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)

The effect of feeding high amounts of polyols on rat metabolism was studied. Adult male rats were fed the basal diet or the same diet to which had been added either galactitol, mannitol or xylitol for 8 wk (final polyol level 200 g/kg diet). Although all three polyols retarded the growth rate of the animals, the polyols were well tolerated. The four experimental groups did not differ significantly (P greater than 0.01) in the following analyses: blood lactic acid and serum transaminases, amylase, lactate dehydrogenase, triglycerides, insulin, glucagon and corticosterone. Compared to rats fed the basal diet, galactitol rats had higher blood hemoglobin levels (P less than 0.01); those fed galactitol or mannitol had lower blood glucose (P less than 0.001 and P less than 0.01, respectively), and those fed mannitol had higher blood pyruvic acid (P less than 0.01). Rats fed any of the polyols had lower serum total cholesterol and liver ascorbic acid (P less than 0.001) than control rats. Rats fed mannitol had higher liver glycogen levels (P less than 0.001) than control rats. Irrespective of the structural differences between the pentitol and the hexitols, a number of common metabolic effects were found. The proposed mechanisms of these effects include 1) the slow absorption and the rapid intraluminal metabolism of the polyols and 2) the similar handling of these polyols in the liver by a dehydrogenase.
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PMID:Metabolic effects in rats of high oral doses of galactitol, mannitol and xylitol. 392 94

A comparative study on the insulinotropic effect of xylitol and glucose was undertaken using isolated rat islets of Langerhans. Xylitol and glucose showed equal insulinotropic effects when compared at equivalent dose levels. Xylitol-induced insulin release was not inhibited by either mannoheptulose or 2-deoxy-D-glucose whereas glucose-induced insulin release was significantly inhibited. Glucagon, caffeine and cyclic-AMP enhanced the insulinotropic effect of glucose and leucine significantly, but insulin release in response to xylitol was not affected. Arginine did not potentiate the insulin releasing effect of xylitol though leucine showed an additive effect. These findings suggest that the mode of action of xylitol may be different from that of glucose.
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PMID:Studies on xylitol-induced insulin secretion in vitro. 638 93

In diabetes, the capacity of urea nitrogen synthesis, ie, a substrate-independent measure of the hepatic conversion of amino nitrogen to urea nitrogen, is increased. Xylitol decreases urea synthesis in normal rats. Capacity of urea nitrogen synthesis and nitrogen balance were measured during intravenous alanine loading in control rats, rats with experimental diabetes (streptozocin 75 mg/kg), and rats with experimental diabetes infused with xylitol to 1 mmol/L. In control rats, capacity of urea nitrogen synthesis was 9.4 +/- 1.1 mumol/min per 100 g of body weight, and nitrogen balance -2.7 +/- 1.2 mumol/min per 100 g of body weight. In the diabetics, these values were markedly increased to 26.6 +/- 1.9 and -16.3 +/- 2.1 mumol/min per 100 g of body weight, respectively (p < 0.01). The infusion of xylitol normalized these values to 11.2 +/- 1.0 and -3.6 +/- 2.1 mumol/min per 100 g of body weight for capacity of urea nitrogen synthesis and nitrogen balance, respectively. Xylitol did not change glucagon or insulin. Xylitol improved the nitrogen economy of uncontrolled diabetic rats by decreasing urea synthesis. The mechanism is not settled, but it does not involve insulin or glucagon.
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PMID:Xylitol normalizes the accelerated hepatic capacity for conversion of amino nitrogen to urea nitrogen in diabetic rats. 827 59

The mechanisms by which triiodothyronine (T3), glucose, insulin, and glucagon regulate acetyl-CoA carboxylase expression in primary cultures of chick embryo hepatocytes have been investigated. Incubating hepatocytes with T3 in the absence of glucose caused a fourfold increase in acetyl-CoA carboxylase activity. Addition of glucose (20 mM) enhanced the T3-induced increase in acetyl-CoA carboxylase activity by threefold but had no effect on enzyme activity in the absence of T3. The effects of T3 and glucose on acetyl-CoA carboxylase activity were accompanied by similar changes in acetyl-CoA carboxylase mRNA levels, indicating that regulation occurred at a pretranslational step. Xylitol mimicked the effect of glucose on acetyl-CoA carboxylase mRNA abundance, suggesting that an intermediate(s) of the nonoxidative branch of the pentose phosphate pathway may be involved in mediating this response. Insulin accelerated the accumulation of acetyl-CoA carboxylase mRNA abundance caused by T3 and glucose but had no effect on steady-state levels of acetyl-CoA carboxylase mRNA in the absence or presence of T3. Glucagon caused a 65% decrease in the accumulation of acetyl-CoA carboxylase mRNA in hepatocytes incubated with T3 and glucose. The effects of T3, glucose, insulin, and glucagon on the abundance of acetyl-CoA carboxylase mRNA were accounted for by changes in the transcription rate of the acetyl-CoA carboxylase gene. These data support the hypothesis that T3, glucose, insulin, and glucagon play a role in mediating the effects of nutritional manipulation on transcription of acetyl-CoA carboxylase in liver.
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PMID:Triiodothyronine stimulates and glucagon inhibits transcription of the acetyl-CoA carboxylase gene in chick embryo hepatocytes: glucose and insulin amplify the effect of triiodothyronine. 901 9

The relation between xylitol concentration (1.0 and 5.5 mmol/1), the Capacity of Urea-N Synthesis, and the rate of Alanine Metabolism was investigated in nephrectomized rats of 200 g and compared with the effect of glucose at concentrations between 5.5 and 15.5 mmol/1. The xylitol and glucose concentrations were controlled by "clamp" techniques and the endogenous hormonal effects by somatostatin. The Capacity of Urea-N Synthesis was determined during alanine infusion to constant amino acid concentrations within the interval 7.3-11.6 mmol/1. The rate of alanine metabolism was assessed as alanine infusion rate corrected for changes in alanine concentration. At normal hormonal response, xylitol at 1.0 mmol/1 and 5.5 mmol/1 reduced urea synthesis from 10.3 +/- 1.1 mumol/(min.100 g) in controls to on average 6.2 +/- 0.9 mumol/(min.100 g) (mean +/- SD, n = 2 x 10, p < 1.01). Alanine metabolism was reduced to the same extent. Glucose concentration increased from 5.4 +/- 1.0 mmol/1 in controls to 8.1 +/- 1.4 mmol/1 at both xylitol concentrations. Xylitol reduced plasma glucagon concentration to one third and tripled plasma insulin concentration. During somatostatin and blood glucose maintained above 8 mmol/1, the Capacity of Urea-N Synthesis fell to 6.1 +/- 1.0 mumol/(min.100 g). In that situation, xylitol at 1.0 mmol/1 reduced neither urea synthesis nor alanine metabolism, whereas xylitol at 5.5 mmol/1 further reduced urea synthesis to 3.4 +/- mumol/(min.100 g) (n = 10, p < 0.05) and almost stopped alanine metabolism. Thus xylitol, independently of glucose and hormonal responses, inhibited urea synthesis and alanine metabolism. This may have therapeutic implications at catabolic conditions.
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PMID:Effects of xylitol versus glucose on urea synthesis and alanine metabolism in rats. 1683 75

With the increasing prevalence of obesity and a possible association with increasing sucrose consumption, nonnutritive sweeteners are gaining popularity. Given that some studies indicate that artificial sweeteners might have adverse effects, alternative solutions are sought. Xylitol and erythritol have been known for a long time and their beneficial effects on caries prevention and potential health benefits in diabetic patients have been demonstrated in several studies. Glucagon-like peptide-1 (GLP-1) and cholecystokinin (CCK) are released from the gut in response to food intake, promote satiation, reduce gastric emptying (GE), and modulate glucose homeostasis. Although glucose ingestion stimulates sweet taste receptors in the gut and leads to incretin and gastrointestinal hormone release, the effects of xylitol and erythritol have not been well studied. Ten lean and 10 obese volunteers were given 75 g of glucose, 50 g of xylitol, or 75 g of erythritol in 300 ml of water or placebo (water) by a nasogastric tube. We examined plasma glucose, insulin, active GLP-1, CCK, and GE with a [(13)C]sodium acetate breath test and assessed subjective feelings of satiation. Xylitol and erythritol led to a marked increase in CCK and GLP-1, whereas insulin and plasma glucose were not (erythritol) or only slightly (xylitol) affected. Both xylitol and erythritol induced a significant retardation in GE. Subjective feelings of appetite were not significantly different after carbohydrate intake compared with placebo. In conclusion, acute ingestion of erythritol and xylitol stimulates gut hormone release and slows down gastric emptying, whereas there is no or only little effect on insulin release.
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PMID:Gut hormone secretion, gastric emptying, and glycemic responses to erythritol and xylitol in lean and obese subjects. 2773 81