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 present study was performed to further clarify the possible role played by insulin deficiency on the steroidogenic capacity of the rat testis. Sprague-Dawley rats weighing 250-300 g were used in all experiments. Diabetes was induced by i.p. injection (40 mg/kg b.w.) of streptozotocin and was monitored at 2-day intervals by measuring body weight and serum glucose, glucosuria and ketonuria levels. The effect of insulin therapy on pituitary LH content and plasma LH concentrations, as well as on the cyclic AMP level in interstitial cell incubation medium and plasma testosterone concentrations, was measured 30 days after the induction of diabetes by radioimmunoassay. Streptozotocin-induced diabetes resulted in significantly reduced pituitary LH (16%, P less than 0.025) and plasma LH (34%, P less than 0.02); insulin treatment completely restored these levels. Similarly, the cyclic AMP content of interstitial cell incubation medium and the plasma testosterone concentrations were dramatically decreased in the diabetic state (50%, P less than 0.005 and 63%, P less than 0.025, respectively) and combined treatment with insulin plus hCG appeared slightly more effective than treatment with either of these hormones alone, suggesting a possible synergistic action. It is concluded that decreased testicular steroidogenesis in the diabetic rat may represent, at least in part, a direct consequence of insulin deficiency at the hypothalamic and/or pituitary levels. However, our findings would also be consistent with other reports suggesting that insulin may play a direct role in the rat testis.
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PMID:Effect of streptozotocin-diabetes and insulin treatment on regulation of Leydig cell function in the rat. 298 62

The activities of either the mitochondrial or cytosolic glycerol phosphate dehydrogenase (mGPD, cGPD) plus that of glycerol kinase are required for the use of glycerol in aerobic metabolism and gluconeogenesis. A knockout mouse lacking mGPD has reduced body weight and fertility but shows remarkably normal liver and muscle metabolite levels. The BALB/cHeA mouse strain, which lacks cGPD, breeds well and is phenotypically normal, although it demonstrates metabolite abnormalities in certain tissues. Crosses were made between these two strains, and mice were generated that lacked both dehydrogenases. These mice, although active and nursing well for several days, failed to grow, and usually died within the first week. Liver glycerol phosphate levels were elevated 30-fold, whereas liver ATP, ADP, and AMP levels were reduced by 30-40%. Plasma glycerol was elevated 30- to 50-fold to 30-50 mm, and urine glycerol exceeded 0.45 m (4% w/v). GPD-deficient mice were hypoglycemic, had a 50% increase in plasma free fatty acids, and developed ketonuria within the first day of life. Uncoupling protein-1 mRNA in brown adipose tissue was reduced 60%. These mice share some features of both glycerol kinase deficiency and hereditary fructose intolerance, suggesting the phenotype may be due to the combined effects of the loss of a gluconeogenic substrate, the osmotic effects of glycerol, and the metabolic effects of the accumulation of a phosphorylated metabolite.
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PMID:Lethal hypoglycemic ketosis and glyceroluria in mice lacking both the mitochondrial and the cytosolic glycerol phosphate dehydrogenases. 1209