Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have described before that different forms of physical exercise induce bidirectional changes of insulin binding of monocytes (Michel G., Vocke T., Fiehn W., Weicker H., Schwarz W., Bieger W.P.: Am J Physiol 246: E 156-E 159, 1984). In vitro experiments suggested these changes to be due to dialyzable serum components. In this study, we investigated several hormones and metabolites as to their capacity to alter insulin binding in vitro. Somatostatin (100 pg/ml) and prostaglandin B1 (10 nmol/l) were the only hormonal agents producing a small and reversible (somatostatin) increase in monocyte insulin binding. Ketones were only effective at concentrations unphysiologically high. Acidosis diminished insulin binding to monocytes to about 35% of that found at pH 7.6. Lactate (10 mmol/l) induced a 28% drop in cellular insulin binding at low pH. The effect persisted after removal of the agent and may hence account for some of the decrease in cellular insulin binding observed after exhaustive exercise. Although the effect of acidosis was reversible in vitro, it may add considerably to the effect of lactate under in vivo conditions. The dialyzable serum factors responsible for the enhancement of binding affinity after long-term moderate exertion remain unknown. Free fatty acids proved effective in increasing monocyte insulin binding (14% with 1 mmol/l oleic acid) in vitro.
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PMID:Exercise-induced regulation of insulin receptor affinity: role of circulating metabolites. 286 Nov 68

We studied the influence of hyperglycemia on glucose homeostasis in man by determining the effect of graded hyperglycemia on peripheral glucose uptake and systemic metabolism in the presence of basal and increased serum insulin concentrations in 10 normal men. This was achieved by the simultaneous application of forearm and clamp techniques (euglycemic and hyperglycemic) during the combined iv infusion of somatostatin, glucagon, and insulin. While mean (+/- SE) basal serum insulin levels (14 +/- 2 microU/ml) were maintained, the elevation of fasting arterial glucose concentrations (90 +/- 1 mg/dl) to 146 +/- 1 and 202 +/- 1 mg/dl (each for 120 min) increased forearm glucose uptake (FGU) only modestly from 0.06 +/- 0.01 to 0.15 +/- 0.02 and then to 0.24 +/- 0.03 mg/100 ml forearm X min, respectively. During physiological hyperinsulinemia (47 +/- 3 microU/ml), the influence of similar graded hyperglycemia on FGU was considerably enhanced. At plasma glucose concentrations of 90 +/- 1, 139 +/- 1, and 206 +/- 1 mg/dl, FGU rose to 0.33 +/- 0.05, 0.59 +/- 0.07, and 0.83 +/- 0.12 mg/100 ml forearm X min, respectively. The glucose infusion rate required to maintain the glucose clamp with basal insulin levels was 1.08 +/- 0.20 and 2.67 +/- 0.39 mg/kg X min at glucose concentrations of 146 +/- 1 and 202 +/- 1 mg/dl, respectively. During physiological hyperinsulinemia, however, the glucose infusion rate required was 4.15 +/- 0.39, 9.45 +/- 1.05, and 12.70 +/- 0.81 mg/kg X min at glucose levels of 90 +/- 1, 139 +/- 1, and 206 +/- 1 mg/dl, respectively. Lactate concentrations rose significantly during hyperglycemia, but the rise in the presence of increased insulin concentrations (from 0.72 +/- 0.06 to 1.31 +/- 0.11 mmol/liter; P less than 0.001) considerably exceeded the increment (from 0.74 +/- 0.05 to 0.92 +/- 0.03 mmol/liter) with basal insulin levels. While both FFA and glycerol concentrations were immediately reduced by euglycemic hyperinsulinemia, the fall in FFA during hyperglycemia in the presence of basal insulin levels preceded the decrease in glycerol concentrations by 45 min. Forearm oxygen consumption did not change throughout the study.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The influence of graded hyperglycemia with and without physiological hyperinsulinemia on forearm glucose uptake and other metabolic responses in man. 287 53

The metabolic responses to infusion of adrenaline (6 micrograms/min) and of noradrenaline (5 micrograms/min) for 120 minutes have each been studied in five normal males with and without concurrent somatostatin (250 micrograms/h). Adrenaline induced marked and sustained hyperglycaemia (maximal blood glucose at 75 min, 9.0 +/- 0.4 mmol/l) while noradrenaline induced only a mild and transient blood glucose rise. Blood lactate was elevated by adrenaline (2.57 +/- 0.47 mmol/l with adrenaline, 0.62 +/- 0.06 mmol/l with saline at 120 min, p less than 0.02). Pyruvate levels rose proportionately less so that the circulating lactate:pyruvate ratio was increased (16.6 +/- 1.3 with adrenaline, 11.4 +/- 0.9 with saline at 120 min, p less than 0.05). Lactate and pyruvate levels were unaffected by noradrenaline. Both catecholamines increased circulating non-esterified fatty acid (NEFA) and glycerol to peak at 30 min, while maximal 3-hydroxybutyrate concentrations were achieved at 50 min (0.26 +/- 0.07 mmol/l with adrenaline; 0.23 +/- 0.06 mmol/l with noradrenaline; 0.03 +/- 0.01 mol/l with saline, both p less than 0.05). Insulin levels were partially suppressed by noradrenaline, while a small rise in circulating insulin was observed with adrenaline which was also associated with a large rebound rise in insulin secretion on cessation of the infusion. Mild and transient hyperglucagonaemia was observed with adrenaline while stimulation of glucagon secretion was more sustained with noradrenaline. Somatostatin suppressed insulin, glucagon and growth hormone secretion and both magnified and prolonged the hyperglycaemic effect of adrenaline (maximal at 105 min, 11.3 +/- 0.5 mmol/l, p less than 0.01 versus adrenaline alone).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic effects of adrenaline and noradrenaline in man: studies with somatostatin. 614 42

The purpose of this study was to examine the temporal plasma glucose, lactate, insulin, and somatostatin responses of 10-day-old (10 d) and 28-day-old (28 d) rats to the effects of an LD90 dose of endotoxin for a 4 h period. Salmonella enteritidis endotoxin was administered to 10 d and 28 d rats at .2 and 30.0 mg/kg, respectively. Hyperglycemia was the initial response to endotoxin, followed by hypoglycemia; this was similar for 10 d and 28 d rats. Lactate levels were significantly elevated in 10 d rats, but only mild hyperlactacidemia was observed in 28 d rats. Hyperinsulinemia was observed in both 10 d and 28 d rats in response to elevated glucose levels; in 10 d rats, decreased insulin levels preceded the hyperinsulinemia. Plasma somatostatin levels were elevated in both 10 d and 28 d rats in response to endotoxin, but the endotoxin-induced somatostatin levels were greater and occurred earlier in 28 d rats than in 10 d rats. The magnitude of the somatostatin response to endotoxin in the developing rats was markedly less than that previously reported in adult rats. Since previous reports indicated that somatostatin supported the glucoregulatory adaptive response to endotoxin in adult rats, the present results suggested that the diminished somatostatin response to endotoxin in developing rats may partially underlie their increased sensitivity to endotoxin and the profound glucose dyshomeostasis that results subsequently.
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PMID:Glucose, lactate, insulin, and somatostatin responses to endotoxin in developing rats. 774 75

We previously reported that simulation of the chronic hyperglucagonemia seen during infection was unable to recreate the infection-induced increase in hepatic glucose production. However, chronic hyperglucagonemia was accompanied by a fall in the arterial levels of gluconeogenic precursors as opposed to a rise as is seen during infection. Thus our aim was to determine whether an infusion of gluconeogenic precursors could increase hepatic glucose production in a setting of hyperglucagonemia. Studies were done in 11 conscious chronically catheterized dogs in which sampling (artery and portal and hepatic veins) and infusion catheters (splenic vein) were implanted 17 days before study. Forty-eight hours before infusion of gluconeogenic (GNG) precursors, a sterile fibrinogen clot was placed into the peritoneal cavity. Glucagon was infused over the subsequent 48-h period to simulate the increased glucagon levels (approximately 500 pg/ml) seen during infection. On the day of the experiment, somatostatin was infused peripherally, and basal insulin and simulated glucagon were infused intraportally. After a basal period, a two-step increase in lactate and alanine was initiated (120 min/step; n = 5). Lactate (Delta479 +/- 25 and Delta1, 780 +/- 85 microM; expressed as change from basal in periods I and II, respectively) and alanine (Delta94 +/- 13 and Delta287 +/- 44 microM) levels were increased. Despite increases in net hepatic GNG precursor uptake (Delta0.7 +/- 0.3 and Delta1.1 +/- 0.4 mg glucose . kg-1 . min-1), net hepatic glucose output did not increase. Because nonesterified fatty acid (NEFA) levels fell, in a second series of studies, the fall in NEFA was eliminated. Intralipid and heparin were infused during the two-step substrate infusion to maintain the NEFA levels constant in period I and increase NEFA availability in period II (Delta -29 +/- 29 and Delta689 +/- 186 microM; n = 6). In the presence of similar increases in net hepatic GNG precursor uptake and despite increases in arterial glucose levels (Delta17 +/- 5 and Delta38 +/- 12 mg/dl), net hepatic glucose output increased (Delta0.6 +/- 0.1 and Delta0.7 +/- 0.2 mg . kg-1 . min-1). In summary, a chronic increase in glucagon, when combined with an acute increase in gluconeogenic precursor and maintenance of NEFA supply, increases hepatic glucose output as is seen during infection.
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PMID:Regulation of glucose production by NEFA and gluconeogenic precursors during chronic glucagon infusion. 972 9