Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162275 (ketonuria)
 553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The absence of ketoacidosis is thought to be characteristic of generalized lipoatrophic diabetes. It is widely believed that lipoatrophic diabetic patients are able to tolerate starvation and therapeutic insulin withdrawal, due to absence of subcutaneous body fat, the substrate essential for ketogenesis. In this article, we document nine episodes of acidosis and accelerated ketone body formation in a 24-yr-old woman whose deterioration followed episodes of dietary excesses without evidence of intercurrent infection or other identifiable forms of metabolic stress. Serum C-peptide measurements demonstrated that an absolute insulin deficiency did not exist. During short-term, experimental, dietary manipulations, excess dietary calories worsened the hyperglycemia and hyperlipidemia but did not reproduce the ketoacidotic state. Excess fat added to the diet was the most poorly tolerated of the food groups, causing ketonuria, hypertriglyceridemia, and abdominal pain. Our experience with this patient suggests that increased food consumption, insufficient insulin relative to an insulin-resistant state, and increased amounts of insulin counterregulatory hormones (stress), acted in concert to cause acidosis and increased ketone body formation.
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PMID:Recurrent ketoacidosis in acquired, total lipodystrophy (lipoatrophic diabetes). 643 2

Myocardial membranes from rats rendered diabetic with streptozotocin were used to determine muscarinic receptors with 3H-quinuclidinyl benzilate. In the acute state of diabetes, four days after induction, the density of receptors were equal in controls, insulin (glucosuria) and non insulin-treated (glucosuria and ketonuria) diabetic animals. In myocardial membranes from diabetic rats agonist binding to the muscarinic receptor was shifted to higher affinity than in controls. Computer modeling revealed that guanine nucleotides transformed agonist binding from two sites to a site of low affinity in controls. In membranes from insulin-treated diabetic animals the shift to lower affinity occurred but two receptor sites remained. In non insulin-treated membranes the nucleotides failed to exert any effect. Inhibition of adenylate cyclase by the muscarinic agonist oxotremorine was amplified in diabetic membranes. This indicates that the function of the inhibitory nucleotide binding protein (NI), as reflected by agonist binding to the receptor and adenylate cyclase inhibition, is sensitive to the hormonal status.
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PMID:Effects of acute ketotic and non-ketotic diabetes on the myocardial muscarinic receptors. 644 90

A rapid paper-strip test for the semiquantitating 3-hydroxybutyrate (3-OHBA) has been developed. The color develops within 5 min after applying the serum to the paper strip, and the purple color was read either visually or by reflectance meter. This can detect 3-OHBA levels as low as 0.1 mmol/L up to 2.0 mmol/L. The more concentrated sample can be measured on serial dilution. Clinical usefulness has been tested in a summer camp for insulin-dependent diabetic children as well as in a routine diabetes clinic. Serum 3-OHBA levels ranged from greater than 100 mumol/L to 4 mmol/L in all the subjects before breakfast in a summer camp. In four subjects, 3-OHBA was elevated to the level of 2-4 mmol/L, and only one of these four subjects exhibited ketonuria by nitroprusside test. In a diabetes clinic, a new paper-strip test for 3-OHBA has revealed ketonemia in 34 (74%) of 46 diabetic subjects, while nitro-prusside test revealed ketonemia in only 4 (13%). The present paper-strip test for 3-OHBA is sensitive enough to detect levels as low as 0.1 mmol/L and is clinically useful for rapid detection of ketosis proneness as well as for monitoring of diabetes control.
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PMID:Development of paper-strip test for 3-hydroxybutyrate and its clinical application. 649 40

For 28 days, four steers received 1,3-butanediol, which causes ketonemia, and phlorizin, which causes glucosuria. Steers also were fasted for 9 days. Effects of treatments on concentrations of metabolites in blood and liver and on kinetics of glucose metabolism were determined. Treatments were: control, control with dietary butanediol plus injected phlorizin, and fasting. Fasting caused hypoinsulinemia and decreased liver glycogen by 60%. Butanediol plus phlorizin and fasting caused 18 and 19% decreases of plasma glucose and 2.5- and 6-fold increases of free fatty acid concentrations in blood plasma. Glucose irreversible loss averaged 371, 541, and 182 g/day during control, butanediol plus phlorizin treatment, and fasting. Butanediol plus phlorizin increased liver ketone body concentrations, caused glucosuria, ketonuria, and ketonemia, but did not affect insulin, glucagon, or growth hormone concentrations in plasma or triglyceride and glycogen contents in liver. Steers given butanediol plus phlorizin did not show all the usual signs of lactation ketosis, but the treatment still offers promise for studying causes and effects of ketosis.
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PMID:Plasma and liver metabolites and glucose kinetics as affected by prolonged ketonemia-glucosuria and fasting in steers. 650 47

Ninety-four infants of 28 weeks gestation or more were born to 85 women, 64 type I and 21 gestational diabetics, between 1969-1972 at Sabbatsberg's Hospital, Stockholm. Perinatal mortality rate was 6.3%. The follow-up study was conducted when the children were approximately 5 years of age and included a physical and a neurological evaluation, IQ determination of mother and child, and an interview of mother by a psychologist. Fifty-three infants of insulin-dependent (IDM) and 20 infants of gestational diabetic mothers (IGDM) (83%) participated, 3 families could not be traced and 12 were unwilling. The group lost to follow-up (13 IDM, 2 IGDM) had more perinatal complications including congenital malformations than the follow-up group. All children had normal physical and neurological development. IQ was normal, the majority were above 100, the average in IDM was 115 (range 98-144) and 112 in IGDM (range 95-133). No obvious relationship was found between maternal acetonuria during pregnancy, infant birthweight, blood glucose during first hours after birth or neonatal complications and IQ of the children. A correlation (r = 0.364, p less than 0.01) was found between maternal and child IQ. Mothers exhibiting emotional disorders (anxiety, depression) had significantly higher life stress scores based on 29 stress variables and reported more frequently about conduct and behavioural disorders in their children than mothers without emotional disturbances.
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PMID:Follow-up of children of insulin-dependent and gestational diabetic mothers. Neuropsychological outcome. 674 37

Insulin binding to monocytes was assessed before and after plasma insulin suppression by diazoxide in 14 obesity-related diabetic subjects. Four of the five patients with mild carbohydrate intolerance (FBS less than 150 mg%) and hyperinsulinism exhibited low monocyte insulin binding. Despite an increase in insulin binding after 7 days of diazoxide therapy, no improvement in carbohydrate tolerance could be demonstrated. Lack of improvement may have been related to persistent diazoxide effect. An additional group of 4 patients with low plasma insulin values and more severe carbohydrate intolerance (FBS greater than 150 mg%) had high monocyte insulin binding. This group, as well as a group of patients with intermediate insulin responses, tolerated diazoxide poorly and developed moderate ketonuria or severe hyperglycemia (plasma glucose greater than 350 mg%) necessitating discontinuation of the drug after 3-6 days. The studies in these patients suggest that obesity-related diabetes may be characterized early by mild elevation of plasma glucose, hyperinsulinism and impaired monocyte insulin binding. As beta cell exhaustion occurs, more severe hyperglycemia intervenes and insulin binding to monocytes increases.
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PMID:Role of insulin receptors in obesity-related diabetes. 675 56

Selection for and against diabetes and subsequent inbreeding of Chinese hamsters started in 1963. Currently there are six inbred sublines that have greater than 85% incidence of glycosuria and two control inbred nondiabetic sublines that are essentially free of glycosuria. At birth, hamsters from inbred sublines are considered prediabetic. There is phenotypic variation between diabetic sublines. Onset time, incidence of ketonuria, blood glucose, plasma insulin, glucagon and glycohydrolase levels vary from subline to subline, but pancreatic insulin and glucagon levels are consistently low and high, respectively, in all diabetic sublines compared with nondiabetics. Experimental breeding data suggest a minimum of two homozygous recessive genes for diabetes. It is not known if the inbred lines are similar diabetic genotypes, but the probability is high that modifier background genes vary from subline to subline. Chinese hamsters have diabetes ranging from mild to severe. Animals weighing 25 g can excrete up to 75 ml of urine containing 3 g of glucose per day. Fasting blood glucose as high as 500 mg/dl and 10 mumol/ml of beta-hydroxybutyrate have been reported. Gluconeogenesis is elevated, and some glycolytic enzymes are decreased in severe diabetes. Low levels of renal acid glycohydrolase enzymes may contribute to glomerular capillary loop basement membrane thickening in diabetic hamsters. Caloric restriction per se or reduction of dietary fat prevented onset of hyperglycemia and hyperinsulinemia in prediabetics. Morphologic changes have been observed in pancreatic islets, kidney, nerve, blood vessels, eyes, brain, and genito-urinary systems of diabetic Chinese hamsters. Pathogenesis of diabetes in this animal appears to be related to an increased demand for insulin. Initially there is a positive response to this demand by beta cells, but exhaustion occurs. This is followed by a decrease in beta-cell mass and relative or absolute insulin deficiency.
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PMID:The Chinese hamster as a model for the study of diabetes mellitus. 676 Nov 91

The large-scale clinical trials of human insulin (recombinant DNA) in the United States consisted of a "New Patient" study and a "Transfer" study. The "New Patient" study involved 101 patients (38% type I) who have never received insulin and who were treated with human insulin and followed for 6 mo using NPH insulin alone or in combination with Neutral Regular Insulin (NRI). Shortly after treatment, serum glucose and total glycohemoglobin concentration fell. No patients developed insulin lipoatrophy or insulin allergy. Two patients developed insulin hypertrophy; in one, it was transient. Intradermal tests to varying dilutions of human insulin did not change over 6 mo. In addition, there was no evidence of development of antibodies to Escherichia coli polypeptide. Two-hundred-and-forty-three patients, 91% of whom had type I diabetes, were transferred in a controlled double-blind study from mixed beef-pork or purified pork insulin (PPI) either to human insulin or back to their previous insulin treatment and followed for 3 mo. While insulin dosage did not change, there was a slight increase in fasting serum glucose and a statistically significant increase in fasting ketonuria. There was no change in the frequency of the complications of insulin treatment. These limited data are consistent with the conclusion that NPH human insulin is slightly shorter acting than its animal insulin counterparts. Overall, human insulin is a safe, effective insulin.
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PMID:The U.S. "new patient" and "transfer" studies. 676 25

Early morning ketonuria, as judged by Ketostix testing, occurred in 19% of urine samples from insulin-independent diabetic pregnant women eating 1000 calorie diets, in 14% from diabetics on higher calorie diets, and in 7% of urines from nondiabetic pregnant women. Ketostix test was never found to be positive in blood, even when it was 2+ in urine samples, and acetoacetate levels were always below 1 mmol/L. Enzymatic estimations of acetoacetate (AA) and beta-hydroxybutyrate (BB) in urine and plasma samples revealed (1) no significant differences in range or mean between the groups receiving different restricted diets or full diets, the highest value observed for plasma AA being 0.34 mmol/L; (2) that Ketostix became positive at a concentration of AA above 1 mmol/L and that such a value in urine corresponded to plasma levels of between 0.06 and 0.1 mmol/L, i.e., double the normal; and (3) a 50-100-fold increase in urine AA when blood levels exceeded 0.08 mmol/L. Neonates born to diabetic mothers with ketonuria had no fetal distress or asphyxia neonatorum. The lowest Apgar score at 5 min was 8; 80% of neonates had a score of 10. Hence, positive Ketostix tests in urine samples do not indicate toxic levels in the blood, and a 1000 calorie diet for obese pregnant diabetics appears to be safe as regards neonatal outcome.
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PMID:Ketonuria in pregnancy--with special reference to calorie-restricted food intake in obese diabetics. 676 24

Seven diabetic patients who had been dependent on insulin before pregnancy (classes B, C, D of White) threatened to go into premature labour between the 31st and 36th week of the pregnancy. They were treated by intravenous administration of Ritodrine, the dosage varying between 100 and 400 micrograms per minute. The changes in the mother consisted in a rise in the blood glucose level which rose from 140 +/- 34 mg % to 212 +/- 56 mg % (p less than 0.01). This occurred in spite of a mean rise of 49% of insulin (p less than 0.0025) and a moderate ketonuria in two patients and a severe acido-ketosis in two further patients. In five patients there were no effects on the fetus as far as repeated observations of the fetal heart rate could detect. On the other hand, in the two mothers who developed acido-ketosis during the transfusion the fetal heart rythm showed signs of acute fetal distress, which however was temporary. Oscillations were reduced and there were late decelerations. These disappeared when the maternal metabolic state was brought back to equilibrium. 13.1 +/- 7.3 days were gained for the fetus by using tocolytic treatment, and this is considered a success. Discussion of these cases is accompanied by a complete review of the literature of the administration of beta-mimetic drugs in diabetic women. The authors point out that special precautions have to be taken and special conditions have to be fulfilled when this type of treatment is used. These consist of changes in the amounts of insulin that are given and particularly careful observation of the fetal heart rhythm before and during treatment.
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PMID:[Intravenous administration of ritodrine to pregnant insulin-dependent diabetics. Metabolic impact]. 681 13


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