Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In normal fed rats the low Km glucose transporter GLUT-1 is expressed only in one row of hepatocytes immediately surrounding a terminal hepatic venule, while the high Km GLUT-2 is expressed in every hepatocyte. Previously, we showed that additional perivenous hepatocytes express GLUT-1 in fasting animals. In diabetes, as in starvation, the liver functions to release glucose into the circulation, but unlike starvation, circulating extracellular glucose is high in diabetes. By immunofluorescence and Western blotting we studied whether glucose or insulin is the primary extracellular signal for inducing GLUT-1 expression in hepatocytes. We observed that streptozocin-induced diabetes causes induction of GLUT-1 expression in the plasma membrane of hepatocytes within four cell rows of a terminal hepatic venule; GLUT-2 expression is unaltered. Chronic insulin treatment of diabetic rats reduces the number of rows of hepatocytes expressing GLUT-1 from approximately four to approximately two. In contrast, chronic insulin infusion into nondiabetic rats does not affect the number of hepatocytes expressing GLUT-1. Thus, both fasting and diabetes induce GLUT-1 expression in specific hepatocytes that normally do not express this gene. This induction correlates with low insulin levels in the blood, and not with circulating glucose levels.
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PMID:Expression of the low Km GLUT-1 glucose transporter is turned on in perivenous hepatocytes of insulin-deficient diabetic rats. 191 77

The effects of a single intraperitoneal injection of methylglyoxal (50-800 mg/kg body wt.) in mice were investigated in the liver after 24 h. The administration of methylglyoxal (400 mg/kg body wt.) resulted in an increase in aniline hydroxylase activity in liver microsomes. At the same time an accumulation of p-amino-phenol, the hydroxylated product of aniline, was observed in isolated hepatocytes upon addition of aniline similarly to conditions (starvation, diabetes mellitus, pyrazole pretreatment) when aniline hydroxylase was induced. Methylglyoxal also decreased the reduced glutathione content in the liver, while the activity of serum glutamate pyruvate transaminase was increased, suggesting the onset of liver injuries. It is assumed that the increased oxidation of aniline hydroxylase combined with decreased glutathione levels after methylglyoxal treatment favours the formation of potentially hazardous phenol derivatives in the liver.
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PMID:Accumulation of phenols in isolated hepatocytes after pretreatment with methylglyoxal. 194 76

To elucidate the peripheral ketone body uptake and the role of insulin in regulating peripheral ketone body utilization in starvation and diabetes mellitus, uptake of beta-hydroxybutyrate (BOHB) was investigated in the perfused hindquarter of starved (72 hour) or streptozotocin-induced (65 mg/kg, intraperitoneally) diabetic rats. Blood concentration of BOHB was significantly higher in diabetic (1,380 +/- 250 mumol/L) and starved (1,229 +/- 245 mumol/L) rats than in controls (104 +/- 8 mumol/L). The hindquarter was perfused with synthetic medium at a flow rate of 0.5 mL/g muscle weight/min. BOHB was added to the medium at a concentration of 0.1, 0.5, 2, or 10 mmol/L, and insulin was added at a concentration of 20, 100, or 500 microU/mL. In the hindquarter perfused with 0.1, 0.5, 2, or 10 mmol/L BOHB, fractional uptake of BOHB in the absence or presence of insulin was significantly lower in diabetic and starved rats than in controls. The addition of 100 or 500 microU/mL insulin significantly increased BOHB uptake in the perfused hindquarter of control rats; however, insulin addition did not significantly increase BOHB uptake in the perfused hindquarter of starved and diabetic rats. These results suggest that BOHB uptake is markedly reduced in the perfused hindquarter of starved and diabetic rats, and that physiological dose of insulin stimulates BOHB uptake in control rats, but not in starved and diabetic rats.
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PMID:Uptake of beta-hydroxybutyrate in perfused hindquarter of starved and diabetic rats. 196 Nov 22

The ability of the initiation factor eIF-2 in skeletal muscle extracts to form ternary initiation complexes ([Met-tRNA(f).eIF-2.GDP]) is decreased by either starvation or diabetes. These conditions also impair the ability of muscle extracts to dissociate [eIF-2.GDP], suggesting inhibition of the guanine nucleotide exchange reaction essential for eIF-2 recycling. We could not, however, detect any change in the phosphorylation state of the alpha subunit of eIF-2. This suggests that eIF-2 activity may be regulated in this system by a mechanism not involving its phosphorylation.
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PMID:Effect of starvation and diabetes on the activity of the eukaryotic initiation factor eIF-2 in rat skeletal muscle. 207 92

Hormonal modulation of hepatic plasma membrane lactate transport was studied in primary cultures of isolated hepatocytes from fed rats to examine the mechanism for the known enhancement of lactate transport in starvation and diabetes. Total cellular lactate entry was increased by 14% in the presence of dexamethasone; this was accounted for by an approximately 40% increase in the carrier-mediated component of entry with no effect on diffusion. A trend of similar magnitude was evident with glucagon. The effects of dexamethasone and glucagon on lactate transport constitute an additional potential mechanism for enhancement of gluconeogenesis by these hormones.
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PMID:Hormonal modulation of hepatic plasma membrane lactate transport in cultured rat hepatocytes. 208 71

The effects of chemical diabetes and fasting on fuel metabolism and insulin secretory activity in late pregnancy were investigated. Female Wistar rats were made chemically diabetic (CD) by intravenous injection of streptozotocine (30 mg/kg) 2 weeks before conception. When CD pregnant rats were fed, plasma glucose and insulin levels were not significantly different from those of normal pregnant rats. Ketone body levels, however, were higher in CD pregnant rats than in normal pregnant rats, indicating insulin resistance in CD rats. Insulin secretion from the perfused pancreas caused by arginine or glucose was markedly decreased in CD pregnant rats. The pregnant rats were fasted for 2 days, from day 19 to 21 of gestation. Plasma glucose and insulin concentrations decreased similarly in the two groups, whereas ketone body concentrations in CD pregnant rats were significantly higher than those in normal pregnant rats. Glucose-induced insulin secretion by the perfused pancreas was markedly attenuated by fasting and was not significantly different in normal and CD pregnant rats. These observations suggest that diabetes mellitus accelerates starvation in late gestation, due to increased insulin resistance and poor insulin secretion, and that fasting in diabetic pregnancy amplifies ketogenesis.
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PMID:Insulin release from the pancreas and fuel metabolism during late gestation in chemically diabetic rats. 215 Aug 11

The response of peripheral tissues to insulin is reduced in fasting and diabetes mellitus. The experiments described herein were designed to determine whether insulin-stimulated glucose oxidation is affected by the free-fatty acid-derived plasma metabolites acetone, acetol, and propylene glycol (1,2-propanediol [1,2-PD]), concentrations of which are elevated in both starvation and diabetic ketosis. In epididymal adipose tissue from fed and 48-h--fasted rats given 3% acetone drinking water for 7 days, insulin-stimulated glucose oxidation was reduced by approximately 30-40%. After ingestion of 2% acetol for 7 days, basal and insulin-stimulated glucose oxidation was lowered approximately 30%, whereas the consumption of 1,2-PD had no influence on either basal or insulin-stimulated glucose oxidation. Similar effects on glucose oxidation were observed in isolated adipocytes from fed rats after ingestion of 3% acetone and 2% acetol for 7 days. The reduction in insulin-stimulated glucose oxidation in adipose tissue in vitro required the consumption of 3% acetone water for greater than 3 days. In 48-h--fasted rats that ingested 3% acetone for 5 days, insulin-stimulated glucose oxidation remained depressed 4 days after withdrawal of acetone from the drinking water. These studies imply that at least part of the insulin resistance indigenous to fasting and diabetic ketosis may be attributed to the metabolic influence of acetone and/or acetol in body fluids.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1990 Apr
PMID:Acetone and acetol inhibition of insulin-stimulated glucose oxidation in adipose tissue and isolated adipocytes. 218 Jul 56

The effects of various metabolic conditions inducing an overproduction of ketone bodies in the rat were studied at different levels of D-beta-hydroxybutyrate dehydrogenase expression, i.e., enzymatic activity and protein content in purified mitochondria, and translational activity of isolated free cytosolic polysomes. The strongest variations were obtained in diabetes mellitus where the D-beta-hydroxybutyrate dehydrogenase expression is largely decreased. Insulin can reverse this strong effect. Modulation of liver enzyme activity and of enzyme content was observed under the other conditions tested, i.e., a decrease and an increase in starvation and hyperlipidemic conditions, respectively. A comparative study was carried out on the enzyme of extrahepatic tissues, i.e., heart, kidney and brain. The results indicate that the D-beta-hydroxybutyrate dehydrogenase function appears to be controlled, at least at the translational, post-translational and catalytic levels.
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PMID:Metabolic control of the expression of mitochondrial D-beta-hydroxybutyrate dehydrogenase, a ketone body converting enzyme. 231 5

To elucidate the possible role of thyroid hormone in somatomedin-C (SmC)/insulin-like growth factor I regulation in diabetes mellitus and starvation, plasma SmC, liver SmC, and kidney SmC concentrations were measured in streptozotocin-induced (60 mg/kg) diabetic and starved (for 72 h) rats. Triiodothyronine (T3, 5.0 micrograms/kg every 24 h) was subcutaneously injected into diabetic rats for 7 days and into starved rats at 12, 36, and 60 h after starvation. Plasma T3, plasma SmC, liver SmC, and kidney SmC concentrations were significantly decreased in diabetic and starved rats. T3 administration restored plasma T3 levels to the normal value in diabetic and starved rats. Plasma SmC and kidney SmC concentrations were significantly increased in T3-treated starved rats, while they were not increased in T3-treated diabetic rats. These results suggest that thyroid hormone may have some role in SmC regulation during starvation, but may have no role in diabetes mellitus in the rat.
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PMID:Possible role of thyroid hormone in decreased somatomedin-C levels in diabetic and starved rats. 233 Nov 41

Serine dehydratase was induced in the kidneys of normal rats by the administration of either glucagon or dexamethasone. The increase in enzyme activity was associated with an increase in both enzyme protein and its mRNA, which were determined respectively by Western blot and RNA blot analysis. No apparent differences were observed between kidney and liver in the molecular weights of serine dehydratase proteins and the sizes of their mRNAs. Although kidney serine dehydratase was dramatically induced by either glucagon or dexamethasone, the liver enzyme was induced by glucagon but not by dexamethasone alone in the intact rat. On the other hand, liver serine dehydratase was induced in starvation, diabetes mellitus, and a high-protein diet. The kidney enzyme could not be induced under any of these conditions.
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PMID:Regulation of the expression of the serine dehydratase gene in the kidney and liver of the rat. 238 71


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