Peptides which stimulate INSULIN release from the PANCREATIC BETA CELLS following oral nutrient ingestion, or postprandially.
A gastrointestinal peptide hormone of about 43-amino acids. It is found to be a potent stimulator of INSULIN secretion and a relatively poor inhibitor of GASTRIC ACID secretion.
A peptide of 36 or 37 amino acids that is derived from PROGLUCAGON and mainly produced by the INTESTINAL L CELLS. GLP-1(1-37 or 1-36) is further N-terminally truncated resulting in GLP-1(7-37) or GLP-1-(7-36) which can be amidated. These GLP-1 peptides are known to enhance glucose-dependent INSULIN release, suppress GLUCAGON release and gastric emptying, lower BLOOD GLUCOSE, and reduce food intake.
Compounds that suppress the degradation of INCRETINS by blocking the action of DIPEPTIDYL-PEPTIDASE IV. This helps to correct the defective INSULIN and GLUCAGON secretion characteristic of TYPE 2 DIABETES MELLITUS by stimulating insulin secretion and suppressing glucagon release.
A serine protease that catalyses the release of an N-terminal dipeptide. Several biologically-active peptides have been identified as dipeptidyl peptidase 4 substrates including INCRETINS; NEUROPEPTIDES; and CHEMOKINES. The protein is also found bound to ADENOSINE DEAMINASE on the T-CELL surface and is believed to play a role in T-cell activation.
Peptides derived from proglucagon which is also the precursor of pancreatic GLUCAGON. Despite expression of proglucagon in multiple tissues, the major production site of glucagon-like peptides (GLPs) is the INTESTINAL L CELLS. GLPs include glucagon-like peptide 1, glucagon-like peptide 2, and the various truncated forms.
Cell surface receptors that bind glucagon with high affinity and trigger intracellular changes which influence the behavior of cells. Activation of glucagon receptors causes a variety of effects; the best understood is the initiation of a complex enzymatic cascade in the liver which ultimately increases the availability of glucose to body organs.
Surgical procedure in which the STOMACH is transected high on the body. The resulting small proximal gastric pouch is joined to any parts of the SMALL INTESTINE by an end-to-side SURGICAL ANASTOMOSIS, depending on the amounts of intestinal surface being bypasses. This procedure is used frequently in the treatment of MORBID OBESITY by limiting the size of functional STOMACH, food intake, and food absorption.
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.
A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511)
The condition of weighing two, three, or more times the ideal weight, so called because it is associated with many serious and life-threatening disorders. In the BODY MASS INDEX, morbid obesity is defined as having a BMI greater than 40.0 kg/m2.
Surgical procedures aimed at affecting metabolism and producing major WEIGHT REDUCTION in patients with MORBID OBESITY.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
A type of pancreatic cell representing about 50-80% of the islet cells. Beta cells secrete INSULIN.
Glucose in blood.
Substances which lower blood glucose levels.
The time frame after a meal or FOOD INTAKE.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
A test to determine the ability of an individual to maintain HOMEOSTASIS of BLOOD GLUCOSE. It includes measuring blood glucose levels in a fasting state, and at prescribed intervals before and after oral glucose intake (75 or 100 g) or intravenous infusion (0.5 g/kg).

Beneficial effects of GLP-1 on endothelial function in humans: dampening by glyburide but not by glimepiride. (1/231)

Sulfonylureas (SU) with glucagon-like peptide-1 (GLP-1)-based therapy are an emerging therapeutic combination for type 2 diabetes. Prior human studies have hinted at endothelial effects of GLP-1 and SU. To study the endothelial effects of GLP-1 per se and to evaluate the modulatory effects, if any, of SU agents on GLP-1-induced changes in endothelial function, healthy, nondiabetic, normotensive, nonsmokers, age 18-50 yr with no family history of diabetes, were studied. Subjects were randomized to either placebo (n = 10), 10 mg of glyburide (n = 11), or 4 mg of glimepiride (n = 8) orally. Euglycemic somatostatin pancreatic clamp with replacement basal insulin, glucagon, and growth hormone was performed for 240 min. Forearm blood flow (FBF) was measured by venous occlusion plethysmography with graded brachial artery infusions of acetylcholine (Ach) and nitroprusside (NTP) before and after intravenous infusion of GLP-1. GLP-1 (preinfusion 3.4 +/- 0.2, postinfusion 25.5 +/- 2.8 pM) enhanced (P < 0.03) Ach-mediated vasodilatation (Delta+6.5 +/- 1.1 vs. Delta+9.1 +/- 1.2 ml.100 ml(-1).min(-1), change from baseline FBF) in those on placebo. However, in contrast, glyburide abolished GLP-1-induced Ach-mediated vasodilatation (Delta+11.7 +/- 2.0 vs. Delta+11.7 +/- 2.5 ml.100 ml(-1).min(-1)). On the other hand, glimepiride did not alter the ability of GLP-1 to enhance Ach-mediated vasodilatation (Delta+7.9 +/- 0.5 vs. Delta+10.2 +/- 1.3 ml.100 ml(-1).min(-1), P < 0.04). Neither GLP-1 nor SU altered NTP-induced vasodilatation. These data demonstrate that GLP-1 per se has direct beneficial effects on endothelium-dependent vasodilatation in humans that are differentially modulated by SU.  (+info)

Incretin receptors for glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide are essential for the sustained metabolic actions of vildagliptin in mice. (2/231)

OBJECTIVE: Dipeptidyl peptidase-4 (DPP4) inhibitors lower blood glucose in diabetic subjects; however, the mechanism of action through which these agents improve glucose homeostasis remains incompletely understood. Although glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP) represent important targets for DPP4 activity, whether additional substrates are important for the glucose-lowering actions of DPP4 inhibitors remains uncertain. RESEARCH DESIGN AND METHODS: We examined the efficacy of continuous vildagliptin administration in wild-type (WT) and dual incretin receptor knockout (DIRKO) mice after 8 weeks of a high-fat diet. RESULTS: Vildagliptin had no significant effect on food intake, energy expenditure, body composition, body weight gain, or insulin sensitivity in WT or DIRKO mice. However, glycemic excursion after oral glucose challenge was significantly reduced in WT but not in DIRKO mice after vildagliptin treatment. Moreover, vildagliptin increased levels of glucose-stimulated plasma insulin and reduced levels of cholesterol and triglycerides in WT but not in DIRKO mice. Vildagliptin treatment reduced the hepatic expression of genes important for cholesterol synthesis and fatty acid oxidation, including phospho-mevalonate kinase (Mvk), acyl-coenzyme dehydrogenase medium chain (Acadm), mevalonate (diphospho)decarboxylase (Mvd), and Acyl-CoA synthetase (Acsl1), in WT but not in DIRKO mice. However, vildagliptin also reduced levels of hepatic mRNA transcripts for farnesyl di-phosphate transferase (Fdft1), acetyl coenzyme A acyltransferase 1 (Acaa1), and carnitine palmitoyl transferase 1 (Cpt 1) in DIRKO mice. No direct effect of GLP-1 receptor agonists was detected on cholesterol or triglyceride synthesis and secretion in WT hepatocytes. CONCLUSIONS: These findings illustrate that although GLP-1 and GIP receptors represent the dominant molecular mechanisms for transducing the glucoregulatory actions of DPP4 inhibitors, prolonged DPP4 inhibition modulates the expression of genes important for lipid metabolism independent of incretin receptor action in vivo.  (+info)

GIP receptor antagonism reverses obesity, insulin resistance, and associated metabolic disturbances induced in mice by prolonged consumption of high-fat diet. (3/231)

The gut hormone gastric inhibitory polypeptide (GIP) plays a key role in glucose homeostasis and lipid metabolism. This study investigated the effects of administration of a stable and specific GIP receptor antagonist, (Pro(3))GIP, in mice previously fed a high-fat diet for 160 days to induce obesity and related diabetes. Daily intraperitoneal injection of (Pro(3))GIP over 50 days significantly decreased body weight compared with saline-treated controls, with a modest increase in locomotor activity but no change of high-fat diet intake. Plasma glucose, glycated hemoglobin, and pancreatic insulin were restored to levels of chow-fed mice, and circulating triglyceride and cholesterol were significantly decreased. (Pro(3))GIP treatment also significantly decreased circulating glucagon and corticosterone, but concentrations of GLP-1, GIP, resistin, and adiponectin were unchanged. Adipose tissue mass, adipocyte hypertrophy, and deposition of triglyceride in liver and muscle were significantly decreased. These changes were accompanied by significant improvement of insulin sensitivity, meal tolerance, and normalization of glucose tolerance in (Pro(3))GIP-treated high-fat-fed mice. (Pro(3))GIP concentrations peaked rapidly and remained elevated 24 h after injection. These data indicate that GIP receptor antagonism using (Pro(3))GIP provides an effective means of countering obesity and related diabetes induced by consumption of a high-fat, energy-rich diet.  (+info)

Gliptins: a new class of oral hypoglycaemic agent. (4/231)

The epidemic of type 2 diabetes worldwide continues unabated. Despite a number of existing therapies, treatment goals are seldom fully achieved. While insulin resistance and beta cell failure remain important in the pathogenesis of the condition, the role of incretin hormones in glucose homeostasis has recently become clearer. Incretins have several glucoregulatory mechanisms, and a novel approach to the treatment of type 2 diabetes focuses on enhancing and prolonging the physiological actions of these hormones. Gliptins inhibit the enzyme dipeptidyl peptidase-IV (DPP-IV), which degrades incretin hormones. These drugs are a promising new class of oral hypoglycaemic medication, which appear to be weight-neutral and have few side-effects, although the published clinical studies are mainly regulatory licensing studies. As these drugs now are available for clinical use, we discuss the mechanism of action, efficacy and potential adverse effects of this new class of oral hypoglycaemic agent.  (+info)

Differential antidiabetic efficacy of incretin agonists versus DPP-4 inhibition in high fat fed mice. (5/231)

OBJECTIVE: We examined whether chronic administration of a glucagon-like peptide 1 (GLP-1) receptor agonist exendin-4 (Ex-4), a glucose-dependent insulinotropic polypeptide (GIP) receptor agonist D-Ala(2)-GIP (DA-GIP), or a dipeptidyl peptidase-4 (DPP-4) inhibitor (DPP-4i) des-fluoro-sitagliptin produced comparable antidiabetic actions in high fat-fed mice. RESEARCH DESIGN AND METHODS: High fat-fed mice were administered twice-daily injections of Ex-4, DA-GIP, vehicle (saline), or vehicle with the addition of des-fluoro-sitagliptin (DPP-4i) in food to produce sustained inhibition of DPP-4 activity. RESULTS AND CONCLUSIONS: Mice treated with vehicle alone or DA-GIP exhibited progressive weight gain, whereas treatment with Ex-4 or DPP-4i prevented weight gain. Although Ex-4 improved oral glucose tolerance and insulin-to-glucose ratios after an intraperitoneal glucose tolerance test (IPGTT), DPP-4i had no significant effect after IPGTT but improved glucose excursion and insulin levels after an oral glucose tolerance test. The extent of improvement in glycemic control was more sustained with continuous DPP-4 inhibition, as evidenced by loss of glucose control evident 9 h after peptide administration and a significant reduction in A1C observed with DPP-4i but not with DA-GIP or Ex-4 therapy. DA-GIP, but not Ex-4 or DPP-4i, was associated with impairment in insulin sensitivity and increased levels of plasma leptin and resistin. Although none of the therapies increased beta-cell mass, only Ex-4-treated mice exhibited increased pancreatic mRNA transcripts for Irs2, Egfr, and Gck. These findings highlight significant differences between pharmacological administration of incretin receptor agonists and potentiation of endogenous GLP-1 and GIP via DPP-4 inhibition.  (+info)

Regulation of cAMP dynamics by Ca2+ and G protein-coupled receptors in the pancreatic beta-cell: a computational approach. (6/231)

In this report we describe a mathematical model for the regulation of cAMP dynamics in pancreatic beta-cells. Incretin hormones such as glucagon-like peptide 1 (GLP-1) increase cAMP and augment insulin secretion in pancreatic beta-cells. Imaging experiments performed in MIN6 insulinoma cells expressing a genetically encoded cAMP biosensor and loaded with fura-2, a calcium indicator, showed that cAMP oscillations are differentially regulated by periodic changes in membrane potential and GLP-1. We modeled the interplay of intracellular calcium (Ca(2+)) and its interaction with calmodulin, G protein-coupled receptor activation, adenylyl cyclases (AC), and phosphodiesterases (PDE). Simulations with the model demonstrate that cAMP oscillations are coupled to cytoplasmic Ca(2+) oscillations in the beta-cell. Slow Ca(2+) oscillations (<1 min(-1)) produce low-frequency cAMP oscillations, and faster Ca(2+) oscillations (>3-4 min(-1)) entrain high-frequency, low-amplitude cAMP oscillations. The model predicts that GLP-1 receptor agonists induce cAMP oscillations in phase with cytoplasmic Ca(2+) oscillations. In contrast, observed antiphasic Ca(2+) and cAMP oscillations can be simulated following combined glucose and tetraethylammonium-induced changes in membrane potential. The model provides additional evidence for a pivotal role for Ca(2+)-dependent AC and PDE activation in coupling of Ca(2+) and cAMP signals. Our results reveal important differences in the effects of glucose/TEA and GLP-1 on cAMP dynamics in MIN6 beta-cells.  (+info)

Glucagon-like peptide-1 and energy homeostasis. (7/231)

A growing body of evidence demonstrates the role of gut-derived hormones in the control of energy homeostasis. Among those intestinal signals, physiological and therapeutic interest has been drawn to glucagon-like peptide-1 (GLP-1). The main reasons are that this hormone 1) is secreted by epithelial intestinal L-cells in response to glucose and lipids, 2) enhances glucose-stimulated insulin secretion, 3) improves blood glucose profiles of type 2 diabetic patients by means of several actions on pancreatic hormone secretions, 4) reduces body weight and food intake, and 5) slows gastric emptying. Furthermore, recent evidence has suggested that the nervous system is a key player accounting for the beneficial role of GLP-1 on the control of energy homeostasis. Hence, the role of GLP-1 on the gut-to-brain axis is reviewed.  (+info)

Effects of protein on glycemic and incretin responses and gastric emptying after oral glucose in healthy subjects. (8/231)

BACKGROUND: Dietary interventions represent a promising therapeutic strategy to optimize postprandial glycemia. The addition of protein to oral glucose has been reported to improve the glycemic profile. OBJECTIVE: The aim of the current study was to evaluate the mechanisms by which protein supplementation lowers the blood glucose response to oral glucose. DESIGN: Nine healthy men were studied on 3 d each in a random order. Subjects consumed 300-mL drinks containing either 50 g glucose (Glucose), 30 g gelatin (Protein), or 50 g glucose with 30 g gelatin (Glucose + Protein) in water labeled with 150 mg [(13)C]acetate. Blood and breath samples were subsequently collected for 3 h to measure blood glucose and plasma insulin, glucagon-like peptide 1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) concentrations and gastric half-emptying time, which was calculated from (13)CO(2) excretion. RESULTS: The blood glucose response was less after Glucose + Protein than after Glucose (P < 0.005); GIP was lower (P < 0.005), and there were no significant differences in plasma insulin or GLP-1. Protein alone stimulated insulin, GLP-1, and GIP (P < 0.05 for each) without elevating blood glucose. The gastric half-emptying time was greater after Glucose + Protein than after Glucose (P < 0.05) and tended to be greater for Glucose than for Protein (P = 0.06). CONCLUSIONS: In healthy humans, the addition of protein to oral glucose lowers postprandial blood glucose concentrations acutely, predominantly by slowing gastric emptying, although protein also stimulates incretin hormones and non-glucose-dependent insulin release.  (+info)

Incretins are hormones that are released from the gut in response to food intake, with two major types being glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). These hormones stimulate the pancreas to produce insulin, suppress the release of glucagon from the pancreas, slow down gastric emptying, and promote satiety. Incretins play a significant role in regulating blood sugar levels after meals, and medications that mimic or enhance incretin action are used in the treatment of type 2 diabetes.

Gastric Inhibitory Polypeptide (GIP) is a 42-amino acid long peptide hormone that is released from the K cells in the duodenum and jejunum of the small intestine in response to food intake, particularly carbohydrates and fats. It is also known as glucose-dependent insulinotropic polypeptide.

GIP has several physiological effects on the body, including:

* Incretin effect: GIP stimulates the release of insulin from the pancreas in a glucose-dependent manner, which means that it only increases insulin secretion when blood glucose levels are high. This is known as the incretin effect and helps to regulate postprandial glucose levels.
* Inhibition of gastric acid secretion: GIP inhibits the release of gastric acid from the stomach, which helps to protect the intestinal mucosa from damage caused by excessive acid production.
* Increase in blood flow: GIP increases blood flow to the intestines, which helps to facilitate nutrient absorption.
* Energy storage: GIP promotes the storage of energy by increasing fat synthesis and reducing fat breakdown in adipose tissue.

Overall, GIP plays an important role in regulating glucose metabolism, energy balance, and gastrointestinal function.

Glucagon-like peptide 1 (GLP-1) is a hormone that is secreted by the intestines in response to food intake. It plays a crucial role in regulating blood sugar levels through several mechanisms, including stimulation of insulin secretion from the pancreas, inhibition of glucagon release, slowing gastric emptying, and promoting satiety. GLP-1 is an important target for the treatment of type 2 diabetes due to its insulin-secretory and glucose-lowering effects. In addition, GLP-1 receptor agonists are used in the management of obesity due to their ability to promote weight loss by reducing appetite and increasing feelings of fullness.

Dipeptidyl-Peptidase IV (DPP-4) inhibitors are a class of medications used to treat type 2 diabetes. They work by increasing the levels of incretin hormones, such as glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP), which help regulate blood sugar levels in the body.

Incretin hormones are released from the gut in response to food intake and promote insulin secretion, suppress glucagon secretion, slow down gastric emptying, and reduce appetite. However, these hormones are rapidly degraded by the enzyme DPP-4, which reduces their effectiveness.

DPP-4 inhibitors block the action of this enzyme, thereby increasing the levels of incretin hormones in the body and enhancing their effects on blood sugar control. Some examples of DPP-4 inhibitors include sitagliptin, saxagliptin, linagliptin, and alogliptin.

These medications are usually taken orally once or twice a day and are often used in combination with other diabetes medications, such as metformin or sulfonylureas, to achieve better blood sugar control. Common side effects of DPP-4 inhibitors include upper respiratory tract infections, headache, and nasopharyngitis (inflammation of the throat and nasal passages).

Dipeptidyl peptidase 4 (DPP-4) is a serine protease enzyme that is widely distributed in various tissues and organs, including the kidney, liver, intestines, and immune cells. It plays a crucial role in regulating several biological processes, such as glucose metabolism, immune function, and cell signaling.

In terms of glucose metabolism, DPP-4 is responsible for breaking down incretin hormones, including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which are released from the gut in response to food intake. These hormones stimulate insulin secretion from pancreatic beta cells, suppress glucagon release, and promote satiety, thereby helping to regulate blood sugar levels. By degrading GLP-1 and GIP, DPP-4 reduces their activity and contributes to the development of type 2 diabetes.

DPP-4 inhibitors are a class of drugs used to treat type 2 diabetes by blocking the action of DPP-4 and increasing incretin hormone levels, leading to improved insulin secretion and glucose control.

Glucagon-like peptides (GLPs) are hormones that are produced in the intestines in response to food consumption. They belong to a class of hormones known as incretins, which play a role in regulating blood sugar levels by stimulating the pancreas to produce insulin and inhibiting the release of glucagon.

There are two main types of GLPs: GLP-1 and GLP-2. GLP-1 is secreted in response to meals and stimulates the pancreas to produce insulin, suppresses glucagon production, slows gastric emptying, and promotes satiety. GLP-2, on the other hand, promotes intestinal growth and improves nutrient absorption.

GLP-1 receptor agonists are a class of medications used to treat type 2 diabetes. They mimic the effects of natural GLP-1 by stimulating insulin secretion, suppressing glucagon release, slowing gastric emptying, and promoting satiety. These medications have been shown to improve blood sugar control, reduce body weight, and lower the risk of cardiovascular events in people with type 2 diabetes.

Glucagon receptors are a type of G protein-coupled receptor found on the surface of cells in the body, particularly in the liver, fat, and muscle tissues. These receptors bind to the hormone glucagon, which is produced and released by the alpha cells of the pancreas in response to low blood sugar levels (hypoglycemia).

When glucagon binds to its receptor, it triggers a series of intracellular signaling events that lead to the breakdown of glycogen (a stored form of glucose) in the liver and the release of glucose into the bloodstream. This helps to raise blood sugar levels back to normal.

Glucagon receptors also play a role in regulating fat metabolism, as activation of these receptors in adipose tissue can stimulate the breakdown of triglycerides (a type of fat) into free fatty acids and glycerol, which can then be used as energy sources.

Abnormalities in glucagon receptor function or expression have been implicated in various metabolic disorders, including diabetes and obesity.

Gastric bypass is a surgical procedure that involves creating a small pouch in the stomach and rerouting the small intestine to connect to this pouch, thereby bypassing the majority of the stomach and the first part of the small intestine (duodenum). This procedure is typically performed as a treatment for morbid obesity and related health conditions such as type 2 diabetes, sleep apnea, and high blood pressure.

The smaller stomach pouch restricts food intake, while the rerouting of the small intestine reduces the amount of calories and nutrients that are absorbed, leading to weight loss. Gastric bypass can also result in hormonal changes that help regulate appetite and metabolism, further contributing to weight loss and improved health outcomes.

There are different types of gastric bypass procedures, including Roux-en-Y gastric bypass and laparoscopic gastric bypass. The choice of procedure depends on various factors such as the patient's overall health, medical history, and personal preferences. Gastric bypass is generally considered a safe and effective treatment for morbid obesity, but like any surgical procedure, it carries risks and requires careful consideration and preparation.

Diabetes Mellitus, Type 2 is a metabolic disorder characterized by high blood glucose (or sugar) levels resulting from the body's inability to produce sufficient amounts of insulin or effectively use the insulin it produces. This form of diabetes usually develops gradually over several years and is often associated with older age, obesity, physical inactivity, family history of diabetes, and certain ethnicities.

In Type 2 diabetes, the body's cells become resistant to insulin, meaning they don't respond properly to the hormone. As a result, the pancreas produces more insulin to help glucose enter the cells. Over time, the pancreas can't keep up with the increased demand, leading to high blood glucose levels and diabetes.

Type 2 diabetes is managed through lifestyle modifications such as weight loss, regular exercise, and a healthy diet. Medications, including insulin therapy, may also be necessary to control blood glucose levels and prevent long-term complications associated with the disease, such as heart disease, nerve damage, kidney damage, and vision loss.

Glucagon is a hormone produced by the alpha cells of the pancreas. Its main function is to regulate glucose levels in the blood by stimulating the liver to convert stored glycogen into glucose, which can then be released into the bloodstream. This process helps to raise blood sugar levels when they are too low, such as during hypoglycemia.

Glucagon is a 29-amino acid polypeptide that is derived from the preproglucagon protein. It works by binding to glucagon receptors on liver cells, which triggers a series of intracellular signaling events that lead to the activation of enzymes involved in glycogen breakdown.

In addition to its role in glucose regulation, glucagon has also been shown to have other physiological effects, such as promoting lipolysis (the breakdown of fat) and inhibiting gastric acid secretion. Glucagon is often used clinically in the treatment of hypoglycemia, as well as in diagnostic tests to assess pancreatic function.

Morbid obesity is a severe form of obesity, defined by a body mass index (BMI) of 40 or higher or a BMI of 35 or higher in the presence of at least one serious obesity-related health condition, such as diabetes, high blood pressure, or sleep apnea. It is called "morbid" because it significantly increases the risk of various life-threatening health problems and reduces life expectancy.

Morbid obesity is typically associated with significant excess body weight, often characterized by a large amount of abdominal fat, that can strain the body's organs and lead to serious medical complications, such as:

* Type 2 diabetes
* High blood pressure (hypertension)
* Heart disease
* Stroke
* Sleep apnea and other respiratory problems
* Nonalcoholic fatty liver disease (NAFLD)
* Osteoarthritis
* Certain types of cancer, such as breast, colon, and endometrial cancer

Morbid obesity can also have significant negative impacts on a person's quality of life, including mobility issues, difficulty with daily activities, and increased risk of mental health problems, such as depression and anxiety. Treatment for morbid obesity typically involves a combination of lifestyle changes, medication, and in some cases, surgery.

Bariatric surgery is a branch of medicine that involves the surgical alteration of the stomach, intestines, or both to induce weight loss in individuals with severe obesity. The primary goal of bariatric surgery is to reduce the size of the stomach, leading to decreased food intake and absorption, which ultimately results in significant weight loss.

There are several types of bariatric surgeries, including:

1. Roux-en-Y gastric bypass (RYGB): This procedure involves creating a small pouch at the top of the stomach and connecting it directly to the middle portion of the small intestine, bypassing the rest of the stomach and the upper part of the small intestine.
2. Sleeve gastrectomy: In this procedure, a large portion of the stomach is removed, leaving behind a narrow sleeve-shaped pouch that restricts food intake.
3. Adjustable gastric banding (AGB): This surgery involves placing an adjustable band around the upper part of the stomach to create a small pouch and limit food intake.
4. Biliopancreatic diversion with duodenal switch (BPD/DS): This is a more complex procedure that involves both restricting the size of the stomach and rerouting the small intestine to reduce nutrient absorption.

Bariatric surgery can lead to significant weight loss, improvement in obesity-related health conditions such as diabetes, high blood pressure, sleep apnea, and reduced risk of mortality. However, it is not without risks and complications, including infection, bleeding, nutrient deficiencies, and dumping syndrome. Therefore, careful consideration and evaluation by a multidisciplinary team are necessary before undergoing bariatric surgery.

Insulin is a hormone produced by the beta cells of the pancreatic islets, primarily in response to elevated levels of glucose in the circulating blood. It plays a crucial role in regulating blood glucose levels and facilitating the uptake and utilization of glucose by peripheral tissues, such as muscle and adipose tissue, for energy production and storage. Insulin also inhibits glucose production in the liver and promotes the storage of excess glucose as glycogen or triglycerides.

Deficiency in insulin secretion or action leads to impaired glucose regulation and can result in conditions such as diabetes mellitus, characterized by chronic hyperglycemia and associated complications. Exogenous insulin is used as a replacement therapy in individuals with diabetes to help manage their blood glucose levels and prevent long-term complications.

Insulin-secreting cells, also known as beta cells, are a type of cell found in the pancreas. They are responsible for producing and releasing insulin, a hormone that regulates blood glucose levels by allowing cells in the body to take in glucose from the bloodstream. Insulin-secreting cells are clustered together in the pancreatic islets, along with other types of cells that produce other hormones such as glucagon and somatostatin. In people with diabetes, these cells may not function properly, leading to an impaired ability to regulate blood sugar levels.

Blood glucose, also known as blood sugar, is the concentration of glucose in the blood. Glucose is a simple sugar that serves as the main source of energy for the body's cells. It is carried to each cell through the bloodstream and is absorbed into the cells with the help of insulin, a hormone produced by the pancreas.

The normal range for blood glucose levels in humans is typically between 70 and 130 milligrams per deciliter (mg/dL) when fasting, and less than 180 mg/dL after meals. Levels that are consistently higher than this may indicate diabetes or other metabolic disorders.

Blood glucose levels can be measured through a variety of methods, including fingerstick blood tests, continuous glucose monitoring systems, and laboratory tests. Regular monitoring of blood glucose levels is important for people with diabetes to help manage their condition and prevent complications.

Hypoglycemic agents are a class of medications that are used to lower blood glucose levels in the treatment of diabetes mellitus. These medications work by increasing insulin sensitivity, stimulating insulin release from the pancreas, or inhibiting glucose production in the liver. Examples of hypoglycemic agents include sulfonylureas, meglitinides, biguanides, thiazolidinediones, DPP-4 inhibitors, SGLT2 inhibitors, and GLP-1 receptor agonists. It's important to note that the term "hypoglycemic" refers to a condition of abnormally low blood glucose levels, but in this context, the term is used to describe agents that are used to treat high blood glucose levels (hyperglycemia) associated with diabetes.

The postprandial period is the time frame following a meal, during which the body is engaged in the process of digestion, absorption, and assimilation of nutrients. In a medical context, this term generally refers to the few hours after eating when the body is responding to the ingested food, particularly in terms of changes in metabolism and insulin levels.

The postprandial period can be of specific interest in the study and management of conditions such as diabetes, where understanding how the body handles glucose during this time can inform treatment decisions and strategies for maintaining healthy blood sugar levels.

Glucose is a simple monosaccharide (or single sugar) that serves as the primary source of energy for living organisms. It's a fundamental molecule in biology, often referred to as "dextrose" or "grape sugar." Glucose has the molecular formula C6H12O6 and is vital to the functioning of cells, especially those in the brain and nervous system.

In the body, glucose is derived from the digestion of carbohydrates in food, and it's transported around the body via the bloodstream to cells where it can be used for energy. Cells convert glucose into a usable form through a process called cellular respiration, which involves a series of metabolic reactions that generate adenosine triphosphate (ATP)—the main currency of energy in cells.

Glucose is also stored in the liver and muscles as glycogen, a polysaccharide (multiple sugar) that can be broken down back into glucose when needed for energy between meals or during physical activity. Maintaining appropriate blood glucose levels is crucial for overall health, and imbalances can lead to conditions such as diabetes mellitus.

A Glucose Tolerance Test (GTT) is a medical test used to diagnose prediabetes, type 2 diabetes, and gestational diabetes. It measures how well your body is able to process glucose, which is a type of sugar.

During the test, you will be asked to fast (not eat or drink anything except water) for at least eight hours before the test. Then, a healthcare professional will take a blood sample to measure your fasting blood sugar level. After that, you will be given a sugary drink containing a specific amount of glucose. Your blood sugar levels will be measured again after two hours and sometimes also after one hour.

The results of the test will indicate how well your body is able to process the glucose and whether you have normal, impaired, or diabetic glucose tolerance. If your blood sugar levels are higher than normal but not high enough to be diagnosed with diabetes, you may have prediabetes, which means that you are at increased risk of developing type 2 diabetes in the future.

It is important to note that a Glucose Tolerance Test should be performed under the supervision of a healthcare professional, as high blood sugar levels can be dangerous if not properly managed.

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