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 12 aged nondiabetic subjects, 10 aged diabetic subjects, and 6 young nondiabetic subjects the glucose, insulin, glucagon and growth hormone responses to the intravenous administration of arginine were studied. A prompt increase in the levels of blood glucose, serum insulin and serum glucagon was observed, but the glucose and glucagon peaks were significantly higher in the aged nondiabetic and diabetic subjects. Growth hormone secretion did not differ between the nondiabetic aged and young subjects. These findings suggest the hypothesis that glucose intolerance in old age is due to increased release of glucagon.
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PMID:Serum glucagon after arginine infusion in aged and young subjects. 698 81

Nine normal subjects ingested 100 gm. glucose, fructose, and sucrose on separate days after an overnight fast. Plasma glucose, fructose, insulin, glucagon, growth hormone, and triglyceride levels were then measured over the following 5 hr. Plasma glucose and insulin peaks were both significantly lower after fructose ingestion as compared with glucose and sucrose. Plasma glucagon suppression was significantly less after fructose. Growth hormone showed a late stimulation after glucose and sucrose but did not rise after fructose intake. Triglyceride levels were significantly increased at 3 to 5 hr. after fructose ingestion.
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PMID:Endocrine responses to sugar ingestion in man. Advantages of fructose over sucrose and glucose. 699 16

Insulin and glucagon secretion in response to common secretagogues were ascertained in the perfused pancreas isolated from essential fatty acid deficient rats. The pattern of insulin secretory response to glucose (16.7 mmol/L) by isolated rat pancreas perfused for 30 min was biphasic in EFA-deficient and control rat pancreas. The amplitude of glucose-stimulated acute secretion (phase I) was significantly greater (p less than 0.01) in magnitude and amplitude in EFA-deficient rats than in the control rats. There was no significant difference in the second phase of glucose-stimulated insulin secretion in the two groups. Glucagon secretion in EFA-deficient and control rats was inhibited by glucose (16.7 mmol/l). Glucagon secretion induced by L-arginine (10 mmol/l) was not significantly different in EFA-deficient and in control rat pancreata (p greater than 0.05). However, arginine (10 mmol/l)-stimulated insulin release was significantly higher in EFA-deficient than in control rats. Growth hormone (100 mumol/l)-induced glucagon and insulin secretion was variable in the two groups but significantly higher than basal secretion. The level of L-leucine (10 mmol/l)-stimulated glucagon and insulin secretion in EFA-deficient rats was minimal but significant. Our results show that isolated pancreata of rats devoid of precursors for endogenous prostaglandin synthesis secreted insulin and glucagon in response to common secretagogues. On the basis of our data, it is concluded that endogenous prostaglandins are probably not obligatory for normal secretory functions of islets of Langerhans.
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PMID:Insulin and glucagon secretion in essential fatty acid deficient rats. 701 48

Insulin tolerance tests were carried out in normal subjects and in adrenalectomized (ADX) patients in order to better understand the importance of counter regulatory hormones for the recovery from hypoglycaemia. Compared to normal subjects recovery of plasma glucose and of free fatty acid levels in adrenalectomized patients is retarded. The levels of glucagon are significantly higher in ADX patients during rest than in normal subjects. As expected, epinephrine and norepinephrine levels did not increase in ADX patients and, accordingly, blood pressure did not change. Growth hormone levels were the same in both groups of subjects. Interestingly, there was no clear-cut difference with regard to subjective symptoms of hypoglycaemia. It would appear that epinephrine is important for the rapid initial recovery from hypoglycaemia, whereas other hormones play a more important role later on.
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PMID:Insulin hypoglycaemia in normal and adrenalectomized subjects: comparison of metabolic parameters and endocrine counter regulation. 702 15

Age-related changes in the hormonal control of glucose homeostasis were examined in immature (5-wk-old), young adult (10-wk-old) and older adult (30 and 60-wk-old mice). In immature mice, basal plasma glucose and insulin concentrations were higher than young adult mice. Glucose tolerance was impaired in immature mice, although the plasma insulin response to glucose and other secretagogues (arginine and glucagon) was well developed, and the hypoglycaemic effect of exogenous insulin was not impaired. Glucagon and epinephrine evoked a greater acute hyperglycaemia in immature mice, suggesting that these hormones exert a stronger rapid glucose-raising effect in preadult life. Basal plasma glucose and insulin concentrations were lowest in young adult mice, and increased with advancing adult age. Glucose tolerance was best in young adult mice and deteriorated with age, while plasma insulin concentrations after administration of glucose, arginine and glucagon were lowest in young adult mice and increased with age. However, in response to these secretagogues, the percentage increase in plasma insulin above basal was reduced in older adult mice. This indicates a defect of stimulus-recognition-secretion-coupling in the B-cells of older adult mice. The raised plasma glucose concentrations of older adult mice could not be attributed to an increase in the acute hyperglycaemic action of glucagon or epinephrine. The hypoglycaemic response to exogenous insulin decreased with age, suggesting that tissue sensitivity to insulin was impaired. Treatment with growth hormone and cortisone for 5 days produced a greater antagonism of insulin in older mice than young adult or immature mice. Growth hormone impaired glucose tolerance at each age, but only produced a marked hyperinsulinaemia in older adult mice. In contrast, cortisone produced a marked hyperinsulinaemia at each age, but only impaired glucose tolerance in older adult mice.
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PMID:Hormonal control of glucose homeostasis during development and ageing in mice. 704 71

Milk production responses to 1) growth hormone injections (51.5 IU/day), 2) a mixture of glucose (274 g/day) and sodium caseinate (441 g/day) infused into the abomasum, 3) a combination treatment, and 4) a placebo treatment were determined in 4 cows in a 4 x 4 Latin square design. Treatment periods were 10 days, and production responses were based on the last 5 days of each treatment. Growth hormone administration increased milk yield 15.2% without changing milk composition or feed intake. Infusions of glucose-sodium caseinate into the abomasum increased milk yield 3.9% and milk protein yield 6.4% but when combined with growth hormone treatment did not stimulate a greater response than observed for growth hormone alone. Plasma concentrations of growth hormone were increased 4-fold with growth hormone injections but were not affected by the infusion of glucose-sodium caseinate into the abomasum. There were no significant changes in plasma concentrations of glucose, free fatty acids, insulin, glucagon, prolactin, triiodothyronine, thyroxine or cortisol with any of the treatments. Growth hormone increased milk synthesis and the efficiency of milk production, but its effect was not enhanced by the postruminal supply of additional nutrients.
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PMID:Lactational response to exogenous growth hormone and abomasal infusion of a glucose- sodium caseinate mixture in high-yielding dairy cows. 710 42

The availability of transfected cell lines expressing the five cloned somatostatin receptors has allowed extensive families of synthetic analogues to be screened for their binding affinities to these receptors. Cyclic octapeptides in the octreotide series have high affinity for sstr2 and low affinity for sstr1 and sstr4. Modifications to these analogues can have profound effects on their residual affinity for sstr3 and sstr5. Several linear peptides, incorporating the critical core-D-Trp-Lys-sequence of all active analogues, exhibit selectivity for either sstr3, sstr5 or both, but little affinity for the other three. From these analogues we have assembled a panel of compounds with a useful degree of specificity for sstr2, sstr3 and sstr5 and these have been used to evaluate receptor involvement in various physiological processes. Inhibition of pituitary growth hormone release correlates completely with sstr2 affinity and it appears from preliminary results that inhibition of pancreatic glucagon release is also sstr2 mediated. Effects on gastric acid secretion show a high degree of dependence on sstr2 affinity. Inhibition in vivo by somatostatin of insulin release, amylase release and binding to rat pancreatic acinar cells is highly correlated with sstr5 receptor affinity. Gastric smooth muscle cells have particularly high affinity for sstr3 receptor ligands. The availability of receptor-specific ligands is proving to be of great value in elucidating the physiological roles of each receptor. It is anticipated that these and future generations of analogues will have distinct therapeutic advantages over somatostatin itself and presently available cyclic octapeptides.
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PMID:Somatostatin analogues and multiple receptors: possible physiological roles. 758 50

Human galanin was recently isolated and sequenced and was found to differ from porcine galanin, hitherto used for studies in humans, in several important respects. We therefore synthesized and purified human galanin and infused it i.v. at a rate of 74 pmol.kg-1.min-1 into six healthy volunteers for 60 min during a hyperglycaemic clamp. The clamp was achieved by i.v. infusion of glucose at a rate which in a control experiment had been demonstrated to maintain the plasma glucose level at 12-13 mmol/l for 90 min. Galanin concentrations reached a plateau of approximately 1500 pmol/l throughout the infusion as opposed to pre-infusion and control levels of 20-30 pmol/l. The glucose levels obtained in the two experiments were indistinguishable. Plasma levels of C-peptide and insulin increased significantly in both experiments and the dynamic concentration curves were almost identical. Glucagon concentrations in plasma decreased significantly and similarly. Growth hormone levels, however, increased eight-fold during galanin infusions. Galanin was eliminated from plasma with a half-life of 3.7 +/- 0.4 min, similar to that of porcine galanin. It is concluded that human galanin powerfully stimulates growth hormone secretion in man, but has no effect on pancreatic endocrine secretion or glucose metabolism in the concentrations obtained in this study.
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PMID:On the effects of human galanin in man. 768 99

Wound healing is a series of complex physicochemical interactions that require various micronutrients at every step. In the critically ill or severely injured patient, wound healing is impaired by the protein-catabolic, hypermetabolic response to stress. The hypothalamus responds to cytokine stimulation by increasing the thermoregulatory set-point and by augmenting elaboration of stress hormones (catecholamines, cortisol, and glucagon). In turn, the stress hormones induce thermogenic futile substrate cycling, lipolysis, and proteolysis. Increased glucose production results at the expense of skeletal muscle degradation, producing amino acid substrate for hepatic gluconeogenesis. Nutritional support of the hypermetabolic state is an essential part of ensuring efficient wound healing in these patients. Protein catabolism cannot be reversed by increased amino acid availability alone, due partly to a defect in amino acid transport. This defect can be reversed by anabolic agents, such as growth hormone and insulin-like growth factor-1. Growth hormone treatment dramatically improves wound healing in severely burned children. Supplementation with protein and vitamins, specifically arginine and vitamins A, B, and C, provides optimum nutrient support of the healing wound.
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PMID:Nutrient support of the healing wound. 792 45

To test the hypothesis that differing physiological insulin levels can modify the counter-regulatory response to prolonged hypoglycemia, experiments were carried out in 10 healthy male subjects. Insulin was infused subcutaneously for 8 h in two separate randomized protocols, so that steady-state levels of 132 +/- 6 pM (low) and 402 +/- 18 pM (high) were obtained. The fall in plasma glucose was controlled by the glucose-clamp technique. Plasma glucose fell slowly and similarly in both groups, reaching an identical steady-state (final 120 min of each study) level of 3.4 +/- 0.1 mM. Steady-state plasma epinephrine (2.5 +/- 0.4 vs. 1.5 +/- 0.2 nM) and norepinephrine (1.5 +/- 0.2 vs. 1.1 +/- 0.1 nM) were significantly (P < 0.05) greater during high- compared with low-dose insulin infusions. Plasma glucagon was reduced during high compared with low infusions (104 +/- 9 vs. 150 +/- 19 ng/l, P < 0.05). Growth hormone, cortisol, and pancreatic polypeptide increased significantly but were not different during the two insulin infusions. Hepatic glucose production (HGP) was equal during the steady-state period (8.4 +/- 1.0 mumol.kg-1.min-1) of each infusion. Blood lactate levels (1,255 +/- 73 vs. 788 +/- 69 mumol/l, P < 0.02) were increased in high compared with low, but nonesterified fatty acid (205 +/- 43 vs. 579 +/- 65 mumol/l) and 3-hydroxybutyrate (40 +/- 36 vs. 159 +/- 51 mumol/l) were reduced (P < 0.002) during the high-compared with low-dose infusions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of physiological hyperinsulinemia on counterregulatory response to prolonged hypoglycemia in normal humans. 794 20


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