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)

Obese Zucker rats are hyperlipemic and mildly hyperglycemic. Because insulin and glucagon are involved in lipid and carbohydrate metabolism and they act via their receptors, we investigated the role of insulin and glucagon receptors in obese and lean female Zucker rats. Because dietary sucrose is more lipogenic than starch, we also studied the effect of dietary carbohydrates on the receptors. Significant phenotypic effect (obese greater than lean) was observed on plasma levels of glucose, triglyceride and insulin. Binding of insulin and glucagon to liver plasma membranes was significantly lower in obese rats than in lean rats. Lower insulin binding was due to a lower number of receptors as well as a lower affinity, whereas the lower glucagon binding was due only to a lower receptor number. Insulin binding in lean rats but not in obese rats was lower in sucrose-fed than in starch-fed rats. Diet had no effect on glucagon binding. We propose that in obese Zucker rats, in addition to hyperinsulinemia, impaired glucagon activity as manifested by decreased glucagon binding to target tissues may be an important contributor to the hyperlipemia and obesity.
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PMID:Effect of dietary carbohydrates on glucagon and insulin receptors in genetically obese female Zucker rats. 303 87

The effects of gastric inhibitory polypeptide (GIP) on glucose and lipid metabolism of isolated rat adipocytes were investigated. In a dose-dependent manner, GIP stimulated 2-deoxy-glucose uptake increasing the glucose transport rate by up to 140% at a concentration of 10(-7) mol/l. GIP also stimulated the conversion of 14C-glucose into extractable lipids by up to 81% at 10(-7) mol/l. Insulin-stimulated 2-deoxy-glucose uptake and lipogenesis were additively enhanced by the presence of GIP. Insulin binding was slightly but not significantly increased by addition of GIP, mainly due to an increase in receptor affinity. GIP had a weak lipolytic activity, but lipolysis elicited by glucagon or isoproterenol was potently reduced. In conclusion, independent of its insulinotropic action, GIP showed a insulin-like activity on glucose metabolism and lipolysis in rat adipose tissue. The possible role of GIP for the development of obesity is discussed.
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PMID:Effects of gastric inhibitory polypeptide on glucose and lipid metabolism of isolated rat adipocytes. 307 52

Several new problems in obesitology were pointed out in this book and commented with respect to experiments and experiences of our working group. The problem of the low triiodothyronine (T3) syndrome was treated in chapter 2. The decrease of serum T3 and increase of serum reverse T3 in obese subjects was induced by several factors, namely by fasting. A resistance to administered thyroxine and triiodothyronine was observed in these patients. This energy saving mechanism is at variance with slimming regimens. The prevention and treatment of this awkward complication was discussed. The next chapter (3) is concerned with the hormonal and metabolic effects of diet and motor activity in the course of slimming regimens. The different effects of diet and motor activity on epinephrine and norepinephrine in obese subjects were similar to those obtained by other investigators in nonobese humans. A great importance was attributed to an increased plasma level of cortisol in obese and nonobese subjects in the course of different forms of motor activity and related to a different intensity of exercise. Parallel to several of these experiments, beta-endorphin, thyroid hormones and glucagon were also estimated. It was suggested that motor activity for exercising subjects should not lead to an enhanced secretion of cortisol in view of the health deteriorating effects of increased cortisolemia and in view of an already stimulated secretion of this hormone in obese subjects on basal conditions. Vice versa, a decreased cortisolemia should be obtained in obese subjects treated with an appropriate motor activity and diet. It has been shown that diet without motor activity reduced the level of plasma androgens but in cooperation with motor activity, the level of androgens remained unaltered in the course of the reducing regimen. The conservation of a normal or even higher level of androgens is probably prerequisite for a positive nitrogen balance observed in the course of a combined slimming regimen, while diet without motor activity led in the studied conditions to a negative nitrogen balance. Chapter 4 was devoted to the role of motor activity in slimming regimens. In view of the metabolic effects of motor activity and the clinical late effects of obesity (osteoarthritis of the knees, hips and spine, arterial hypertension, overload of the cardiovascular system, diabetes mellitus etc.), a selection of motor activities was proposed. According to our long experience, we do not recommend jogging, running, jumping and all sports leading to collisions of players.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:New trends in obesitology. 307 25

Effects of gold thioglucose on the insulin and glucagon secretion by the isolated perfused pancreas of Wistar rats in vivo and in vitro Gold thioglucose (GTG), hitherto administered predominantly to mice can also be used in rats in a non toxic dosage, if GTG is injected intravenously (i.v.) together with sodium hexobarbital. Wistar rats tolerate a single injection of GTG in doses ranging from 40 to 1200 mg/kg bw. GTG (10 mmol/l in the perfusion medium) has no in vitro effect--tested by the isolated perfused rat pancreas--on the basal (5.5 mmol/l glucose) or stimulated (11 mmol/l glucose) insulin (IRI)-secretion. This is valid also for glucagon (IRG)-secretion. After in vivo injection of GTG (600 mg/kg bw, together with sodium hexobarbital (10 mg/100 g bw, i.v.] extensive alterations of IRI- and IRG-secretion result as tested under in vitro conditions in the isolated perfused pancreas of the rat, Glucose stimulation (11 mmol/l) causes a hyperinsulinism and a hypersecretion of IRG, a so-called paradoxical glucagon secretion, lasting for 2 days while IRI secretion is already diminished. At the same time food intake is very low and the body weight decreases. Ten days later the body weight has reached the starting value again and the IRI secretion shows again signs of hyperinsulinism. Six months after a single injection of GTG (600 mg/kg bw, i.v.) the rats were obese and react after glucose stimulation with hyperinsulinism and again with a paradoxical glucagon secretion. The blood glucose levels were normoglycaemic, whereas serum IRI rose in parallel with development of the obesity. Also with histological methods we could distinguish an acute from a chronic phase of GTG toxicity visible in the tested organs (liver, kidney, thyroid gland). The endocrine pancreas reacts after a single injection of GTG with a lowered number of B cells. The remaining cells reveal variable amounts of degranulation. In the early phase the hypothalamus, in particular the ventromedial hypothalamic nucleus, shows most clearly signs of destruction and 6 months after a single injection of GTG the number of cells is still reduced in this region. We conclude that GTG reacts primarily on the hypothalamus and modulates the reactivity of the endocrine pancreas in a permanent manner via the vegetative nervous system, because we test the function of the pancreas in an in vitro system. As a consequence the threshold of the B and A cell against the stimulus glucose is altered in two ways.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[In vitro and in vivo effect of gold thioglucose on the insulin- and glucagon-secretion of the isolated perfused rat pancreas]. 308 62

Adrenalectomy of gold thioglucose (GTG)-treated hyperphagic obese mice had been shown by us earlier to result in anorexia, weight loss, hypoglycemia and subsequent death of all mice. More recent studies suggest that adipose tissue mass may not be the critical determinant of anorexia since a large proportion of GTG-treated non obese (pair-fed to curb obesity) mice when challenged with adrenalectomy also developed anorexia. The aim of the present studies was to determine whether the changes in circulating metabolites, namely, glucose, free fatty acids and hormones, including insulin, glucagon and ACTH, which accompany adrenalectomy, might provide a clue to the causative agent for the onset of anorexia in GTG obese and non obese mice. Accordingly, plasma levels of glucose, free fatty acids, insulin, glucagon and ACTH were measured in GTG-treated obese, non obese and in normal untreated mice following adrenalectomy or a sham operation. Preoperatively, plasma insulin levels were significantly elevated in GTG obese mice whereas plasma glucose, free fatty acids and glucagon levels were not appreciably different than those of untreated controls. Upon adrenalectomy and onset of anorexia, GTG obese mice exhibited a progressive decline in blood glucose and insulin levels; plasma free fatty acids increased precipitously but only after the first day. Plasma glucagon levels declined immediately following adrenalectomy, however, by the 6th day postoperatively they were significantly elevated above the sham operated obese and untreated controls. Prior to adrenalectomy, the pair-fed GTG non obese mice exhibited blood glucose and insulin levels well below the levels of untreated controls and GTG obese mice whereas plasma free fatty acids and glucagon levels were markedly elevated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adrenalectomy induced anorexia in gold thioglucose-treated obese mice: metabolic and hormonal changes. 309 86

Chronic treatment of rats with dexfenfluramine decreased the concentrations of circulating corticosterone, fatty acid, glycerol, and triacylglycerol after feeding a test load of fructose. It also decreased the rise in adrenalin in the blood of rats that were anaesthetized with urethane. These effects of dexfenfluramine probably result from changes in the metabolism of 5-HT in the CNS and consequent alterations in hormonal balance. It is proposed that the long-term metabolic effects of dexfenfluramine could be explained by a decrease in the effectiveness of stress hormones (e.g., glucocorticoids, corticotropin, catecholamines, glucagon) in regulating metabolism since these hormones antagonize many of the actions of insulin. This hypothesis also identifies the possibility that the ability of dexfenfluramine to decrease an exaggerate stress response could alleviate some of the potential risk factors associated with atherosclerosis including obesity and maturity onset diabetes.
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PMID:Metabolic and hormonal effects of dexfenfluramine on stress situations. 318 Jan 10

Serum lipids and lipoproteins were studied in 149 non-insulin-dependent diabetic subjects treated with diet or oral drugs (75 men, 74 women) and in 101 nondiabetic control subjects (49 men, 52 women) in relation to endogenous insulin secretion capacity measured by plasma C-peptide response to intravenous glucagon. Serum HDL- and HDL2-cholesterol concentrations were lower and VLDL-cholesterol and total and VLDL-triglyceride concentrations higher in subjects with high C-peptide response (above the median) than in subjects with low C-peptide response (lower or equal to median) both in diabetic and control subjects of both sexes. Adjustment for the effect of obesity abolished these differences in serum lipids and lipoproteins in diabetic subjects but not in control subjects. This may indicate that obesity has stronger influence on serum lipids in diabetic subjects than in nondiabetic subjects.
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PMID:Association of serum lipids and lipoproteins with plasma C-peptide concentration in non-insulin-dependent diabetic and non-diabetic subjects. 330 77

Diabetes, the most common metabolic disease, is responsible for the deaths of over 300,000 Americans annually. The incidence of the disease increases with age and since the U.S. population is graying, prevalence is also increasing. Obesity and family history are strong predictors of diabetes. The etiology of Type II diabetes is heterogeneous. The hyperglycemia of Type II diabetes can result from a variety of metabolic defects including impaired beta cell secretion, receptor deficiencies, or abnormal hepatic production or uptake of glucose. Other glucoregulatory hormones such as glucagon, growth hormone, cortisol, thyroid hormones, somatostatin, and gastric inhibitory polypeptide may contribute to the aberrations of carbohydrate metabolism. Environmental factors including stress, diet, and exercise may also contribute to the disease. Since most diabetics are obese, weight loss should be the first priority in improving status. A variety of diet and exercise regimens may help achieve this goal or even improve glucose control without weight loss. Due to the heterogeneity of the disease individualized treatment must be used to improve status of patients with the various metabolic defects of Type II diabetes.
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PMID:Dietary sugars and carbohydrate metabolism in type II diabetes. 330 10

Islets of Langerhans in sections from the tail of the pancreas of corpulent LA/N-cp rats and lean controls aged 1, 3, 6 and 9 mo were examined by immunocytochemistry and morphometrically using an automatic image analyzer. The corpulent rats had significantly greater islet volumes at all ages, although islet hypertrophy tended to plateau after 6 mo. By 12 mo age the architecture of the islets was disrupted with large islets fused and showing areas of fibrosis and deposits of hemosiderin. The volume density (v/v, %) of islets in the parenchyma was significantly increased at each age step in corpulent rats reaching over 20% at 9 mo, and was greater in corpulent than in lean rats at all ages. In the corpulent rats, B-cell volume density dramatically with age and at all ages was significantly greater in corpulent than in lean rats. A-cell volume density was significantly greater in the corpulent rats than in lean rats at 1 and 9 mo. The mean B:A cell ratio was greater in corpulent than in lean rats at 3, 6 and 9 mo. There were more D cells per islet in corpulent than in lean rats up to 9 mo. These changes in cell populations were paralleled by qualitative changes in islet morphology and cellular topography such as increasingly irregular islet shape in corpulent animals and by variations in plasma levels of insulin and glucagon. In this strain of rats, obesity is associated with major changes in pancreatic morphology and this correlates strongly with the susceptibility of the strain to atherosclerosis.
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PMID:Age-related qualitative and quantitative changes in the endocrine pancreas of the LA/N-corpulent rat. 332 19

Circulating levels of insulin, glucagon, thyroid hormones as well as lipid levels were determined in an obese strain of chicken and their lean controls. Hepatic and muscle glycogen and lipids were also measured. Obese birds had higher plasma lipids accompanied by significantly higher insulin and lower glucagon levels compared to lean controls. Hepatic and muscle triglycerides were also higher in obese birds. Plasma T4 level was significantly higher in obese but T3 was not different in the two groups. Results suggest that genetically obese birds have significantly increased insulin/glucagon ratios as previously reported in the PTU induced hypothyroid-obese chicks (Horm. Metab. Res. 12: 51, 1980) and this could have causal relationship to hyperlipidemia and obesity observed in these birds.
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PMID:Possible role of pancreatic insulin and glucagon in the hyperlipidemia and obesity of obese strain of chicken. 351 30


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