Ketosis: A condition characterized by an abnormally elevated concentration of KETONE BODIES in the blood (acetonemia) or urine (acetonuria). It is a sign of DIABETES COMPLICATION, starvation, alcoholism or a mitochondrial metabolic disturbance (e.g., MAPLE SYRUP URINE DISEASE).3-Hydroxybutyric Acid: BUTYRIC ACID substituted in the beta or 3 position. It is one of the ketone bodies produced in the liver.Diabetic Ketoacidosis: A life-threatening complication of diabetes mellitus, primarily of TYPE 1 DIABETES MELLITUS with severe INSULIN deficiency and extreme HYPERGLYCEMIA. It is characterized by KETOSIS; DEHYDRATION; and depressed consciousness leading to COMA.Ketone Bodies: The metabolic substances ACETONE; 3-HYDROXYBUTYRIC ACID; and acetoacetic acid (ACETOACETATES). They are produced in the liver and kidney during FATTY ACIDS oxidation and used as a source of energy by the heart, muscle and brain.Ketogenic Diet: A course of food intake that is high in FATS and low in CARBOHYDRATES. This diet provides sufficient PROTEINS for growth but insufficient amount of carbohydrates for the energy needs of the body. A ketogenic diet generates 80-90% of caloric requirements from fats and the remainder from proteins.Hydroxybutyrates: Salts and esters of hydroxybutyric acid.Acetoacetates: Salts and derivatives of acetoacetic acid.Parturient Paresis: A disease of pregnant and lactating cows and ewes leading to generalized paresis and death. The disease, which is characterized by hypocalcemia, occurs at or shortly after parturition in cows and within weeks before or after parturition in ewes.Acidosis: A pathologic condition of acid accumulation or depletion of base in the body. The two main types are RESPIRATORY ACIDOSIS and metabolic acidosis, due to metabolic acid build up.Cattle Diseases: Diseases of domestic cattle of the genus Bos. It includes diseases of cows, yaks, and zebus.Butylene Glycols: 4-carbon straight chain aliphatic hydrocarbons substituted with two hydroxyl groups. The hydroxyl groups cannot be on the same carbon atom.Peripartum Period: The period shortly before, during, and immediately after giving birth.Acetone: A colorless liquid used as a solvent and an antiseptic. It is one of the ketone bodies produced during ketoacidosis.Diabetic Coma: A state of unconsciousness as a complication of diabetes mellitus. It occurs in cases of extreme HYPERGLYCEMIA or extreme HYPOGLYCEMIA as a complication of INSULIN therapy.Megasphaera: A genus of gram-negative bacteria in the family ACIDAMINOCOCCACEAE, found in the RUMEN of SHEEP and CATTLE, and also in humans.Abomasum: The fourth stomach of ruminating animals. It is also called the "true" stomach. It is an elongated pear-shaped sac lying on the floor of the abdomen, on the right-hand side, and roughly between the seventh and twelfth ribs. It leads to the beginning of the small intestine. (From Black's Veterinary Dictionary, 17th ed)Selenomonas: Curved bacteria, usually crescent-shaped rods, with ends often tapered, occurring singly, in pairs, or short chains. They are non-encapsulated, non-sporing, motile, and ferment glucose. Selenomonas are found mainly in the human buccal cavity, the rumen of herbivores, and the cecum of pigs and several rodents. (From Bergey's Manual of Determinative Bacteriology, 9th ed)Hyperglycemic Hyperosmolar Nonketotic Coma: A serious complication of TYPE 2 DIABETES MELLITUS. It is characterized by extreme HYPERGLYCEMIA; DEHYDRATION; serum hyperosmolarity; and depressed consciousness leading to COMA in the absence of KETOSIS and ACIDOSIS.Placenta, Retained: A placenta that fails to be expelled after BIRTH of the FETUS. A PLACENTA is retained when the UTERUS fails to contract after the delivery of its content, or when the placenta is abnormally attached to the MYOMETRIUM.KetonesLameness, Animal: A departure from the normal gait in animals.Fatty Acids, Nonesterified: FATTY ACIDS found in the plasma that are complexed with SERUM ALBUMIN for transport. These fatty acids are not in glycerol ester form.DairyingCoenzyme A-Transferases: Enzymes which transfer coenzyme A moieties from acyl- or acetyl-CoA to various carboxylic acceptors forming a thiol ester. Enzymes in this group are instrumental in ketone body metabolism and utilization of acetoacetate in mitochondria. EC 2.8.3.Stomach Diseases: Pathological processes involving the STOMACH.
KetosisDiabetic ketoacidosisKetogenesisCyclic ketogenic diet: A cyclic ketogenic diet (or carb-cycling) is a low-carbohydrate diet with intermittent periods of high or moderate carbohydrate consumption. This is a form of the general Ketogenic diet that is used as a way to maximize fat loss while maintaining the ability to perform high-intensity exercise.Polyhydroxybutyrate: Polyhydroxybutyrate (PHB) is a polyhydroxyalkanoate (PHA), a polymer belonging to the polyesters class that are of interest as bio-derived and biodegradable plastics.Frieder W.Acetoacetic acidDowner (animal): A downer is an animal, usually livestock, that cannot stand on its own and therefore is to be killed. A downed animal, one that is unable to stand, is not necessarily a downer.AcidosisSecoisolariciresinol diglucosidePeripartum cardiomyopathyPhenylacetoneDiabetic comaAbomasitis: Abomasitis (abomasal bloat) is a relatively rare ruminant disease characterized by inflammation of abomasum in young calves, lambs, and goat kids. It occurs with gastroenteritis but is seldom diagnosed as a separate condition, and its causes are as yet unknown.Hyperosmolar syndrome: Hyperosmolar syndrome or diabetic hyperosmolar syndrome is a medical emergency caused by a very high blood glucose level.Friesian horseDiketoneSidebone: Sidebone is a common condition of horses, characterized by the ossification of the collateral cartilages of the coffin bone. These are found on either side of the foot protruding above the level of the coronary band.Supercow (dairy): Supercow (or super cow) is a term used in the dairy industry to denote lines or individual animals that have superior milk production: that is, which produce more milk per day, or in some cases produce more fat per gallon of milk. Biology of the super cow.Reactive gastropathy: In gastroenterology, reactive gastropathy, also chemical gastropathy, is an abnormality in the stomach caused by chemicals, e.g.
(1/154) Effect of acute ketosis on the endothelial function of type 1 diabetic patients: the role of nitric oxide.
In type 1 diabetic patients, acute loss of metabolic control is associated with increased blood flow, which is believed to favor the development of long-term complications. The mechanisms for inappropriate vasodilation are partially understood, but a role of endothelium-derived nitric oxide (NO) production can be postulated. We assessed, in type 1 diabetic patients, the effect of the acute loss of metabolic control and its restoration on forearm endothelial function in 13 type 1 diabetic patients who were studied under conditions of mild ketosis on two different occasions. In study 1, after basal determination, a rapid amelioration of the metabolic picture was obtained by insulin infusion. In study 2, seven type 1 diabetic patients underwent the same experimental procedure, except that fasting plasma glucose was maintained constant throughout. Basal plasma venous concentrations of nitrites/nitrates (NO2- + NO3-) were determined both before and after intravenous insulin infusion. Endothelium-dependent and -independent vasodilation of the brachial artery was assessed by an intra-arterial infusion of N(G)-monomethyl-L-arginine (L-NMMA) and sodium nitroprusside (SNP), respectively. The same parameters were determined in 13 control subjects at baseline conditions and during a hyperinsulinemic-euglycemic glucose clamp. Baseline forearm blood flow (4.89 +/- 0.86 vs. 3.65 +/- 0.59 ml x (100 ml tissue)(-1) x min(-1)) and NO2- + NO3- concentration (30 +/- 8 vs. 24 +/- 3 micromol/l) were higher in type 1 diabetic patients than in control subjects (P < 0.05). Insulin infusion was associated with lower forearm blood flow and plasma (NO2- + NO3-) concentration (P < 0.05), irrespective of the prevailing glucose levels, as compared with patients under ketotic conditions. The responses to L-NMMA were significantly lower in type 1 diabetic patients during euglycemia and hyperglycemic hyperinsulinemia (-11 +/- 5 and -10 +/- 4%, respectively, of the ratio of the infused arm to the control arm) than in control subjects at baseline (-18 +/- 6%, P < 0.05) and during hyperinsulinemia (-32 +/- 11%, P < 0.01). We conclude that the acute loss of metabolic control is associated with a functional disturbance of the endothelial function characterized by hyperemia and increased NO release during ketosis and blunted NO-mediated vasodilatory response during restoration of metabolic control by intravenous insulin. This functional alteration is unlikely to be explained by hyperglycemia itself. (+info)
(2/154) Human brain beta-hydroxybutyrate and lactate increase in fasting-induced ketosis.
Ketones are known to constitute an important fraction of fuel for consumption by the brain, with brain ketone content generally thought to be low. However, the recent observation of 1-mmol/L levels of brain beta-hydroxybutyrate (BHB) in children on the ketogenic diet suggests otherwise. The authors report the measurement of brain BHB and lactate in the occipital lobe of healthy adults using high field (4-T) magnetic resonance spectroscopy, measured in the nonfasted state and after 2- and 3-day fasting-induced ketosis. A 9-mL voxel located in the calcarine fissure was studied, detecting the BHB and lactate upfield resonances using a 1H homonuclear editing sequence. Plasma BHB levels also were measured. The mean brain BHB concentration increased from a nonfasted level of 0.05 +/- 0.05 to 0.60 +/- 0.26 mmol/L (after second day of fasting), increasing further to 0.98 +/- 0.16 mmol/L (after the third day of fasting). The mean nonfasted brain lactate was 0.69 +/- 0.17 mmol/L, increasing to 1.47 +/- 0.22 mmol/L after the third day. The plasma and brain BHB levels correlated well (r = 0.86) with a brain-plasma slope of 0.26. These data show that brain BHB rises significantly with 2- and 3-day fasting-induced ketosis. The lactate increase likely results from ketones displacing lactate oxidation without altering glucose phosphorylation and glycolysis. (+info)
(3/154) Reduction in serum lecithin:cholesterol acyltransferase activity prior to the occurrence of ketosis and milk fever in cows.
Lecithin:cholesterol acyltransferase (LCAT) is the enzyme responsible for production of cholesteryl esters in plasma. The LCAT activity is reduced in cows with fatty liver developed during the nonlactating stage and those with the fatty liver-related postparturient diseases such as ketosis. The purpose of the present study was to examine whether reduced LCAT activity during the nonlactating stage could be detected before the occurrence of postparturient diseases. Sera from 24 cows were collected at approximately 10-day intervals from -48 to +14 days from parturition. Of the 24 cows, 14 were apparently healthy, whereas 7 had ketosis and 3 had milk fever at around parturition. Of the 14 healthy cows, 7 had unaltered LCAT activity during the observation period, whereas 7 showed reduced activity from -20 to +14 days. Ketosis and milk fever occurred at from -3 to +10 days, but reductions of LCAT activity in diseased cows had already been observed from days -20 to 0. These results suggest that LCAT activity is virtually unaffected during the peripartum period at least in some healthy cows and also that the reduction in LCAT activity can be detected before the occurrence of ketosis and milk fever. (+info)
(4/154) Decreased concentration of serum apolipoprotein C-III in cows with fatty liver, ketosis, left displacement of the abomasum, milk fever and retained placenta.
Apolipoprotein (apo) C-III is a low molecular mass protein mainly distributed in the high-density lipoprotein (HDL) fraction. In cows with postparturient diseases such as ketosis, concentrations of cholesterol, phospholipids and apoA-I and the activity of lecithin:cholesterol acyltransferase, which are mainly distributed in or functionally associated with HDL, are reduced. The purpose of the present study was to examine whether the serum concentration of apoC-III was similarly decreased in the postparturient diseases. Compared with healthy controls, the apoC-III concentration was significantly (P<0.01) decreased in cows with fatty liver, ketosis, left displacement of the abomasum, milk fever and retained placenta. Concentrations of apoC-III in the HDL fractions from diseased cows were also lower than in controls. Of the diseased cows, the decreased apoC-III concentration was particularly distinct in cows with milk fever. Increased nonesterified fatty acid and reduced free cholesterol, cholesteryl ester and phospholipid concentrations were observed in cows with milk fever, as in the other diseased cows. The decrease in the apoC-III concentration is suggested to be closely associated with the postparturient disorders, in particular with milk fever. (+info)
(5/154) Diabetic ketoacidosis associated with recurrent pulmonary edema and rhabdomyolysis in a patient with Turner's syndrome.
Turner's syndrome is a condition involving total or partial absence of one X chromosome and has been associated with a number of diseases including non insulin dependent diabetes mellitus, abnormalities of glucose metabolism and hypothreosis. There have been many case reports in which Turner's syndrome is associated with type 2 diabetes, but the association with type 1 diabetes and/or life threatening complications is very rare. We present an unusual case of a patient with Turner's syndrome who has type 1 diabetes and is complicated with ketoacidosis, severe acute and recurrent pulmonary edema and rhabdomyolysis. (+info)
(6/154) Field study of dairy cows with reduced appetite in early lactation: clinical examinations, blood and rumen fluid analyses.
The study included 125 cows with reduced appetite and with clinical signs interpreted by the owner as indicating bovine ketosis 6 to 75 days postpartum. Almost all of the cows were given concentrates 2 to 3 times daily. With a practitioners view to treatment and prophylaxis the cows were divided into 5 diagnostic groups on the basis of thorough clinical examination, milk ketotest, decreased protozoal activity and concentrations, increased methylene blue reduction time, and increased liver parameters: ketosis (n = 32), indigestion (n = 26), combined ketosis and indigestion (n = 29), liver disease combined with ketosis, indigestion, or both (n = 15), and no specific diagnosis (n = 17). Three cows with traumatic reticuloperitonitis and 3 with abomasal displacement were not grouped. Nonparametric methods were used when groups were compared. Aspartate aminotransferase, glutamate dehydrogenase, gamma-glutamyl transferase and total bilirubin were elevated in the group with liver disease. Free fatty acids were significantly elevated in cows with ketosis, compared with cows with indigestion. Activity and concentrations of large and small protozoas were reduced, and methylene blue reduction time was increased in cows with indigestion. The rumen fluid pH was the same for groups of cows with and without indigestion. Prolonged reduced appetite before examination could have led to misclassification. Without careful interpretation of the milk ketotest, many cases with additional diagnoses would have been reported as primary ketosis. Thorough clinical examination together with feasible rumen fluid examination and economically reasonable blood biochemistry did not uncover the reason(s) for reduced appetite in 14% of the cows. More powerful diagnostic methods are needed. (+info)
(7/154) Lipid metabolism in the cow during starvation-induced ketosis.
1. Concentrations and compositions of liver, serum and milk lipids of cows were measured during 6 days' starvation and serum lipids during 60 days' re-feeding. 2. The concentration of free fatty acid in serum increased fivefold during starvation. 3. The content of total lipid in liver (g/100g of liver dry matter) doubled owing to a 20-fold increase in triglyceride, an eightfold increase in cholesterol ester, a three fold increase in free fatty acid and a 20% increase in cholesterol. There were no changes in the content or composition of liver phospholipids. 4. Starvation lowered the concentrations of total lipid, phospholipid and cholesterol ester of dextran sulphate-precipitable serum lipoproteins. Total lipid and cholesterol ester concentrations in lipoproteins of d greater than 1.055 and in lipoproteins not precipitable by dextran sulphate decreased from day 4 of the starvation period and during the first 20 days' re-feeding. 5. During starvation there were decreases in percentages of stearic acid and increases in oleic acid in serum free fatty acids and triglycerides and in liver neutral lipid. 6. Throughout starvation total milk lipid yield decreased, yields and percentages of C4-14 fatty acids decreased and percentages of C18 fatty acids increased. 7. It is suggested that accumulation of triglyceride in liver may be caused by increased uptake of plasma free fatty acids without corresponding increase in lipoprotein secretion. (+info)
(8/154) Breath acetone as a measure of systemic ketosis assessed in a rat model of the ketogenic diet.
BACKGROUND: The mechanism of a high-fat, low-carbohydrate ketogenic diet (KD) in alleviating drug-resistant epilepsy is unknown but may be related to systemic ketosis induced under this treatment. The need for frequent measurement of systemic ketosis, which is essential for improving maintenance of the KD in patients and for studying mechanism of the KD action, has prompted us to validate the breath acetone test as a fast, reliable, and noninvasive tool for ketosis assessment. METHODS: A rat model of the KD that allowed frequent blood sampling was used to investigate how well breath acetone reflects plasma beta-hydroxybutyrate (beta-HBA), the most commonly measured ketone body. Rat pups (20 days of age) were introduced to and maintained on a KD or control diet for 33 days. During this period, breath acetone, plasma beta-HBA, blood glucose, and body weight were measured approximately every 4th day. A correlational analysis of breath acetone and plasma beta-HBA was conducted. RESULTS: Breath acetone was found to be a significant predictor of plasma beta-HBA over a clinically relevant range of beta-HBA concentrations (r(2) = 0.75; P <0.001). We have proposed a general formula that allows the value of plasma beta-HBA to be estimated based on breath acetone measurement. CONCLUSIONS: Breath acetone is an accurate measure of mild to moderate systemic ketosis. The noninvasive nature of this test will be useful for day-to-day implementation of the KD, searching for better forms of this diet, and understanding the role of ketosis in the mechanism of the KD action. (+info)