Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vivo studies in the rat during the weaning period and in vitro studies on cultured cells have shown that nutriments and pancreatic hormones play a major role in lipogenic enzyme gene expression in liver and adipose tissue. Activation of lipogenic enzyme gene expression in liver and adipose tissue is dependent upon the increased supply of glucose and the concomitant hyperinsulinemia that occur after weaning. In contrast, an elevated supply of polyunsaturated or an increased plasma glucagon level prevent lipogenic enzyme gene expression in liver and adipose tissue. Glucose-6-phosphate seems to be the intracellular metabolite that mediates the transcriptional activation of lipogenic enzyme genes in response to glucose.
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PMID:[Regulation of expression of genes coding for lipogenesis enzymes during development in the rat]. 758 Nov 99

Long term feeding a sucrose-rich diet (SRD) to normal Wistar rats led to multiphasic changes in the activity of the pyruvate dehydrogenase complex (PDH), characterized by a significant decrease in PDHa (active form) in the short term on SRD (3 weeks) when compared to control rats fed the standard chow (STD). Although PDHa returned spontaneously to control values in the medium term (6-8 weeks) on SRD, an even more pronounced decrease was recorded when rats were kept long term on the SRD (15 weeks). Low PDHa levels recorded in the short and long term were accompanied by a two fold increase in heart acetyl-CoA concentration and the acetyl-CoA/CoASH ratio. Tissue long-chain acyl-CoA and triacylglycerol levels were also significantly higher in SRD fed rats. Spontaneous normalization of all the above metabolic parameters was observed during the medium term on SRD. Glucose-6-phosphate levels remained within control values during the short and medium term, in contrast to a two fold increase recorded in the long term on SRD. Glycogen concentrations were found moderately elevated only in the long term. Citrate concentrations were slightly increased in the short and greatly in the long term, and the fructose-2,6-bisphosphate/citrate ratio was found significantly decreased only during the long term on SRD. After 3 weeks on SRD, the protal vein Insulin/Glucagon (I/G) molar ratio was three times higher in SRD than STD rats, as opposed to an unchanged I/G ratio found in the long term.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multiphasic metabolic changes in the heart of rats fed a sucrose-rich diet. 783 21

The effect of small amounts of fructose on net hepatic glucose uptake (NHGU) during hyperglycemia was examined in the presence of insulinopenia in conscious 42-h fasted dogs. During the study, somatostatin (0.8 microg.kg(-1).min(-1)) was given along with basal insulin (1.8 pmol.kg(-1).min(-1)) and glucagon (0.5 ng.kg(-1).min(-1)). After a control period, glucose (36.1 micromol.kg(-1).min(-1)) was continuously given intraportally for 4 h with (2.2 micromol.kg(-1).min(-1)) or without fructose. In the fructose group, the sinusoidal blood fructose level (nmol/ml) rose from <16 to 176 +/- 11. The infusion of glucose alone (the control group) elevated arterial blood glucose (micromol/ml) from 4.3 +/- 0.3 to 11.2 +/- 0.6 during the first 2 h after which it remained at 11.6 +/- 0.8. In the presence of fructose, glucose infusion elevated arterial blood glucose (micromol/ml) from 4.3 +/- 0.2 to 7.4 +/- 0.6 during the first 1 h after which it decreased to 6.1 +/- 0.4 by 180 min. With glucose infusion, net hepatic glucose balance (micromol.kg(-1).min(-1)) switched from output (8.9 +/- 1.7 and 13.3 +/- 2.8) to uptake (12.2 +/- 4.4 and 29.4 +/- 6.7) in the control and fructose groups, respectively. Average NHGU (micromol.kg(-1).min(-1)) and fractional glucose extraction (%) during last 3 h of the test period were higher in the fructose group (30.6 +/- 3.3 and 14.5 +/- 1.4) than in the control group (15.0 +/- 4.4 and 5.9 +/- 1.8). Glucose 6-phosphate and glycogen content (micromol glucose/g) in the liver and glucose incorporation into hepatic glycogen (micromol glucose/g) were higher in the fructose (218 +/- 2, 283 +/- 25, and 109 +/- 26, respectively) than in the control group (80 +/- 8, 220 +/- 31, and 41 +/- 5, respectively). In conclusion, small amounts of fructose can markedly reduce hyperglycemia during intraportal glucose infusion by increasing NHGU even when insulin secretion is compromised.
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PMID:Inclusion of low amounts of fructose with an intraportal glucose load increases net hepatic glucose uptake in the presence of relative insulin deficiency in dog. 1567 Oct 83