Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic and hormonal effect of glucose loads, ranging from 125 to 504 g/70 kg/day, were studied in severely injured patients. There was little or no correlation of glucose intake with nitrogen balance, plasma glucose, fatty acid concentrations, or epinephrine excretion. Increased norepinephrine excretion correlated with and may have resulted from increased glucose intake. Serum glucagon concentrations averaged 320 pg/ml and were not depressed by glucose intake. Insulin concentrations rose with glucose intake but were low for the level of plasma glucose. Glucose oxidation and non-oxidative metabolism, including glycogen deposition, correlated well with glucose intake. Gluconeogenesis from alanine was much higher than normal but was completely suppressed at very high intakes. The data imply that cycling of glucose, with glycerol, glycogen, or both, increased with increasing glucose intake.
 ...
PMID:Influence of increasing carbohydrate intake on glucose kinetics in injured patients. 11 34

The effect of increased endogenous plasma insulin and glucagon concentrations on the free fatty acid (FFA) levels in the circulating blood was investigated in sheep, 2 baboons and 1 vervet monkey. Elevation of the plasma insulin level was obtained by vagal stimulation or intravenous glucose administration and vagal stimulation, whereas increased glucagon levels were induced by sympathetic stimulation, increased plasma insulin levels, with simultaneous increased plasma glucose concentrations (in our experiments with sheep), produced a pronounced lowering of the FFA levels. From this observation a lipogenetic function could be ascribed to insulin. However, in the primate experiments, increased plasma insulin without concomitant glucose administration caused an elevation of FFA levels, and would indicate a lipolytic rather than a lipogenetic action of insulin. Increased glucagon levels, as produced by sympathetic stimulation, did not alter the FFA concentrations significantly. It thus appears that glucagon has no lipolytic effect, as claimed by previous investigators. In our experiment on the vervet monkey, sympathetic stimulation, with increased plasma glucagon, even caused a decrease in FFA levels.
 ...
PMID:[The influence of endogenous insulin and glucagon on the free fatty acids in the circulating blood plasma]. 11 97

Changes in plasma glucose, nonesterified fatty acids, insulin, glucagon, cortisol, growth hormone, and prolactin have been studied in baboons during the course of generalized epileptic seizures induced by intravenous bicuculline. Plasma glucose rose to a peak at 25 min but fell to hypoglycemic levels after 60 min of seizure activity. This hypoglycemia was accompanied by a marked elevation in plasma insulin. Plasma glucagon rose to a peak at 14 min, then returned to normal. Plasma growth hormone levels were elevated after 60 min of seizure activity. Plasma prolactin and cortisol levels also rose during the seizure. These changes result from sequential interaction of (1) autonomic activation at seizure onset, (2) spread of neuronal activity to the hypothalamus leading to the liberation of releasing factors, and (3) indirect physiologic consequences of seizure activity.
 ...
PMID:Endocrine factors and glucose metabolism during prolonged seizures in baboons. 11 9

Chronic renal failure results in a variety of metabolic derangements that perturb glucose homeostasis. These may in part result from the fact that the kidney plays a prominent role in the metabolism of insulin as well as a number of other low-molecular-weight peptide hormones that affect carbohydrate metabolism. Specific abnormalities in glucose utilization that appear to be related to alterations in membrane receptors, resulting in increased glucagon sensitivity and decreased insulin action, are a newly recognized factor in intolerance to oral glucose. Glucose production and utilization are both abnormally increased in patients with chronic uremia, and these disturbances are only partially corrected by hemodialysis treatment. The mechanism(s) contributing to these changes is unclear, but seems to involve a combination of humoral and cellular factors. These include some degree of insulin resistance, probably inadequately modulated proteolytic responses to glucagon and parathyroid hormone, and a basic defect in energy production that alters intracellular concentrations of high-energy phosphate-containing nucleotides. It is unclear whether these changes in carbohydrate tolerance pose an increased risk for the premature development of cardiovascular disease in patients with renal failure, as they appear to do in the nonuremic population. The occasional patient with renal failure may develop clinical hypoglycemia when glucose utilization continues in a setting in which the hepatic capacity to produce glucose is reduced, probably as a consequence of altered substrate delivery and/or inhibition of one or more key gluconeogenic enzymes.
 ...
PMID:Disorders of glucose metabolism in uremia. 11 52

Glibenclamide has been shown to stimulate an insulin releasing factor in the duodenum. The possibility that this effect is of importance in its hypoglycaemic action was investigated by studying the effect of galactose on insulin release before and after treatment with glibenclamide; galactose stimulates insulin release when given orally but has no effect when given parenterally; thus its ability to release insulin appears to reside in an action on a gut factor. Measurements of plasma glucose, insulin and glucagon were made on twelve maturity onset diabetic patients following an oral glucose tolerance test and an oral galactose tolerance test before and after one week of treatment with glibenclamide. Glibenclamide significantly reduced the blood glucose levels. Both basal insulin and basal glucagon levels were unchanged. The insulin response to oral glucose was enhanced. Glucagon levels before treatment did not suppression of glucagon levels. Galactose stimulated insulin release but insulin levels before and after treatment were identical. An effect of glibenclamide on gut insulin releasing activity was not demonstrated but the galactose tolerance test provides a useful technique by which to examine the enteroinsular axis.
 ...
PMID:The effect of glibenclamide treatment on the insulin and glucagon responses to oral glucose and galactose in maturity onset diabetics. 11 30

This study reviews the pathogenic hormonal abnormalities (insulin deficiency and stress hormone excess) in diabetic ketoacidosis. The data both supporting and negating a primary role for insulin deficiency in the pathogenesis of diabetic ketoacidosis are examined. Evidence implicating excess stress hormone secretion as a necessary event in the development of severe metabolic decompensation is discussed. The data suggest that diabetic ketoacidosis may be prevented by correcting either the relative deficiency of insulin or the excess secreation of one or a combination of the stress hormones. Studies supporting a primary role for insulin deficiency in the pathogenesis of diabetic ketoacidosis include the beneficial therapeutic response to insulin administration in ketoacidosis, development of ketoacidosis; and (3) stress hormone excess is necessary for fulminant ketoacidosis to be manifested.s following insulin withdrawal from diabetic man and animals, and hypoglycemic and hypoketonemic effects of insulin. Studies negating a primary role for insulin deficiency in ketoacidosis include the "normal" plasma insulin concentration in the majority of ketoacidotic cases, delayed onset of ketoacidosis after insulin withdrawal from diabetic man, and lack of hypolipolytic and hypoketonemic effect of insulin without prior stress hormone adipocyte and hepatocyte stimulation. Evidence that stress hormones (glucagon, catecholamines, cortisol, and growth hormone) contribute to the metabolic decompensation of ketoacidosis includes: (1) in all cases of ketoacidosis, at least one stress hormone is always elevated; (2) pharmacologic blockade of each of the stress hormones reduces the rate and/or frequency of metabolic decompensation in diabetic man; (3) removal of the pituitary and/or the adrenal gland in diabetic animals completely prevents the development of ketoacidosis after insulin withdrawal; and (4) administration of each of the four stress hormones under appropriate conditions induces metabolic decompensation in diabetic man with "normal" circulating levels of plasma insulin concentration. From these studies, the following conclusions are supported: (1) absolute insulin deficiency is an unusual cause of ketoacidosis; (2) the presence of relative insulin deficiency is necessary for the development of ketoacidosis; and (3) stress hormone excess is necessary for fulminant ketoacidosis to be manifested.
 ...
PMID:Pathogenesis of diabetic ketoacidosis: a reappraisal. 11 31

Glucose tolerance and insulin and glucagon secretion were examined sequentially during 6 months of calorie and carbohydrate restriction in an obese, recent-onset, ketosis-resistant diabetic adult. The subject was then followed for 9 additional months, during which some weight was regained. Fasting plasma glucose levels returned to normal after 6 week of calorie restriction and remained normal during periods of carbohydrate refeeding. Normalization of 2-h plasma glucose concentrations after a standard oral carbohydrate load required 5 months, and glucose disposal after an iv glucose load did not return to normal until the end of the study. Insulin secretion in response to oral glucose reached maximal levels during the first months of weight reduction and then decreased as glucose tolerance continued to improve. Acute phase insulin release in response to iv glucose gradually increased throughout the study. Glucagon stimulation by iv arginine and suppression by iv glucose also returned to normal levels slowly over several months. Abnormalities in glucose tolerance and glucoregulatory hormone secretion of ketosis-resistant diabetes are totally reversible with prolonged dietary therapy. Reduction in tissue resistance to the action of insulin also appeared to be of major importance in the recovery of normal glucose tolerance in this subject.
 ...
PMID:Normalization of insulin and glucagon secretion in ketosis-resistant diabetes mellitus with prolonged diet therapy. 11 19

Increased gastric acid secretion occurs after extensive intestinal resection in man, dog, rat, and monkey. Hypergastrinemia has been observed in patients with short gut syndrome and appears to accompany the hyperacidity after intestinal resection in dog, rat, and monkey. Postresectional hypergastrinemia is caused by increased release of gastrin and/or decreased degradation of the hormone. Other hormonal changes after extensive resection include increased insulin, GIP, pancreatic glucagon, and decreased enteroglucagon.
 ...
PMID:Hyperacidity and hypergastrinemia following extensive intestinal resection. 11 43

The effect of a sulfonylurea, glibenclamide, on the release of insulin, glucagon, and somatostatin was studied in the isolated perfused rat pancreas. At glucose concentrations of 1.1 mM or less, the drug stimulated somatostatin release, whereas glucagon release, after 2-3 min of increase, was markedly inhibited. Insulin release was moderately stimulated, and maximal release occurred relatively late. A moderate glucose load (6.7 mM) inhibited glibenclamide-induced release of somatostatin, whereas the two in combination exerted an additive action on insulin release. Greater glucose loads, which by themselves would stimulate somatostatin release, only marginally suppressed glibenclamide-induced somatostatin release. The insulinogenic effect of these glucose levels was not modified by glibenclamide. Glibenclamide may thus stimulate both the alpha and beta as well as delta cells of the pancreas, depending on glucose concentration. We suggest a paracrine (local) interaction of somatostatin with the alpha and beta cells, which has an important role in the kinetics of insulin and glucagon release induced by sulfonylureas.
 ...
PMID:Effect of glucose/sulfonylurea interaction on release of insulin, glucagon, and somatostatin from isolated perfused rat pancreas. 11 58

We have examined the pattern of the capillaries of the pancreas in rabbits, rats, mice, guinea-pigs, cats and baboons, using arterial and venous injections of Berlin blue. In all these species we found extensive, direct connexions between the capillary beds of the islets and the exocrine tissue of the gland, forming a highly developed portal system. Some of the functional implications of these vascular connexions are discussed, particularly the influence of the islet hormones insulin, glucagon and somatostatin upon the exocrine cells.
 ...
PMID:A comparative study of the portal vessels connecting the endocrine and exocrine pancreas, with a discussion of some functional implications. 11 78


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>