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 examined the effect of hyperglycemia per se on net splanchnic glucose balance. In 2 groups of normal postabsorptive men who had undergone hepatic vein catheterization, somatostatin was administered to block endogenous insulin and glucagon secretion. Exogenous glucose was infused in both groups to maintain euglycemia for 2 h in one group (n = 7) and to induce hyperglycemia of 220-240 mg/dl after 30 minutes of euglycemia in the second group (n = 4). In both groups the induction of insulinopenia and glucagonopenia with euglycemia maintained resulted in an initial 75% fall in net splanchnic glucose production (NSGP). In the group in which euglycemia was maintained NSGP returned to basal rates (157 +/- 31 mg/min) within 2 h. However, in the group in which hyperglycemia was induced, NSGP did not return to basal rates but remained suppressed (28 +/- 4 mg/min) for the duration of the study. These data in normal man indicate that hyperglycemia per se with insulin and glucagon acutely withdrawn can suppress splanchnic glucose production but does not induce net splanchnic glucose storage.
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PMID:Hyperglycemia per se (insulin and glucagon withdrawn) can inhibit hepatic glucose production in man. 42

Somatostatin (SRIF) has been tested for its actions on the central nervous system to affect glucoregulation. In doses ineffective when given systemically , SRIF and SRIF analogs given intracisternally (ic) reduce hyperglycemia and hyperglucagonemia after ic bombesin administration. The SRIF analog, des-AA1, 2, 4, 5, 12, 13-[D-Trp8]SRIF, decreases plasma insulin and elevates plasma glucose and glucagon when given systemically. However, when given ic, this peptide prevents the rise in glucose and glucagon after ic bombesin administration and is 10 times more potent than SRIF in reducing bombesin-induced hyperglycemia. Other analogs of SRIF and various unrelated peptides were found to be ineffective in reducing bombesin-induced hyperglycemia. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF prevented the hyperglycemia induced by surgical stress or by ic administration of beta-endorphin or carbacol. des-AA1, 2, 4, 5, 12, 13-[D-Trp]SRIF given ic did not prevent hyperglycemia induced by systemic administration of epinephrine, arginine, or glucagon. These studies suggest that SRIF and its analogs may act within the brain to affect glucoregulation.
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PMID:Somatostatin: central nervous system actions on glucoregulation. 44 91

Bombesin acts within the brain to produce a prompt and sustained hyperglycemia, hyperglucagonemia, and relative or absolute hypoinsulinemia. Bombesin does not decrease plasma glucose turnover. Acute adrenalectomy but not hypophysectomy prevents hyperglycemia and hyperglucagonemia after intracisternal administration of bombesin. Administration of bombesin into the lateral ventricle of awake, unrestrained animals results in elevation of plasma glucose, preceded by a significant increase in plasma epinephrine and no increase in plasma norepinephrine or dopamine. Systemic administration of somatostatin prevents bombesin-induced hyperglycemia and hyperglucagonemia. These data support the conclusion that bombesin acts within the brain to increase sympathetic outflow resulting in increased adrenalmedullary epinephrine secretion, followed by depression of plasma insulin and elevation of plasma glucagon and glucose.
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PMID:Central nervous system action of bombesin: mechanism to induce hyperglycemia. 46 25

The effect of somatostatin (SRIF) and of insulin on the plasma levels of immunoreactive glucagon (IRG) and glucose was examined in normal (N) and depancreatized (PX) dogs. The infusion of SRIF (3 microgram/min for 15 min) caused a rapid decrease of the total IRG measured by means of an antiglucanon serum (AGS 10) which cross reacts with extracts of intestinal mucosa. This decrease was due primarily to a fall in the IRG fraction measured by an antiserum (AGS 18) specific for the carboxyl terminus of pancreatic or A-cell IRG. When the dose of SRIF was increased to 10 microgram/min for 90 min, the difference between total and A-cell IRG in the systemic blood also decreased, indicating that other IRG fractions, such as gut IRG, had also been suppressed. The introduction of 50 ml of a 5% glucose solution into a loop of ileum was followed by an increase of gut IRG measured in the regional mesenteric blood. This response was suppressed by the infusion of SRIF (3 microgram/min). Insulin suppressed the basal level of total IRG, but did not alter the gut IRG response to glucose. The SRIF- and insulin-induced reduction in plasma IRG was not associated with a reduction in plasma glucose, suggesting that the high levels of total and A-cell IRG observed in depancreatized dogs were not essential for the maintenance of hyperglycemia.
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PMID:A-Cell and gut glucagon in normal and depancreatized dogs. Inhibition by somatostatin and insulin. 47 84

The present study provides evidence that changes in glucagon secretion are influential in determining the hyperglycemic activity of catecholamines in normal and diabetic rats. In normal fed rats, epinephrine (EPI) stimulated large increments in glucagon release and inhibited insulin secretion. In contrast, the modest hyperglycemic activity of isoproterenol (ISO) in normal fed rats correlated with its weak glucagon-releasing activity and its strong insulin-releasing activity. In alloxan-diabetic rats, the augmented hyperglycemic response to ISO was accompanied by larger increments in plasma glucagon levels than the catecholamine produced in normal fed rats. When glucagon release was inhibited by a concurrent infusion of somatostatin, the hyperglycemic responses of normal fed rats to EPI were reduced by approximately 67%. ISO-induced hyperglycemia in alloxan-diabetic rats was even more sensitive to inhibition by somatostatin since this response was reduced by approximately 90% when glucagon release was inhibited by somatostatin. These findings indicate that more than half of the hyperglycemic response to EPI in normal fed rats and nearly all of the hyperglycemia produced by ISO in diabetic rats result from increased glucagon release. Moreover, the impotence of ISO as a hyperglycemic agent in normal fed rats is probably due to insulin release which tends to suppress glucagon release.
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PMID:The influence of endogenous glucagon release on hyperglycemic responses to catecholamines in normal fed and diabetic rats. 48 Jan 94

Normal subjects were infused 1) with epinephrine (50 ng/(kg.min)) for 180 min followed by epinephrine plus glucagon (3 ng/(kg.min)) for 60 min after which the epinephrine infusion rate was increased (125 ng/(kg.min)) or 2) with epinephrine plus somatostatin (500 microgram/h) for 180 min. Epinephrine increased glucose production and plasma glucagon transiently but caused persistent suppression of glucose clearance and sustained hyperglycemia (despite increased plasma insulin and gluconeogenic substrates); glucose production increased again on addition of glucagon and on increasing the epinephrine infusion rate. During epinephrine plus somatostatin, glucose production still increased transiently, but further suppression of glucose clearance caused more marked hyperglycemia. In conclusion, 1) in man hyperepinephrinemia within the physiological range caused sustained suppression of glucose clearance but only a transient increase in glucose production; 2) this transient hepatic response a) was not due to glycogen or substrate depletion, b) occurred without changes in plasma glucagon or insulin, c) was specific for epinephrine but permitted subsequent responses to changes in plasma epinephrine; 3) epinephrine can serve as a physiological regulator of glucose homeostasis in man both by increasing glucose production and by decreasing glucose clearance.
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PMID:Differential effects of epinephrine on glucose production and disposal in man. 49 14

The present study was designed to examine the effects of intravenously injected alloxan (75 mg/kg) upon plasma somatostatin-like immunoreactivity (SLI), glucagon (IRG), insulin (IRI) and glucose levels in 6 dogs. Within 2 hours of the injection of alloxan, SLI and IRI levels decreased significantly below their respective baselines, while IRG and plasma glucose concentrations increased. At 8 hours SLI levels had increased significantly by 55 pg/ml, together with a rise in IRI and a decrease in IRG and glucose concentrations. After 24 hours, marked hyperglycemia and hyperglucagonemia had developed whereas SLI levels were not different from preinjection values.
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PMID:Response of plasma somatostatin-like immunoreactivity to the administration of alloxan in dogs. 49 95

Depancreatized dogs have plasma immunoreactive glucagon (IRG), which is of gastric origin and is immunologically indistinguishable from pancreatic glucagon. The effects of extrapancreatic IRG on the tracer-determined rate of glucose production were examined to establish whether this hormone contributes to the hyperglycemia observed in six conscious, depancreatized dogs after insulin withdrawal. The dogs were initially maintained normoglycemic with an intraportal insulin infusion. Insulin withdrawal resulted in a 53 and 70% decrease of serum immunoreactive insulin (IRI) at 60 and 210 min, respectively. At 60 min, plasma glucose rose and Ra increased by 50%. A somatostatin-induced decrease in IRG prevented a further increase in Ra and glucose; after somatostatin withdrawal, IRG, Ra, and plasma glucose increased. Arginine given 1 or 3 h after insulin withdrawal increased IRG by 100 pg/ml, and mean Ra rose by 8.9 mg/kg-min. Thus, in depancreatized dogs with low but detectable serum IRI, IRG suppression is associated with inhibition of Ra and further rise in plasma glucose is prevented. Stimulation of IRG release increases Ra and results in marked hyperglycemia. It is concluded that extrapancreatic glucagon has a diabetogenic effect during acute insulin defiency.
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PMID:Extrapancreatic glucagon in control of glucose turnover in depancreatized dogs. 62 97

Oral glucose tolerance was examined in five maturity-onset diabetics during the infusion of somatostatin or saline. Somatostatin inhibited glucose-stimulated insulin release and reduced plasma glucagon by 50%--65%. The rise in plasma glucose after glucose ingestion was initially (at 30--120 min) reduced by somatostatin. However, beyond 3 hr, plasma glucose levels were 50--200 mg/100 ml higher, with somatostatin reaching concentrations at 6 hr that were twofold higher than those observed with saline ( p less than 0.005). The degree of late glucose intolerance was inversely related to postglucose plasma insulin concentrations (p less than 0.01). These findings demonstrate a biphasic effect of somatostatin on oral glucose tolerance in maturity-onset diabetes. The exaggerated later hyperglycemia is related to suppression of insulin secretion. The initial blunting of postprandial hyperglycemia may reflect decreased carbohydrate absorption and/or hypoglucagonemia-mediated enhancement of glucose disposal.
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PMID:Biphasic effect of somatostatin on oral glucose tolerance in maturity-onset diabetes. 66 68

The first aim of this study was to determine whether the plasma glucose level can regulate hepatic glucose balance in vivo independent of its effects on insulin and glucagon secretion. To accomplish this, glucose was infused into conscious dogs whose basal insulin and glucagon secretion had been replaced by exogenous intraportal insulin and glucagon infusion after somatostatin inhibition of endogenous pancreatic hormone release. The acute induction of hyperglycemia (mean increment of 121 mg/dl) in the presence of basal levels of insulin (7+/-1 muU/ml) and glucagon (76+/-3 pg/ml) resulted in a 56% decrease in net hepatic glucose production but did not cause net hepatic glucose uptake. The second aim of the study was to determine whether a decrease in the plasma glucagon level would modify the effect of glucose on the liver. The above protocol was repeated with the exception that glucagon was withdrawn (83% decrease in plasma glucagon) coincident with the induction of hyperglycemia. Under this circumstance, with the insulin level basal (7+/-1 muU/ml) and the glucagon levels reduced (16+/-2 pg/ml), hyperglycemia (mean increment of 130 mg/dl) promoted marked net hepatic glucose uptake (1.5+/-0.2 mg/kg per min) and glycogen deposition. In conclusion, (a) physiological increments in the plasma glucose concentration, independent of their effects on insulin and glucagon secretion, can significantly reduce net hepatic glucose production in vivo but at levels as high as 230 mg/dl cannot induce net hepatic glucose storage and (b) in the presence of basal insulin the ability of hyperglycemia to stimulate net hepatic glucose storage is influenced by the plasma glucagon concentration.
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PMID:Glucose disposal during insulinopenia in somatostatin-treated dogs. The roles of glucose and glucagon. 67 Apr 4


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