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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the dynamics of insulin and of glucagon secretion in response to several sequential stimuli administered shortly after an arginine pulse (5 g), 20 nonobese, apparently healthy volunteers were given arginine (5 g), glucose (5 g), and tolbutamide (1 g) by rapid intravenous injection. The early insulin and glucagon area 0-8 min was studied. At the intervals and with the dosages used in this study, different stimuli with and without prestimulation with arginine did not lead to changes in early secretion of insulin. There was no exhaustion of the pool of insulin released after multiple sequential pulses. These results suggest a pattern in which stimulation induces a rapid release of insulin and activates the interchange between the stored and labile insulin pool; the 8-min interval is sufficient for the rapid return of the two compartments to a state of equilibrium. Also for glucagon, subsequent different stimuli did not exhaust glucagon release; nevertheless, glucagon is immediately suppressed by a submaximal glucose pulse.
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PMID:Early insulin and glucagon response to subsequent pulses of arginine, glucose, and tolbutamide in normal man. 36 91

Seven young, healthy subjects performed bicycle exercise with a working load leading to exhaustion after one hour of work. The tests were done in the afternoon in the fed state. The serum insulin concentrations decreased from 22 to 4 mU/l and plasma glucagon increased from 241 to 340 pg/l already after 30 min of work. The level of adipose tissue lipoprotein lipase activity (LPLA) did not fall as had been expected, but increased. The skeletal muscle LPLA was unchanged. The results indicate that during the first hour of heavy exercise the heparin-releasable LPLA in tissues is not influenced by the work induced changes in serum hormone levels.
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PMID:Lipoprotein-lipase activity of human skeletal-muscle and adipose tissue after intensive physical exercise. 44 62

The importance of autonomic nervous activity for the pancreatic hormonal response to exercise in man was studied. 7 men ran at 58% of V(O2)max (determined without administration of drugs) to exhaustion during alpha-adrenergic blockade with phentolamine (P), during parasympathetic blockade with atropine (A), or without drugs (C). At rest phentolamine increased the plasma concentrations of both insulin and norepinephrine. During exercise norepinephrine concentrations increased and were in P experiments 3 times the concentrations in C experiments. Insulin always declined during exercise but in P experiments never decreased below basal levels. At identical times neither glucagon nor glucose differed significantly in the different expts. Thus during exercise alpha-adrenergic blockade increased insulin concentrations but did not diminish the glucagon response. Nor was this response increased when beta-receptor stimulation in P experiments was intensified by the particularly high catecholamine concentrations. The concentrations of FFA, glycerol and lactate were highest in P experiments and identical in A and C experiments. These findings indicate that during prolonged moderate exercise in man insulin secretion is depressed by stimulation of alpha-adrenergic receptors whereas glucagon secretion is not influenced by adrenergic receptors. Stimulation of beta-adrenergic receptors enhances lipolysis but neither lipolysis nor pancreatic hormonal secretion is influenced by cholinergic activity during exercise.
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PMID:Catecholamines and pancreatic hormones during autonomic blockade in exercising man. 59 18

Seven men ran at 60% of individual maximal oxygen uptake to exhaustion during beta-adrenergic blockade with propranolol or without drugs. After propranolol administration the increases during exercise in plasma glucagon and epinephrine concentrations as well as the decrease in plasma glucose concentrations were faster than in control experiments. When euglycemia was maintained by glucose infusion during beta-adrenergic blockade, glucagon and epinephrine responses to exercise, although not abolished, were markedly reduced. The diminution of the exercise-induced decline in glucose concentrations correlated significantly with the diminution of the glucagon as well as the epinephrine responses. Thus decreased glucose concentrations may significantly enhance the secretion of glucagon and epinephrine during prolonged exercise in man. Since the diminution of the glucagon response produced by glucose infusion was not accompanied by significant alterations in the levels of nonesterified fatty acid (NEFA) and glycerol, increased glucagon secretion does not seem to be a major determinant of lipolysis during exercise in man. During glucose infusion, glycogen utilization rates in muscle (n = 4) tended to decrease, whereas carbohydrate combustion rate and concentrations of norepinephrine, insulin, alanine, and lactate were unchanged.
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PMID:Glucose-induced decrease in glucagon and pinephrine responses to exercise in man. 86 12

Seven men ran at 60% of individual maximal oxygen uptake to exhaustion during beta-adrenergic blockade with propranolol (P), during lipolytic blockade with nicotinic acid (N), or without drugs (C). The total work times (83 +/- 9 (P), 122 +/- 8 (N), 166 +/- 10 (C) min, mean and SE) differed significantly. Epinephrine rose progressively above preexercise levels (0.06 +/- 0.01 ng/ml); at exhaustion concentrations in P experiments (2.15 +/- 0.41) were larger than in N (1.08 +/- 0.31) and C (0.72 +/- 0.28) experiments. Norepinephrine increased consistently while insulin decreased. After an initial decrease glucagon concentrations increased progressively in parallel with declining plasma glucose and were at exhaustion always three times preexercise values. Thus beta-adrenergic blockade did not diminish the glucagon response. Nor was this response increased when alpha-receptor stimulation in P experiments was intensified. Carbohydrate combustion was smaller and NEFA and glycerol concentrations in serum larger during C experiments. Alanine concentrations were never raised at exhaustion. Accordingly, neither stimulation of adrenergic receptors nor NEFA and alanine concentrations are major determinants for the exercise-induced glucagon secretion in man. It is suggested that decreased glucose availability enhances the secretion of glucagon and epinephrine during prolonged exercise.
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PMID:Glucagon and plasma catecholamines during beta-receptor blockade in exercising man. 93 21

Plasma calcitonin, glucagon and parathyroid hormone were measured in patients with acute pancreatitis. Plasma calcitonin was not detectable in 6 specimens obtained from the hypocalcaemic patients. Plasma glucagon values were similar in patients with acute pancreatitis and control subjects and were unrelated to hypocalcaemia, which was not even induced by glucagon infusion. High or rising parathyroid hormone levels were noted in association with hypo-and normocalcaemia, suggesting that parathyroid hormone rises and maintains plasma calcium within normal limits. Plasma parathyroid hormone was, however, undetectable in 8 patients with prolonged hypocalcaemia. Deficiency of parathyroid hormone due to its destruction by proteolytic enzymes or because of parathyroid gland exhaustion is suggested as the major factor inducing persistent hypocalcaemia in acute pancreatitis. Administration of parathyroid hormone should, therefore, be considered in patients with acute pancreatitis when hypocalcaemia does not respond to intravenous calcium therapy.
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PMID:The aetiology of hypocalcaemia in acute pancreatitis. 111 72

Glucagon-like peptide-I(7-37) [GLP-I(7-37)] is an intestinal peptide hormone that is released in response to oral nutrients and that potently augments glucose-mediated insulin secretion. GLP-I(7-37) has potent insulin-releasing activities in vivo in response to oral nutrients, in situ in the isolated perfused pancreas, and in vitro in cultured pancreatic B-cells. As such GLP-I(7-37) is a potent hormonal mediator in the enteroinsular axis involved in the regulation of glucose homeostasis. We now show that in addition to stimulating the release of insulin, GLP-I(7-37) stimulates proinsulin gene expression at the levels of gene transcription and cellular levels of proinsulin messenger RNA as well as the translational biosynthesis of proinsulin. These findings of the positive anabolic actions of GLP-I(7-37) on the synthesis of insulin in B-cells support the notion that GLP-I(7-37) may be of therapeutic use in stimulating the production of insulin in patients with noninsulin-dependent diabetes mellitus and that overproduction of insulin with subsequent hypoglycemia will not occur in response to the administration of GLP-I(7-37). Furthermore, these positive actions of GLP-I(7-37) on insulin production obviate the possibility of B-cell exhaustion in response to such a potent secretagogue.
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PMID:Insulinotropic hormone glucagon-like peptide-I(7-37) stimulation of proinsulin gene expression and proinsulin biosynthesis in insulinoma beta TC-1 cells. 130 25

Intense exercise to exhaustion is expected to be associated with rapid and large changes in glucose production (Ra) and utilization (Rd). To quantify these, and to determine their mechanisms and those of the prolonged postexercise hyperglycemia, we measured circulating metabolic regulators and glucose kinetics, the latter by the method of enriched tracer [3-3H] glucose infusion during exercise. Eighteen fit, lean young male subjects exercised to exhaustion at 80% of maximal workload (approximately 100% VO2max) on a cycle ergometer. Plasma glucose was 4.90 +/- 0.08 mM/L at rest, increased during exercise, then abruptly to 6.91 +/- 0.40 mM/L at 4 min recovery then gradually declined. Plasma insulin was constant during exercise, then doubled to 162 +/- 28 pmol/l until 20 min recovery, before declining. Plasma glucagon increased by 71 +/- 11 pg/mL. Plasma norepinephrine increased 18-fold and epinephrine 14-fold, both declining by 20 min recovery. Ra increased 7-fold by exhaustion to 13.0 +/- 1.18 mg/kg/min, then decreased to 2.43 +/- 0.24 mg/kg/min by 9 min, then to about 2 mg/kg/min the rest of recovery. Rd rose 3-fold (6.61 +/- 0.70 mg/kg/min), and remained lower than Ra to 7 min recovery, but thereafter declined more slowly. Thus, the rapid and extremely large increase in Ra was not matched by the increment in Rd during exercise and early recovery. We suggest that unlike in exercise of lesser intensity, the major mediators of both the increase in Ra and the restraint of the increase in Rd are the catecholamines. The post exercise hyperglycemia and hyperinsulinemia are appropriate to muscle glycogen repletion.
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PMID:Glucose turnover and its regulation during intense exercise and recovery in normal male subjects. 145 13

The purpose of this investigation was to examine the effect of phenylethanolamine N-methyltransferase (PNMT) inhibition on the regulation of peripheral metabolic and hormonal responses during treadmill exercise in the rat. Changes in plasma catecholamine (epinephrine, norepinephrine, and dopamine), glucagon and glucose, and the glycogen content of the liver and two skeletal muscles were studied in four groups of rats. Two groups of rats were studied at rest: one group had been treated with LY134046, an inhibitor of PNMT, and the second group was treated with physiological saline. A third group treated with LY134046 was studied after treadmill exercise (28 m.min-1 and 8% slope). In this group of rats, exhaustion came after 37.5 +/- 7.9 minutes of exercise. In order to make appropriate comparisons, a fourth group of rats treated with physiological saline was exercised for 37.5 min. Running endurance during the treadmill exercise was thus reduced in LY134046-treated rats. Plasma epinephrine and glucagon concentrations and other metabolic (plasma glucose and gastrocnemius lateralis and superficial vastus lateralis muscles and liver glycogen contents) responses were similar between LY134046- and saline-treated rats at rest and after exercise. These results suggest that PNMT inhibition in epinephrine brain neurons might be the principal factor involved in the LY134046-induced reduction of exercise endurance.
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PMID:PNMT inhibition decreases exercise performance in the rat. 152 68

Eleven Type 2 (non-insulin-dependent) diabetic patients, islet cell autoantibodies negative, nonobese with secondary failure to oral hypoglycemic agents (OHA) [glyburide (7.5 mg/day) and phenformin (75 mg/day)] and HbA1c 10.2 +/- 0.6% were studied. Insulin receptors on circulating monocytes, glucose utilization at supraphysiological insulin concentrations, and plasma C-peptide after i.v. glucagon were evaluated before and after 2 months of combined therapy with OHA and insulin (Ultratard HM Novo). A significant improvement was demonstrated in HbA1c and glycemia after two months of treatment. Glucose MCR was increased after two months of treatment whilst basal C-peptide was decreased as well as receptor binding to monocytes. After three years of combined therapy, body weight, glycemia and HbA1c did not increase. After three years the C-peptide basal values were significantly increased with respect to values found after 2 months of therapy. These results demonstrate that insulin treatment may restore insulin sensitivity in NIDDM patients resistant to OHA treatment and that after three years there is no exhaustion of B-cell function.
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PMID:The beta cell function in NIDDM patients with secondary failure: a three year follow-up of combined oral hypoglycemic and insulin therapy. 163 93


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