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)

Changes in glucagon, growth hormone (GH), cortisol, renin and aldosterone accompanying the metabolic disturbances and dehydration of severe diabetic ketoacidosis were studied over a 24 h period in eight patients treated with a constant intravenous insulin infusion. Mean steady state plasma-free insulin levels achieved were 28.6--49 mu/1 in patients receiving 2 u/h but a satisfactory rate of fall of glucose was not always obtained until the infusion dose was increased to 4 u/h or more. The total insulin dose administered was positively correlated with the level of plasma glucagon and cortisol on admission. During insulin infusion, both glucagon and cortisol fell but the rate of fall was not related to dose or plasma level of free insulin achieved. In six of eight patients studied increments in plasma GH above admission levels were observed during insulin treatment. Admission values of both plasma renin activity and plasma aldosterone were raised. The renin levels were highest in newly diagnosed diabetics, and two patients with long-established diabetes showed only small increments despite profound dehydration. Plasma renin activity, but not plasma aldosterone correlated with the fluid and sodium retention over the initial 24 h treatment period, but not with potassium requirements. The urinary excretion rates of the small molecular weight proteins GH and insulin, were considerably elevated over the treatment and convalescent periods.
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PMID:Hormonal responses during treatment of acute diabetic ketoacidosis with constant insulin infusions. 10 71

Two transplant procedures have been investigated in which one third of the pancreas was autotransplanted into the splenic pulp of dogs. The two procedures consist of simple mechanical dissociation of the pancreas or mechanical dissociation followed by collagenase digestion. The ability of the endocrine segment of the transplant to survive and function was assessed by stimulation with arginine and measurement of insulin and glucagon response. The results demonstrate that both transplant procedures result in functioning beta and alpha cells that rapidly secrete both insulin and glucagon in response to arginine stimulation. However, greater insulin responses were obtained when mechanically dissociated but nonenzyme digested pancreatic tissue was used for transplantation. The spleen appears to be an excellent transplant site for the reception of endocrine pancreatic tissue and allowed both beta and alpha cells to survive following transplantation.
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PMID:Insulin and glucagon responses of transplanted intrasplenic pancreatic islets. 10 13

"Gastric inhibitory peptide" or "glucose-dependent insulin-releasing peptide" (GIP) is a member of the gut hormone family. Its physiological action is thought to be related to its insulinotrophic effect. The occurrence and distribution of GIP was studied by immunohistochemistry. In all species examined including man, GIP immunoreactivity was found to reside in the glucagon cells of the pancrease and gut. Three pancreatic glucagonomas were found to contain numerous cells displaying GIP and glucagon immunoreactivity. The GIP antiserum used did not cross react with either pancreatic-type or gut-type glucagon (GLI).
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PMID:Is GIP a glucagon cell constituent? 10 36

The effects of low-dose intramuscular insulin therapy on endogenous glucagon secretion in diabetic ketoacidosis were compared prospectively with a conventional regimen. Ten patients, 4 to 15 years of age, who had 13 episodes of diabetic ketoacidosis, were alternately assigned to either group. Either 0.1 unit/kg regular insulin was given every two hours im, or 1.0 unit/kg regular insulin was given, half subcutaneously and half intravenously, every 4 hours. In both groups, a significant and equal fall in both serum glucose and glucagon concentrations was observed. No complications were encountered. It is concluded that 0.1 unit/kg of regular insulin given im every two hours is as effective in correcting hyperglycemia and hyperglucagonemia of diabetic ketoacidosis as is conventional therapy, and avoids the risks of secondary hypoglycemia known to occur when the larger insulin dosages are employed.
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PMID:Glucagon suppression with low-dose intramuscular insulin therapy in diabetic ketoacidosis. 10 14

Studies in 7 patients after total duodenopancreatectomy showed a raised insulin sensitivity and a prolonged effect of depot insulin. Insulinemia is not the only reason for the tendency to hypoglycemia shown by these patients, which seems rather to be due to the lack of pancreatic glucagon, which is not available to antagonize the inhibition of glucose release from the liver by insulin (and also in alcohol abuse).
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PMID:[Insulin sensitivity and glucose utilization of patients after total duodenopancreatectomy (author's transl)]. 10 69

The binding and degradation of insulin and glucagon to kidney cell membranes was examined. Time- and temperature-dependent specific binding of [125I]iodo-insulin to kidney cell membranes was demonstrated. The membranes also degraded insulin in a time-, temperature-, and protein concentration-dependent manner. The apparent Km of the degradation was 2.7 x 10(-7) M. Glucagon degradation by the kidney membranes was extremely active. Per milligram of protein the kidney membrane was over 20 times as active as the liver membrane. Even at 4 C, significant glucagon degradation occurred. Because of this very active degradation, glucagon binding could not be accurately assessed. The kidney glucagon-degrading activity was inhibited by glutahione and EDTA but unaffected by N-ethylmaleimide, ACTH, or insulin, all potent inhibitors of liver glucagon degradation. The apparent Km for glucagon degradation by the kidney, however, was essentially identical with that for the liver, 2.4 x 10(-6) M.
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PMID:Insulin and glucagon binding and degradation by kidney cell membranes. 10 82

The effects of low-dose continuous insulin therapy were compared to those of high-dose subcutaneous and intravenous insulin therapy in six episodes of diabetic ketoacidosis. Time for correction of acidosis, ketosis, and hyperglycemia were similar for both regimens. The high-dose method required more exogenous glucose and supplemental potassium to avoid hypoglycemia and/or hypokalemia during treatment. Levels of cortisol, human growth hormone, and glucagon, initially elevated in most patients, showed a progressive decline with both modes of therapy. Plasma insulin remained remarkably stable during both treatment regimens, but remained within the physiologic range only in patients receiving low-dose therapy. Our study suggest that either modality is effective in the treatment of diabetic ketoacidosis.
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PMID:Low-dose versus high-dose insulin therapy for diabetic ketoacidosis. 10 76

TRH has been shown to be present in the pancreas. To examine a possible role for TRH in the control of endocrine pancreatic function, we have studied the effects of TRH on the isolated perfused rat pancreas preparation. Arginine caused release of TRH from the preparation. The mean maximum TRH peak was 85 +/- 12 pg/ml and occurred later than the first phase of glucagon release. Glucagon (2000 pg/ml) did not release TRH from the preparation. There was no detectable basal release of TRH. Glucose did not stimulate release of TRH from the pancreas preparation. TRH (10 ng/ml) by itself had no effect on insulin or glucagon release. TRH enhanced arginine-induced glucagon release; mean summated glucagon was 8228 +/- 1138 (SE) pg/ml compared to controls (4530 +/- 447 pg/ml; P less than 0.01). There was a tendency for TRH to enhance second phase glucose-induced insulin release. Pancreatic physiology is in part regulated by locally acting hormones and TRH may be one of these hormones.
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PMID:The effects of thyrotropin-releasing hormone on the endocrine pancreas. 10 72

Severe resistance to subcutaneous insulin but sensitivity to intravenous insulin persisted for 15 months in a 17-year-old diabetic girl. Heat-labile insulin-degrading activity was present in the patient's ketotic sera and in the 100,000 g fraction (soluble fraction) of adipose tissue. Serum-degrading activity was not inhibited by N-ethylmaleimide. The soluble fraction also degraded glucagon and B chain but not growth hormone or myoglobin. It was inhibited by incubation with the patient's nonketotic sera, normal sera, or Trasylol. Glutathione-insulin-transhydrogenase (GIT) activity was 66% of normal. The biopsy of adipose tissue at remission showed a normal level of insulin- and glucagon-degrading activity. The activity was eluted from Sephadex G200 as a single peak and had properties consistent with those of the insulin-specific protease (ISP). The increased degrading activity present during insulin resistance had properties not shared with ISP, suggesting the presence of an uncharacterized protease.
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PMID:Insulin resistance caused by massive degradation of subcutaneous insulin. 10 40

For more than half a century the management of hyperglycemia in diabetes mellitus has included rigid diets and intermittent subcutaneous insulin administration. These methods have been totally unsuccessful in restoring glucose homeostasis to normal in most diabetic patients. This review focuses on techniques that offer promise as alternatives or adjuncts to the current modalities of treatment. Specific areas discussed include pancreatic transplantation, islet cell transplantation, artificial beta cell devices, and the glucagon-suppressing agent somatostatin. Although many of these show promise for the future, a cure for the metabolic abnormalities of diabetes is not imminent.
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PMID:Treatment of diabetes mellitus: the future. 10 34


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