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 effects in man of adrenergic blocking agents on plasma insulin, glucagon, growth hormone, and lipid metabolism are reviewed. Whereas basal insulin may be slightly inhibited by beta- and enhanced by alpha-adrenergic blockade, more marked suppression may be achieved under circumstances of high exogenous or endogenous catecholamine stimulation. The relative effects of beta1 or combined beta 1 and beta2 blockers in man are unknown. Glucagon release is probably provoked by beta- and inhibited by alpha-stimulation in man. Muscle glycogenolysis is inhibited by propranolol, and under situations of hepatic glycogen depletion, clinical hypopglycemia may occur. This may also account for the failure of significant hyperglycemia to be observed in short-term experiments on fasting subjects in whom insulin release may be suppressed and glucagon release enhanced. Growth-hormone release is enhanced by beta-adrenergic blockade. Free fatty acid formation in vivo is inhibited by intravenous beta blockade, but the effects of oral administration on triglyceride production and lipoprotein profiles remain uncertain. The inter-relationships between the effects of adrenergic blockade at different sites of hormone and substrate release are unclear but may have important consequences in alteration in carbohydrate tolerance and lipid metabolism. The relative effects of beta-blocking drugs with differing specificity must be determined.
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PMID:The metabolic consequences of adrenergic blockade: a reveiw. 23 94

We have studied a 2-year-old girl with acanthosis nigricans, glucose intolerance, marked hyperinsulinemia, and somatic features characteristic of the leprechaunism syndrome. Circulating plasma insulin levels were increased up to 50-fold and the patient showed a blunted hypoglycemic response to an injection of exogenous insulin (0.2 units/kg), indicating the presence of severe insulin resistance. Insulin purified from the patient's plasma was normal on the basis of chromatographic, electrophoretic, and immunologic criteria. Furthermore, the purified insulin competed effectively with (125)I-labeled insulin for binding to insulin receptors on cultured IM-9 lymphocytes and rat fat cells and also exhibited normal biological potency when tested on rat fat cells. Anti-insulin receptor and anti-insulin antibodies were not detected in the patient's plasma, and plasma levels of glucagon, growth hormone, and cortisol were normal. Insulin binding to the patient's circulating monuclear leukocytes was only slightly depressed into the low normal range and could not account for the severe insulin resistance. Studies on the patient's fibroblasts revealed normal levels of insulin receptors but a total absence of insulin's ability to accelerate glucose transport. Because rates of glucose transport and metabolism were normal in the basal state in the absence of insulin, we conclude that this patient's insulin resistance is due to an inherited cellular defect in the coupling mechanism between occupied insulin receptors and the plasma membrane glucose transport system.
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PMID:Insulin resistance due to a defect distal to the insulin receptor: demonstration in a patient with leprechaunism. 27 48

Somatostatin, a peptide inhibitor of growth hormone release originally isolated from the hypothalamus, is also present in D cells of pancreatic islets. Its ability to inhibit the secretion of insulin and glucagon suggests that it may be a local regulator of pancreatic A- and B-cell function. Studies using synthetic somatostatin have provided evidence that glucagon is a physiologically important hormone that exacerbates the consequences of insulin deficiency in human diabetes mellitus. The ability of somatostatin to diminish both fasting and post-prandial hyperglycemia and to forestall the development of ketoacidosis after withdrawal of insulin in insulin-dependent diabetics suggests a potential therapeutic use of this agent in diabetes. Presently, however, its short half-life and diverse actions preclude such use and have prompted the search for more specific and longer-acting analogs.
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PMID:Somatostatin. Its possible role in carbohydrate homeostasis and the treatment of diabetes mellitus. 32 23

The prevailing concept of etiologic heterogeneity for the diabetes mellitus syndrome is one of multiple genetic factors interacting with a variety of environmental influences. Variation in expression of the disorder, particularly the need for insulin, does not correlate with known etiologic distinctions. There is much evidence for genetic heterogeneity, as well as phenotypic variation when etiology can be presumed to be identical. The vascular manifestations of diabetes include microangiopathy unique to diabetes and larger vessel disease that differs from that of normal aging only by its prematurity. There is as much evidence for heterogeneity of the vascular expression as there is for glucose intolerance. Approximately 25% of persons with insulin-dependent diabetes may never develop the microvascular disease. The pathogenesis of vascular disease in diabetes may involve a number of abnormalities of plasma, circulating cells, and vascular tissue. Were absolute control of glycemia possible, some of the contributing factors involved in vasculopathy would possibly be alleviated. In the absence of automated physiologic insulin replacement the potential deleterious effect of our current methods of treatment might be reduced by specific inhibition of excess catecholamine, growth hormone and/or glucagon responses.
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PMID:Nature and nurture in the expression of diabetes mellitus and its vascular manifestations. 33 1

In the first part of the study oral glucose tolerance tests (GTT) or insulin tolerance tests (ITT) were performed in 22 lean and 22 obese nondiabetics before and after fasts of at least 6 days' duration. Deterioration of glucose tolerance was greater in lean than in obese individuals. Plasma levels of factors known to influence glucose tolerance (glucagon, growth hormone, free fatty acids, ketones) were significantly higher in fasting lean than in fasting obese subjects. Furthermore, delayed insulin rise (GTT) and decreased insulin sensitivity (ITT) were observed after starvation in lean subjects but not in the obese, which could explain the greater deterioration of glucose tolerance in the lean population. In the second part of the study glucose and fructose tolerance were compared during 4-hour infusions of these substrates (0.5 g/kg/h) in 8 normal subjects before and after two 4-day fasts. After starvation, glucose as well as fructose infusion resulted in plasma levels of the infused hexose significantly higher than in control, and the rise in plasma lactate and pyruvate was delayed. These results contradict the view widely held in the literature, that fructose metabolism remains unimpaired in the fasting state.
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PMID:[Carbohydrate intolerance during complete fasting]. 33 74

1. The effect of somatostatin and eighteen somatostatin analogues on pentagastrin-stimulated gastric acid and pepsin secretion was investigated in the conscious vagotomized cat prepared with chronic gastric fistulae. The majority of the analogues are peptides where D-amino acids are incorporated into the molecule instead of the natural L-isomers. 2. The ID50 for cyclic-somatostatin inhibition of near-maximal gastric acid secretion stimulated by pentagastrin 8 microgram kg-1 hr-1 was found to be 1.29 +/- 0.13 n-mole kg-1 hr-1. Pentagastrin-stimulated pepsin secretion had a lower threshold to somatostatin inhibition than did acid secretion. 3. D-Phe6, D-Phe7, D-Thr10, D-Thr12 and D-Phe6-D-Trp8 analogues all show low biological activity against the secretion of gastric acid and pepsin, growth hormone, insulin and glucagon. None of these analogues are antagonists of the cyclic-somatostatin inhibition of gastric secretion, suggesting that they have low affinity for this somatostatin receptor. 4. The analogues under investigation show parallel changes in activity against gastric and growth hormone secretion, suggesting a similarity between the gastric and growth hormone receptors for somatostatin. 5. D-Cys14 analogues are equipotent with or have a greater potency than cyclic-simatostatin in inhibiting the secretion of gastric acid, growth hormone and glucagon but show low insulin inhibiting activity.
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PMID:Structure-activity relationships of eighteen somatostatin analogues on gastric secretion. 34 35

Variations in concentrations of growth hormone, insulin, glucagon, prolactin, adrenal corticoids, and thyroid hormones in blood plasma of ruminants as related to circadian rhythms, environmental factors and nutrition are reviewed. Rhythms in prolactin concentrations are related to light and temperature. Concentrations of prolactin in plasma are higher in warm environments and during longer photoperiods. There is episodic secretion of growth hormone in cattle with frequent peaks in plasma concentrations during 24 h. Marked increases in environmental temperature result in greater secretion of growth hormone for short times followed by a decline in plasma concentration with prolonged exposure. Extreme cold temperature also increases growth hormone concentrations in plasma. Secretion of thyroid hormones increases in cold and decreases in warm environments. Circadian rhythms are definite for plasma concentrations of adrenal corticoids in ruminants adjusted to their surroundings. Peaks occur late in dark periods, and lows occur during the end of light periods. Circadian patterns have not been consistent for secretion of insulin. Prolonged subjection to stresses such as noise, handling, and restraint can modify concentrations of prolactin, growth hormone, and adrenal corticoids. Changes in concentrations of insulin may occur if blood glucose is increased. After feeding, concentrations of growth hormone in plasma decrease and concentrations of insulin and glucagon increase. Relationships of these changes with metabolism are discussed.
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PMID:Relation of hormonal variations to nutritional studies and metabolism of ruminants. 35 Sep 15

We have considered the evidence, first, that the presence of glucagon is essential in the pathogenesis of the full syndrome that results from complete insulin deficiency; second, that in the diabetic in whom insulin levels are relatively fixed, a rise in glucagon concentration contributes to endogenous hyperglycemia; and, third, that conventional methods of treatment of diabetes do not fully correct either the abnormal glucagon levels or the hyperglycemia, but when insulin therapy is supplemented with somatostatin, an agent which suppresses both glucagon and growth hormone, both hyperglycemia and hyperglucagonemia are corrected. These facts may one day provide a rationale for therapeutic efforts to suppress excess glucagon secretion in the management of diabetes in man.
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PMID:Glucagon and diabetes. 35 37

Fifty-two percent of patients with chronic heavy intake of ethanol had an abnormally low growth hormone (GH) response to propranolo-glucagon. The effect of ethanol is transient, since the GH response was normal in patients studied 2 wk or more after withdrawal of ethanol. The low GH response was not due to a difference in the levels of glucose or insulin. Ethanol probably suppresses the GH response by acting on the hypothalamus or pituitary gland. Along with previous data suggesting transient ACTH deficiency in chronic alcoholic patients, our findings suggest that these patients may have multiple hypothalamic-pituitary deficiencies.
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PMID:Transient suppression of growth hormone secretion after chronic ethanol intake. 35 54

The tetradecapeptide somatostatin is widely distributed in the body in endocrine-like calls and in nervous tissues. When produced in endocrine cells, it seems to inhibit the secretion of hormones at the site of production, for example, it inhibits the secretion of growth hormone in the pituitary gland, insulin and glucagon in the pancreas, and the local hormones in the gastrointestinal tract. Its role in the nervous system is not clear, but it may act as an inhibitory transmitter substance or modulator. As for its mode of action, the data suggest that interference with the levels of cyclic nucleotides, within the cells as well as with Ca++ fluxes may be important. The clinical uses of somatostatin have been explored, especially in diseases characterized by hypersecretion of hormones known to be inhibited by somatostatin. But the wide distribution and multipotent inhibitory action calls for attention. Analogues to somatostatin with specific actions have already been produced and await clinical evaluation.
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PMID:Extrahypophyseal effects of somatostatin. 36 38


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