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Query: UMLS:C0162275 (ketonuria)
 553 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pregnancy in diabetic mothers is associated with intrauterine death, perinatal mortality, and birth weight greater than that of infants born of normal mothers. The use of rodents made diabetic by alloxan or streptozotocin as an animal model for human diabetic pregnancy has been controversial because of the severity of the diabetes as well as the direct effect of diabetogenic drugs on the developing organism. Among our female NOD (nonobese diabetic) mice, insulin-dependent diabetes occurs spontaneously in 9% by 12 weeks and in 80% by 29 weeks of age. Offspring born within 21 days of conception to mildly hyperglycemic NOD pregnant mice between 26 and 52 weeks of age, and prior to the onset of maternal ketonuria are macrosomic with an average of 31% increase in body weight and 44% increase in kidney weight, in comparison to controls. Besides organomegaly, the macrosomic offspring have significantly higher pancreatic insulin content which was elevated 80% when compared with that of controls, and litter sizes are significantly 50% smaller. These results suggest that the mildly hyperglycemic pregnant NOD mouse represents a promising model for the study of pregnancy complicated by diabetes.
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PMID:The offspring of the female diabetic "nonobese diabetic" (NOD) mouse are large for gestational age and have elevated pancreatic insulin content: a new animal model of human diabetic pregnancy. 354 10

Biosynthetic Human Insulin (BHI) was administered to 20 diabetics for six months. A clinical examination, glycaemia before and after eating, total glycosuria-ketonuria, and glycosylated haemoglobin tests were performed at fixed intervals, and the results were statistically analysed. It is concluded that human insulin produces no significant side effects. More important that the type of insulin treatment is effective outpatients surveillance of the diabetic, to ensure an adequate metabolic compensation.
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PMID:[Our experience with biosynthetic human insulin]. 390 39

Plasma lipoprotein and lipoprotein lipase activity have been evaluated in young diabetics with and without ketonuria and in healthy controls of the same age. Fifteen (age range 7-23 years) newly detected diabetics (8 with ketonuria, 7 non ketonuric) have been examined before starting the treatment. Five healthy medical students (age range 19-21 years) have also been studied. Both ketotic and non ketotic patients showed an impaired insulin and C-peptide response to the glucose load in comparison to controls. Ketotic patients had low lipoprotein lipase activity (p less than 0.01) and high density lipoprotein (p less than 0.01); total plasma Triglycerides and VLDL Triglyceride and Cholesterol were higher than in controls. Plasma Triglyceride and VLDL Triglyceride and Cholesterol were inversely related to lipoprotein lipase activity. Low lipoprotein lipase activity, from adipose tissue and muscle, has been found to be associated with hypertriglyceridemia and reduced HDL Cholesterol in young diabetic patients with ketonuria.
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PMID:Plasma lipoproteins and lipoprotein lipase in young diabetics with and without ketonuria. 390 44

In an attempt to explain the rarity of ketonuria in Indian diabetics, plasma glucose, insulin and free fatty acid (FFA) levels were measured in 35 non-obese patients with non-insulin-dependent diabetes in the young and 35 matched controls during a 100 g oral glucose tolerance test. Compared with the controls, the patients had a severe degree of hyperglycaemia, fasting hyperinsulinism, and an attenuated and delayed insulinaemic response. However, in addition to the fasting plasma FFA levels being similar in the two groups, the decrement in the FFA responses was equivalent. Thus, the hormone-sensitive lipase of the adipose tissue appeared to be sensitive to inhibition by insulin. Also, the fasting insulin:glucagon molar ratios were computed and found to be no different in the two groups. The normal fasting FFA levels, relative sensitivity to insulin of lipolysis in the adipocyte and normal insulin: glucagon molar ratios may help to explain in part the general rarity of ketosis-prone diabetes in the South African Indian population.
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PMID:A plausible explanation for the aketonuria of young Indian non-insulin-dependent diabetics. 392 67

The relationship between the dose of intravenously administered streptozotocin (a N-nitroso derivative of glucosamine) and the diabetogenic response has been explored by use of the following indices of diabetogenic action: serum glucose, urine volume, and glycosuria, ketonuria, serum immunoreactive insulin (IRI), and pancreatic IRI content. Diabetogenic activity could be demonstrated between the doses of 25 and 100 mg/kg, all indices used showing some degree of correlation with the dose administered. Ketonuria was only seen with the largest dose, 100 mg/kg. The most striking and precise correlation was that between the dose and the pancreatic IRI content 24 hr after administration of the drug, and it is suggested that this represents a convenient test system either for both related and unrelated beta cytotoxic compounds or for screening for modifying agents or antidiabetic substances of a novel type. Ability to produce graded depletion of pancreatic IRI storage capacity led to an analysis of the relationship between pancreatic IRI content and deranged carbohydrate metabolism. Abnormal glucose tolerance and insulin response were seen when pancreatic IRI was depleted by about one-third, while fasting hyperglycemia and gross glycosuria occurred when the depletion had reached two-thirds and three-quarters, respectively. The mild yet persistent anomaly produced by the lowest effective streptozotocin dose, 25 mg/kg, exhibits characteristics resembling the state of chemical diabetes in humans and might thus warrant further study as a possible model. Finally, the loss of the diabetogenic action of streptozotocin by pretreatment with nicotinamide was confirmed and was shown to be a function of the relative doses of nicotinamide and streptozotocin and of the interval between injections.
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PMID:Diabetogenic action of streptozotocin: relationship of dose to metabolic response. 424 8

A survey of ketonuria in insulin-treated diabetics showed that its significance might vary according to the time of day at which the test was performed. Some of the patients had uncontrolled diabetes in the early morning, when severe hyperglycaemia and hyperketonaemia occurred together, while later during the same day or night an episode of hypoglycaemia caused hyperketonaemia, indicating that too much insulin had been given. Correct assessment of the significance of ketonuria is obviously important, because some patients would probably require a decrease rather than an increase of insulin dosage. Ketonuria does not necessarily indicate impending ketoacidosis.
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PMID:Interrelationships of blood sugar and ketones in insulin-treated diabetics. 498 85

The metabolic effects of oral ingestion of minute quantities of carbohydrate during prolonged starvation were studied in nine obese subjects. Measurements were made during a control period of total starvation, during the ingestion of 7.5 g carbohydrate daily, and finally during the ingestion of 15.0 g carbohydrate daily. Daily ketoacid excretion fell after carbohydrate ingestion and was significantly correlated (r = 0.62, P < 0.01) with the amount of carbohydrate administered. Despite this fall in ketoacids, the concentration of blood ketoacids, plasma free fatty acids, and serum insulin remained constant throughout the study. Urinary ammonium excretion, closely correlated with ketoacid output (r = 0.95, P < 0.001), also fell significantly after carbohydrate ingestion. No significant changes were present in extracellular or urinary pH. Urea nitrogen excretion did not change when urinary ammonium output fell. These results indicate that: the excretion of ketoacids and ammonium in starving man is exquisitely sensitive to minute amounts of ingested carbohydrate; the change in ketonuria appears to be due to increased renal ketoacid reabsorption after carbohydrate ingestion; and the nitrogen-sparing effect of reducing renal ammonium output in starvation can be dissociated from nitrogen sparing occurring because of changes in urine urea excretion.
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PMID:The effect of carbohydrates on ammonium and ketoacid excretion during starvation. 505 66

The effects of late pregnancy on metabolic fuels, liver composition, gluconeogenesis, and nitrogen metabolism have been examined in fed and fasted rats. Plasma free fatty acid (FFA) and immunoreactive insulin (IRI) are greater and glucose and ketones are lower in fed 19-day pregnant than they are in agematched virgin rats. A 48 hr fast elicits greater increases in FFA and ketones and more profound reductions in glucose in the pregnant rats and obliterates the differences in IRI. Fetal weight is not modified by such fasting but maternal weight losses exceed that of the nongravid rats. Livers from rats 19 days pregnant contain more and larger hepatocytes. Per mumole hepatic deoxyribonucleic acid (DNA)-phosphorus, water and protein are more abundant, whereas glycogen is unaffected. Livers from fed pregnant rats contain more lipid phosphorus and less neutral lipid fatty acid. After a 48 hr fast, hepatic steatosis supervenes in gravid animals due to accumulated neutral fat. The contents of hepatic acetyl-coenzyme A (CoA) and citric acid are not different in fed pregnant and virgin rats but are greater in the pregnant rats after fasting. Formation of glucose-(14)C and glycogen-(14)C from administered pyruvate-(14)C are the same in fed pregnant and virgin rats, but greater in the pregnant ones after a 24 or 48 hr fast. Pregnancy does not affect creatinine excretion, and urinary urea is not different in fed pregnant, virgin, and postpartum animals. Contrariwise, more nitrogen, potassium, and phosphorus are excreted by the pregnant animals during a 2 day fast. The increment in urinary nitrogen is due largely to urea on the 1st day, whereas heightened ammonia accounts for half the increase on the 2nd and correlates with the enhanced ketonuria. Muscle catabolism, gluconeogenesis, and diversion to fat are activated more rapidly and to a greater degree when food is withheld during late gestation in the rat. These catabolic propensities are restrained in the fed state. The capacity for "accelerated starvation" may confer survival benefit upon an intermittently eating mother in the presence of a continuously feeding fetus.
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PMID:Carbohydrate metabolism in pregnancy. VI. Plasma fuels, insulin, liver composition, gluconeogenesis, and nitrogen metabolism during late gestation in the fed and fasted rat. 535 39

The metabolic response to human growth hormone (HGH) was studied in five obese subjects in the fed state and during prolonged (5-6 wk) starvation. In the fed state (three subjects), HGH induced an elevation in basal serum insulin concentration, a minimal increase in blood and urine ketone levels, and a marked reduction in urinary nitrogen and potassium excretion resulting in positive nitrogen and potassium balance. In prolonged fasting (four subjects), HGH administration resulted in a 2- to 3-fold increase in serum insulin which preceded a 50% elevation in blood glucose. Persistence of the lipolytic effects of HGH was indicated by a rise in free fatty acids and glycerol. The response differed markedly from the fed state in that blood beta-hydroxybutyrate and acetoacetate levels rose by 20-40%, resulting in total blood ketone acid concentrations of 10-12 mmoles/liter, ketonuria of 150-320 mmoles/day, and increased urinary potassium loss. The subjects complained of nausea, vomiting, weakness, and myalgias. Despite a 50% reduction in urea excretion during HGH administration, total nitrogen loss remained unchanged as urinary ammonia excretion rose by 50% and correlated directly with the degree of ketonuria. It is concluded that in prolonged starvation (a) HGH may have a direct insulinotropic effect on the beta cell independent of alterations in blood glucose concentration, (b) persistence of the lipolytic action of HGH results in severe exaggeration of starvation ketosis and interferes with its anticatabolic action by necessitating increased urinary ammonia loss, and (c) failure of HGH to reduce net protein catabolism in starvation suggests that this hormone does not have a prime regulatory role in conserving body protein stores during prolonged fasting.
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PMID:Metabolic response to human growth hormone during prolonged starvation. 554 Jan 76

To delineate the hormonal mechanism of dietary-induced changes in sodium balance, the role of insulin and glucagon in natriuresis of fast was evaluated in obese subjects submitted to a total starvation and given either glucagon or somatostatin infusion on day 4 of fast. While large amounts of glucagon (1 mg over 6 h) stimulated concomitantly ketonaemia, ketonuria and renal sodium losses, the ten-times lower amounts of glucagon induced an increase in renal ketone body and sodium excretion without any significant change in ketonaemia. It was concluded, therefore, that elevated plasma glucagon level may enhance renal sodium loss in ketotic states, through a direct renal effect reducing tubular ketone body reabsorption, hence increased ketonuria and natriuresis. It appears nevertheless that decreased insulin secretion, rather than an increase in plasma glucagon level must be considered as a key hormonal factor responsible for natriuresis attending starvation. Indeed, the concomitant reduction in plasma glucagon and insulin levels, resulting from somatostatin infusion on day 4 of fast, was followed by significant increase in natriuresis. The latter observation supports several previous studies indicating that insulin stimulates sodium reabsorption by the kidney and that the reduction in insulin secretion may induce an increase in renal sodium excretion. It was concluded, therefore, that not only sodium intake but also the carbohydrate content of the diet should be reduced in an attempt to induce a negative sodium balance and to correct hypertension in obese subjects.
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PMID:Influence of insulin and glucagon on sodium balance in obese subjects during fasting and refeeding. 611 18


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