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)

Insulin resistance was estimated in nine subjects with impaired glucose tolerance (IGT) and eleven healthy, age and body-weight matched controls. Glucose tolerance and insulin response were evaluated by means of a 2h-glucose infusion test. Insulin resistance was determined by measuring the steady state plasma glucose response (SSPG) to a continuous infusion of glucose (6 mg . kg-1 . min-1 or 12 mg . kg-1 . min-1), insulin, epinephrine and propranolol for 150 minutes as described previously by other authors. The endogenous insulin secretion (C-peptide) was inhibited by epinephrine and propranolol in controls and subjects with IGT irrespective of a low (6 mg . kg-1 . min-1) or high (12 mg . kg-1 . min-1) glucose infusion. Steady-state plasma levels of exogenous insulin were virtually identical in all groups studied. There were no significant differences in the pancreatic glucagon, growth hormone, FFA and glycerol response during the SSPG period between controls and subjects with IGT. In comparison to controls the mean SSPG was significantly higher in subjects with IGT (during low and high glucose infusion) suggesting the existence of insulin resistance in these subjects. A higher glucose dose as described earlier by other investigators does not provide a better discrimination of controls and subjects with IGT concerning their degree of insulin resistance. Finally, there was a direct correlation between the SSPG and glucose tolerance in the total group. In conclusion, our results have confirmed the validity of an infusion technique of glucose, insulin, epinephrine and propranolol for evaluation of insulin sensitivity in vivo. In addition, our findings have added further support for insulin resistance in subjects with IGT which is directly proportional to the degree of glucose intolerance.
 ...
PMID:Evaluation of insulin resistance in non-obese subjects with impaired glucose tolerance. 675 94

Beta-blockade is known to induce muscle fatigue and tendency to hypoglycaemia during prolonged exercise. In addition, beta-blocking agents influence the secretion of many hormones, which regulate glucose. We have investigated the effects of a beta 1-selective (metoprolol) and a non-selective (propranolol) beta-blocking agent on muscle glycogenolysis, blood glucose and lactate levels, plasma levels of free fatty acids and on secretion of insulin, growth hormone, glucagon and cortisol during physical exercise in a double blind cross-over study in seven healthy male volunteers. They participated in three bicycle ergometer tests each lasting for 30 minutes under treatment of placebo (C), metoprolol (M) or propranolol (P). A biopsy was obtained from the vastus lateralis muscle before and immediately after the exercise for muscle glycogen assay. The glycogen concentration after exercise tended to be lower in C than in M or P experiment. The blood glucose level decreased during P and at 30 min there was a significant difference between P and C. The blood lactate was significantly lower before exercise during P than C or M. The increase of blood lactate during exercise, however, was not inhibited by P. Both beta-blocking agents counteracted the increase of FFA during exercise. There was a marked increase of growth hormone secretion during beta-blockade. The secretion of glucagon and cortisol were slightly increased by P and M, but the plasma insulin level was not affected by beta-blockade.
 ...
PMID:Modification of the metabolic and hormonal response to physical exercise by beta-blocking agents. 675 73

There seems little doubt that there are signals for the increased mobilization of fat in shock, trauma, and sepsis. Whether those signals are reflected by an actual increase in mobilization is dependent on many variables including cardiovascular status. A hypothetical scheme based on our own experiments in the hyperdynamics phases of response to burn injury and to sepsis is presented in Figure 8. According to this scheme, catecholamines stimulate lipolysis in the adipose tissue, resulting in the release of glycerol and FFA into the plasma at increased rates. The glycerol is cleared by the liver and converted into glucose--a process stimulated by, among other things, glucagon. Some of the increased flux of FFA is also cleared by the liver, whereupon the fatty acids are incorporated into VLDL and released again into the plasma. The increased FFA levels also exert a dampening effect on the factors stimulating hepatic glucose production. At the periphery, plasma FFA as well as VLDL fatty acids are taken up at an increased rate. The tissues are attuned to the oxidation of fat, and as a consequence most of the energy production is derived from fat oxidation. The increased fatty acids exert an inhibitory effect on the complete oxidation of glucose, so although glucose may be taken up at an accelerated rate, the relative contribution of glucose oxidation to total energy production may fall. Rather than being completely oxidized, pyruvate is reduced to lactate and released into the plasma at an accelerated rate. The lactate then contributes to the production of glucose in the liver, completing a cyclical process called the Cori Cycle. Although all aspects of this scheme are supported by data highlighted in this paper, it certainly must be an oversimplification of the overall response of substrate metabolism to trauma and sepsis. It is presented for the purpose of highlighting the potential role of fat as a controller of the metabolic response, and to suggest that the enhanced mobilization and oxidation of fat is one of the fundamental responses to stress.
 ...
PMID:Energy metabolism in trauma and sepsis: the role of fat. 686 23

The role of physiological hypercortisolemia in the regulation of fuel metabolism in man was examined during a 5-h primed-continuous infusion of cortisol which raised plasma cortisol levels to 40 microgram/dl. Plasma glucose increased by 15--20 mg/dl (P less than 0.005) in spite of unchanged rates of glucose production. Glucose uptake and clearance, on the other hand, fell by 15% (P less than 0.05) and 30% (P less than 0.005), respectively, thereby accounting for cortisol-induced hyperglycemia. Total blood ketones during cortisol infusion increased 3-fold above saline control values (P less than 0.01) despite comparable FFA levels in the two groups. In addition, there was a selective 40% rise in total branched chain amino acids (P less than 0.005) during cortisol infusion. These effects of cortisol on glucose, ketone, and amino acid metabolism occurred in the absence of significant changes in the plasma insulin or glucagon concentration. Furthermore, cortisol infusion had no effect on [125I]insulin binding to circulating monocytes. Our data thus suggest that acute elevations of plasma cortisol have antiinsulin effects in man which may occur independent of alterations in insulin receptors.
 ...
PMID:The influence of acute physiological increments of cortisol on fuel metabolism and insulin binding to monocytes in normal humans. 610 51

This study aimed at evaluating the effect of acetylsalicylic acid (ASA) on blood glucose, plasma FFA, glycerol, 3-hydroxybutyrate, alanine, C-peptide, glucagon and growth hormone responses to arginine in subjects with insulin-dependent diabetes. For this purpose, seven insulin-requiring diabetics were submitted to a standard arginine tolerance test before and after a three day treatment with ASA (50 mg/kg/daily, plus 1 g before the second test). ASA treatment resulted in no significant changes in either basal or arginine-stimulated blood glucose, but it significantly decreased the basal concentrations of plasma FFA (p less than 0.05), 3-hydroxybutyrate (p less than 0.05) and glycerol (p less than 0.05). In addition, the fall in plasma FFA concentrations during arginine infusion was significantly less after ASA than levels observed without ASA (--262 +/- 100 microEq/l vs --35 +/- 57 microEq/l, p less than 0.02). No significant changes in either basal or arginine-stimulated glucagon concentrations were observed after ASA; by contrast, the growth hormone peak was significantly reduced after ASA (11.3 +/- 4.2 ng/ml vs 5.1 +/- 1.1 ng/ml, p less than 0.05). These metabolic effects exerted by ASA in insulin-dependent diabetes seem not to be related to alterations in endogenously secreted insulin since C-peptide circulating levels were similar during the pre- and post-treatment arginine tests.
 ...
PMID:Effects of acetylsalicylic acid on blood glucose, plasma FFA, glycerol, 3-hydroxybutyrate, alanine, C-peptide, glucagon and growth hormone responses to arginine in insulin-dependent diabetics. 698 60

Resistance to both insulin and glucagon have been considered as possible causes of primary hypertriglyceridemia. In the present research, we have compared insulin and glucagon secretion in five hyperlipidemic patients with familial dysbetalipoproteinemia with five normolipidemic control subjects matched for age, sex and adiposioty. Plasma insulin and glucagon concentrations mesaured during standard oral glucose tolerance and arginine infusion tests were similar in the two groups. Blood glucose fell transiently in the controls, but not in the patients, during the Himsworth test (100 g glucose orally plus 0.05 U insulin per kg body weight intravenously). There were no significant differences in plasma FFA concentrations and responses during all tests between the groups. The percentage reduction in plasma triglyceride concentration during infusion of arginine was similar in the two groups. These results suggest that the patients with familial dysbetalipoproteinemia were slightly less insulin sensitive than the controls. However, primary insensitivity to glucagon or insulin does not appear to be fundamental to the pathogenesis of hyperlipidemia in familial dysbetalipoproteinemia.
 ...
PMID:Pancreatic alpha and beta cell function in familial dysbetalipoproteinemia. 700 Jun 52

The existence of plasma metabolites (glucose, free fatty acids [FFA[, aminoacids [AA])--pancreatic hormones (insulin, glucagon) feedback mechanisms and of insulin-glucagon relationships were studied in hypophysectomised ducks; the insulinogenic effect of glucagon was also studied in normal ducks in physiological conditions. Glucose infusion stimulated insulin secretion in hypophysectomised ducks; during oleic acid infusion, plasma IRI (immunoreactive insulin) was not modified whereas plasma GLI (glucagon like immunoreactivity) level drops slightly. Arginine induced insulin and glucagon secretion. Plasma GLI did not decrease during insulin infusion. In normal ducks glucagon was insulinogenic, hyperglycaemic and hypoaminoacidaemic. These biological properties of glucagon were lost in hypophysectomised ducks, except the effect on plasma aminoacids. It is concluded that the anterior pituitary and the adrenal cortex indirectly control the endocrine function of the pancreas, via the plasma metabolites and the insulin-glucagon interactions. In normal ducks, glucagon is probably insulinogenic in physiological conditions.
 ...
PMID:Pituitary and adrenal control of pancreatic endocrine function in the duck. III. Effects of glucose, oleic acid, arginine, insulin and glucagon infusions in hypophysectomized or normal ducks. 700 47

We have previously shown that during swimming muscular glycogen breakdown was diminished and plasma glucagon and insulin were lower and higher, respectively, in adrenodemedullated rats compared to controls. These findings might be due to a lower work intensity or higher efficiency in adrenodemedullated rats than in controls. Furthermore, they might be due to either an acute or a chronic influence of epinephrine. Rats were adrenodemedullated (DM) or sham-operated (C). They were chronically cannulated and either rested or ran in a metabolism chamber for 45 min. Running DM rats had either saline (DM-S) or epinephrine (normalizing the concentration in plasma) (DM-E) infused. During running, oxygen uptake was identical in C and DM rats. Muscular glycogen breakdown was similar in DM-E and C rats and higher than in DM-S rats. Blood glucose, lactate, and heart rate increased in C and DM-E, but not in DM-S rats. In spite of the differences in blood glucose, plasma insulin was the same in all groups and plasma glucagon increased identically in all running rats. Plasma FFA and liver glycogen were similar in all groups. In conclusion. in running rats, epinephrine exerts an acute enhancing effect on muscular glycogenolysis, glucagon secretion, and heart rate and an acute depressing effect on insulin secretion.
 ...
PMID:Role of epinephrine for muscular glycogenolysis and pancreatic hormonal secretion in running rats. 701 78

In normal dogs epinephrine stimulates glucose production (Ra) independently of glucagon. To investigate the role of this interaction in diabetes, epinephrine (0.1 micrograms . kg-1 . min-1) was infused for 90 min in five alloxan-diabetic dogs in the presence or absence of somatostatin (0.1 micrograms . kg-1 . min-1). In response to epinephrine, glycemia rose by 40% reflecting a near maximal (122%) increase in Ra. Plasma glucagon (IRG) rose to 953 pg/ml, whereas insulin (IRI) increased minimally. When somatostatin was infused with epinephrine to prevent the rise of IRG and IRI, there was only a marginal increase of glucose concentration (12%) and production (38%). The effect of somatostatin was reversed by infusing glucagon (10 ng . kg-1 . min-1) together with epinephrine and somatostatin into five additional alloxan-diabetic dogs. Increments in IRG, glycemia, and Ra were fully reestablished. A 100% FFA increase was observed in all three groups, indicating that the lipolytic effect of epinephrine was independent of glucagon. In conclusion, in diabetic dogs, in contrast to normal dogs, epinephrine induced a marked and prolonged increase in glucose concentration and production mostly through a stimulation of IRG secretion.
 ...
PMID:Importance of glucagon in mediating epinephrine-induced hyperglycemia in alloxan-diabetic dogs. 703 19

Thirty hospitalized, severely obese patients (40 +/- 2 yr, 82 +/- 4 percent weight excess) were submitted to a 13-d protein-supplemented fast (PSF) with 70 g milk proteins/d (1.26 MJ or 300 kcal). The mean weight loss during PSF was 5.4 +/- 0.3 kg corresponding to 422 +/- 39 g/d. Comparison of the urinary nitrogen excretion with daily protein intake revealed that the nitrogen balance was equilibrated during PSF. Blood glucose decreased moderately but significantly during the whole PSF period whereas plasma insulin was only reduced during the first 9 d and tended to rise thereafter. Plasma FFA increased rapidly and remained elevated until the end of the study (+ 60 per cent); serum total cholesterol and plasma triglycerides showed a 26 and a 35 per cent decrease respectively. Basal plasma glucagon was slightly increased. Due to the low sodium intake (42 mmol/d) urinary sodium excretion dropped rapidly. Simultaneously both systolic (-13 mmHg) and diastolic (-7 mmHg) arterial blood pressure decreased significantly. The biological tolerance was good: metabolic acidosis was prevented with sodium bicarbonate, excessive rise in serum uric acid was corrected with allopurinol and a marked decrease in serum potassium was avoided with an appropriate dose of spironolactone. Twenty-six patients could be weighed 6 to 15 months after PSF: 12 showed a further weight reduction (6.6 +/- 1.6 kg) and seven a discrete weight gain (1.0 +/- 0.4 kg). Thus, PSF was well accepted and was profitable in 19 out of our 30 patients. It should be restricted to cases of severe and refractory obesity and performed under careful medical supervision.
 ...
PMID:Hormonal and metabolic adaptation to protein-supplemented fasting in obese subjects. 704 25


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