglycemia, and idiopathic hypoglycemia. (cdc.gov)
- These agents lower postprandial glucose by slowing glucose absorption and delaying the hydrolysis of ingested complex carbohydrates and disaccharide. (medscape.com)
- Macromineral enrichment of refined carbohydrates may have a promising role in lowering postprandial glucose and triglycerides, and thus decrease their negative health consequences. (who.int)
- therefore, serum tri- spectively ( 3 ), and are known to improve postprandial glyceride (TG) levels are expected to increase in a setting glucose and insulin metabolism ( 4 , 5 ). (who.int)
Disorders6
- Carbohydrate metabolism disorders are a group of metabolic disorders. (medlineplus.gov)
- If you have one of these disorders, you may not have enough enzymes to break down the carbohydrates. (medlineplus.gov)
- Carbohydrate metabolism disorder is a severe systemic disease leading to the development of a full range of metabolic disorders, accompanied by obesity , vascular pathology , connective tissue damage. (bvsalud.org)
- Changes of liver metabolite concentrations in adults with disorders of fructose metabolism after intravenous fructose by 31P magnetic resonance spectroscopy. (medscape.com)
- This battery of measurements are used in the diagnosis and treatment of certain liver, heart, and kidney diseases, acid-base imbalance in the respiratory and metabolic systems, other diseases involving lipid metabolism and various endocrine disorders as well as other metabolic or nutritional disorders. (cdc.gov)
- Inherited Disorders of Metabolism: Approach to the Patient With a Suspected Inherited Disorder of Metabolism. (howstuffworks.com)
Insulin3
- Because carbohydrate is the major secretagogue of insulin, some form of carbohydrate restriction is a prima facie candidate for dietary control of diabetes. (biomedcentral.com)
- These data show low carbohydrate diets to be comparable or better than traditional low fat high carbohydrate diets for weight reduction, improvement in the dyslipidemia of diabetes and metabolic syndrome as well as control of blood pressure, postprandial glycemia and insulin secretion. (biomedcentral.com)
- Macleod's main work was on carbohydrate metabolism and his efforts with Frederick Banting and Charles Best in the discovery of insulin. (biographybase.com)
Metabolic3
- In this review, we discuss the current evidence for a low carbohydrate diet versus a low fat diet in the management of people with diabetes, highlighting the potential role of low carbohydrate diet in ameliorating various metabolic abnormalities associated with diabetes. (biomedcentral.com)
- You will learn about diseases caused by defects in metabolism, such as diabetes, which will emphasise the importance of metabolic control. (manchester.ac.uk)
- Diseases caused by defects in metabolism will be studied to emphasise the importance of metabolic control. (manchester.ac.uk)
Liver1
- This work is the first to provide metabolomic and transcriptomic data to uncover molecular targets for the effect of prolonged molecular hydrogen treatment on liver metabolism. (nature.com)
Diabetes4
- A low fat, high carbohydrate diet in combination with regular exercise is the traditional recommendation for treating diabetes. (biomedcentral.com)
- Moreover, the current epidemic of diabetes and obesity has been, over the past three decades, accompanied by a significant decrease in fat consumption and an increase in carbohydrate consumption. (biomedcentral.com)
- Some form of low carbohydrate diet, in combination with exercise, is a viable option for patients with diabetes. (biomedcentral.com)
- Impact of increased growth hormone secretion on carbohydrate metabolism in adolescents with diabetes. (ox.ac.uk)
Biosynthesis3
- Both transcripts and metabolites enriched in H 2 -treated rats revealed alteration of amino acid metabolism pathways and activation of purine nucleotides and carbohydrate biosynthesis pathways. (nature.com)
- starch/sugar metabolism and fermentation for biofuels, storage lipid biosynthesis: regulation and applications. (manchester.ac.uk)
- Cellular processes in biosynthesis (anabolism) and degradation (catabolism) of CARBOHYDRATES. (bvsalud.org)
Endogenous1
- A number of endogenous systems, such as the aerobic metabolism and electron transport chains, generate highly reactive molecules with important biological functions known as reactive oxygen species (ROS), including superoxide and hydrogen peroxide (H2O2). (bvsalud.org)
Amino1
- control of protein turnover, nitrogen handling, links to nucleic acid metabolism, amino acid oxidation, integration with citric acid cycle. (manchester.ac.uk)
Regulation2
Degradation1
- Carbohydrate metabolism describes all processes of absorption, transport and degradation of carbohydrates. (akuryprodukte.de)
Oxidation1
- Over the past few decades, there have gradual but signif- in carbohydrate phosphorylation and oxidation, such icant changes in eating behaviour worldwide in light of as protein kinases and phosphatases. (who.int)
Grapevine3
- Modulation of the Activity of Enzymes Involved in Carbohydrate Metabolism during Flower Development of Grapevine ( Vitis Vinifera L. (univ-reims.fr)
- Modulation of the Activity of Enzymes Involved in Carbohydrate Metabolism during Flower Development of Grapevine ( Vitis Vinifera L. ). Open Journal of Plant Science , 2016, 1 (1), pp.010-017. (univ-reims.fr)
- Osmotic stress-induced change in polyamine metabolism can modulate grapevine defense responses and resistance to Botrytis cinerea . (univ-reims.fr)
Cellular3
- To provide students with an understanding of the essential features of cellular metabolism, and the mechanisms through which metabolism is controlled. (manchester.ac.uk)
- Describe the key features of cellular metabolism, including central catabolic and anabolic pathways. (manchester.ac.uk)
- Explain how different control mechanisms may be integrated to coordinate cellular metabolism, with reference to specific examples. (manchester.ac.uk)
Proteins1
- Food is made up of proteins, carbohydrates, and fats. (medlineplus.gov)
Adaptation1
- The presence of lacS and lacZ genes is the major dairy adaptation affecting lactose metabolism pathways also due to the disruption of lacIIABC . (biomedcentral.com)
Dietary1
- This apparent failure of low fat diets in curbing the obesity pandemic calls into question the effectiveness and long-term usefulness of such dietary recommendation and has led to renewed interest in alternative dietary interventions, notably those recommending reduced carbohydrate intake. (biomedcentral.com)
Type1
- Differences in the quantitative and qualitative content of monosaccharides in saliva are determined by the type of carbohydrate metabolism disorder. (bvsalud.org)
Diets1
- Furthermore, the ability of low carbohydrate diets to reduce triglycerides and to increase HDL is of particular importance. (biomedcentral.com)
Genes1
- The same subspecies exhibits expansion of its carbohydrate metabolism gene repertoire including the acquisition of a genomic island strongly enriched in glycosyltransferase genes involved in exopolysaccharide synthesis. (biomedcentral.com)
Important1
- It is important to understand that there is no clear cut definition of a low carbohydrate diet in the literature. (biomedcentral.com)
Study1
- Within the framework of the study, a protocol was formed containing the values of anthropometric indices and assessments of body parameters , the results of the study of lipid and carbohydrate spectrum parameters in plasma . (bvsalud.org)
Energy1
- Metabolism is the process your body uses to make energy from the food you eat. (medlineplus.gov)
Growth1
- Heterogeneous growth in the Nile tilapia: social stress and carbohydrate metabolism. (bvsalud.org)
Role1
- E. rectale produces butyrate and other short-chain fatty acids (SCFAs) from carbohydrates not directly accessible by the host, which play a role in promoting intestinal health in the host [ 4 ]. (biomedcentral.com)
Development1
- 2 ) strongly emphasize the importance of reducing sim- would ultimately favour the onset and development of ple carbohydrates. (who.int)
Treatment1
- Enzyme Replacement as an Effective Treatment for the Common Symptoms of Complex Carbohydrate Intolerance. (howstuffworks.com)
Patients1
- Nous avons génotypé les deux polymorphismes mononucléotidiques du gène ADIPOQ chez 140 patients atteints de DNID sans lien de parenté et 66 témoins non diabétiques en recourant à l'analyse du polymorphisme de longueur des fragments de restriction par réaction en chaîne de polymérase. (who.int)
Affect1
- variations during pregnancy affect lipid metabolism. (who.int)
Discuss1
- Discuss how metabolism is coordinated in mammals, and explain how disturbances in metabolism contribute to disease. (manchester.ac.uk)