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 an attempt to define the pancreatic B cell function in the elderly, we subjected 88 non-obese individuals (aged between 21 and 88) to an oral glucose tolerance test (OGTT), a simple glucagon test (SGT) and OGTT-glucagon test, in which the plasma glucose, insulin and serum C-peptide (CPR) were measured. We investigated heterogeneity in glucose intolerance in the elderly and its relationship to atherosclerosis. In the OGTT and SGT test, the insulin responses (SIRI/SPG ratios) for normal, borderline and DM1 (fasting plasma glucose less than 140 mg/dl and 2 h-PG greater than or equal to 200 mg/dl) groups of the elderly (60 and above) were not significantly different from those for normal group of young and middle-aged (below 60) and were significantly higher for elderly group than for the young and middle-aged group in each glucose tolerance group. But the insulin responses for the DM2 (fasting plasma glucose greater than or equal to 140 mg/dl and 2 h-PG greater than or equal to 200 mg/dl) group of the elderly were not significantly different from those for the DM1 and DM2 groups of young and middle-aged. The insulin responses of normal, borderline and DM1 groups of the elderly with atherosclerosis were significantly higher than those of the comparable groups without atherosclerosis, while the insulin responses of the borderline and DM1 groups of the elderly with atherosclerosis were similar to those of the control group of the young. In the OGTT-glucagon test, there were no differences in the insulin response or serum CPR response among the normal, borderline and DM1 groups of the elderly, and these responses were significantly higher for the elderly group than the for young and middle-aged group in each glucose tolerance group. But these responses for the DM2 group of the elderly were not significantly different from those for the DM1 and DM2 groups of the young and middle-aged. These results indicate that the pancreatic B cell function of the normal group in the elderly remains favorable while mildly impaired glucose tolerance was exhibited by the borderline and DM1 groups, who are comparable with the normal group of the young and middle-aged. But this function was clearly reduced in the DM2 group of the elderly. These findings suggest that there is a subgroup in the elderly, which has clinically evident atherosclerosis, mild glucose intolerance and high insulin response. Their pancreatic B cell function remains favorable.
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PMID:[Pancreatic B cell function and glucose intolerance in the elderly]. 265 22

The meal-stimulated release of pancreatic polypeptide (PP), gastrin, somatostatin and glucagon was studied in nine patients with myotonic dystrophy (MD) and in 11 healthy controls. PP-release was significantly reduced in MD compared to controls. This reduction may be related to the abnormal gut motility demonstrated in MD. The release of gastrin, somatostatin and glucagon was not significantly different in the two groups.
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PMID:Diminution of postprandial release of pancreatic polypeptide in myotonic dystrophy. 357 61

To clarify the possible participation of glucagon in glucose intolerance in myotonic dystrophy, six patients with myotonic dystrophy were examined. Three of the six patients had abnormal oral glucose tolerance curves; two had frank diabetic glucose tolerance curves, and the other had a high glucose value 30 min after glucose loading, which fell beyond the normal range (mean +/- 2 SD). The total insulin response to oral glucose, calculated as the insulin area, was significantly exaggerated (P less than 0.01 vs. the control value). In addition to these results, hyperglucagonemia was observed throughout the test in two patients with myotonic dystrophy. In the arginine infusion test, the insulin response was not as exaggerated. Plasma glucagon, however, was significantly higher (P less than 0.05 vs. the control value) 30, 45, and 60 min after arginine infusion, and the mean glucagon area under the curves was significantly greater (P less than 0.05 vs. the control value). None of the myotonic patients showed GH or cortisol excess during an arginine infusion and/or insulin tolerance test. Three patients with myotonic dystrophy who had abnormal glucose tolerance curves showed absolutely or relatively high glucagon levels and exaggerated responses to arginine infusion. These findings suggested that hyperglucagonemia might contribute to the appearance of glucose intolerance in myotonic dystrophy.
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PMID:Hyperglucagonemia in myotonic dystrophy. 700 30

In order to clarify the possible participation of glucagon in glucose intolerance in myotonic dystrophy, six patients with myotonic dystrophy were examined. Three out of the six patients had an abnormal oral glucose tolerance curve. Two had frank diabetic glucose tolerance curves and the other had a high glucose value at 30 min after glucose loading, which fell beyond the normal range (Mean +/- 2 S.D.). Total insulin response to oral glucose, calculated as insulin area, was significantly exaggerated (p less than 0.01 vs control value). In addition to these results, hyperglucagonemia was observed throughout the test in two patients with myotonic dystrophy. In the arginine infusion test, insulin response was not so exaggerated but plasma glucagon was significantly higher (p less than 0.05 vs control value) at each 30, 45, 60 minutes after arginine infusion, and the mean glucagon area under the curves was significantly greater (p less than 0.05 vs control value). None of the myotonic patients showed growth hormone or cortisol excess during an arginine infusion and/or insulin tolerance test. Three patients with myotonic dystrophy who had abnormal glucose tolerance curves showed absolutely or relatively high glucagon levels and exaggerated response to arginine infusion. These findings suggested that hyperglucagonemia might contribute to the appearance of glucose intolerance in myotonic dystrophy.
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PMID:[Clinical evaluation of hyperglucagonemia in patients with myotonic dystrophy (author's transl)]. 703 34

It has been suggested that insulin-induced suppression of endogenous glucose production (EGP) may be counteracted independently of increased epinephrine (Epi) or glucagon during moderate hypoglycemia. We examined EGP in nondiabetic (n = 12) and type 1 diabetic (DM1, n = 8) subjects while lowering plasma glucose (PG) from clamped euglycemia (5.6 mmol/l) to values just above the threshold for Epi and glucagon secretion (3.9 mmol/l). Individualized doses of insulin were infused to maintain euglycemia during pancreatic clamps by use of somatostatin (250 microg/h), glucagon (1.0 ng. kg(-1). min(-1)), and growth hormone (GH) (3.0 ng. kg(-1). min(-1)) infusions without need for exogenous glucose. Then, to achieve physiological hyperinsulinemia (HIns), insulin infusions were fixed at 20% above the rate previously determined for each subject. In nondiabetic subjects, PG was reduced from 5.4 +/- 0.1 mmol/l to 3.9 +/- 0.1 mmol/l in the experimental protocol, whereas it was held constant (5. 3 +/- 0.2 mmol/l and 5.5 mmol/l) in control studies. In the latter, EGP (estimated by [3-(3)H]glucose) fell to values 40% of basal (P < 0.01). In contrast, in the experimental protocol, at comparable HIns but with PG at 3.9 +/- 0.1 mmol/l, EGP was activated to values about twofold higher than in the euglycemic control (P < 0.01). In DM1 subjects, EGP failed to increase in the face of HIns and PG = 3.9 +/- 0.1 mmol/l. The decrease from basal EGP in DM1 subjects (4.4 +/- 1.0 micromol. kg(-1). min(-1)) was nearly twofold that in nondiabetics (2.5 +/- 0.8 micromol. kg(-1). min(-1), P < 0.02). When PG was lowered further to frank hypoglycemia ( approximately 3.1 mmol/l), the failure of EGP activation in DM1 subjects was even more profound but associated with a 50% lower plasma Epi response (P < 0. 02) compared with nondiabetics. We conclude that glucagon- or epinephrine-independent activation of EGP may accompany other counterregulatory mechanisms during mild hypoglycemia in humans and is impaired or absent in DM1.
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PMID:Hormone-independent activation of EGP during hypoglycemia is absent in type 1 diabetes mellitus. 1071 Apr 96

The adipose tissue is an endocrine organ that produces a variety of protein hormones. One of them is leptin, which regulates several critical functions at the central nervous system such as caloric intake, basal energy expenditure, reproduction, glucose and lipid metabolism and osteogenesis. Acting at a local level, leptin modulates the immune system and promotes liver fibrogenesis. The most promising therapeutic implications of leptin will possibly be in type 1 diabetes mellitus (DM1). Its supplementation in animal models of DM1 prevents hyperglycemia and ketoacidosis. These actions depend on the activation of leptin receptors in the central nervous system and the suppression of glucagon signaling in the liver.
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PMID:[Novel physiological and therapeutic implications of leptin]. 2532 19