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)

Intestinal ischemia shock was induced by 35 to 40-min portal vein occlusion (PVO). After treatment with rat plasma a severe hypoglycemia ensues which is caused by a block in gluconeogenesis. This hypoglycemia is not affected by treatment with adrenaline, glucagon, nicotinadenine dinucleotide (NAD), adenosine triphosphate (ATP) alanine (A), or pyruvate (P), while fructose (F) and dihydroxyacetone (DHA) slightly increase the plasma glucose concentration. If F or DHA are combined with NAD a considerable hyperglycemic effect is observed, but NAD plus A or P is ineffective. A similar marked rise in plasma glucose is observed if F is combined with nicotinamide, adenylic acid, or histamine. NAD causes vasodilatation in the splanchnic area and an increased portal flow. It is concluded that the effect of NAD is the result of an increased uptake of suitable substrates of gluconeogenesis from the peritoneal cavity and/or an increased availability of these substrates to the liver. During the development of PVO shock, portal venous flow diminishes considerably. This reduced flow may be the result of vasoconstriction caused by the high level of plasma adrenaline.
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PMID:Studies on the site of the block in gluconeogenesis causing severe hypoglycemia in intestinal ischemia shock in rats. 405 96

Intestinal ischemia shock is obtained in fasted rats by 40-minute splanchnic arterial occlusion (SAO) or by 35-minute portal vein occlusion (PVO). Survival is prolonged by plasma treatment; further prolongation is obtained by additional administration of glucose. After SAO early hyperglycemia is marked. Plasma adrenaline rises steeply after opening of the arteries and remains high, while plasma insulin remains unaltered. The hyperglycemia is abolished by adrenalectomy and section of the major splanchnic nerves (MSN) proximal to the adrenals but not by section of the MSN distal from the adrenals or by vagotomy. It is concluded that the sympathetic nervous system is stimulated by a substance, possibly related to VIP, released from the intestines. After PVO hyperglycemia is less marked. Plasma adrenaline as well as insulin are increased. During late and fatal hypoglycemia after PVO plus plasma treatment, the liver still appears to be functionally intact. It is assumed that gluconeogenesis is reversibly inhibited by as yet unknown factors. The hypoglycemia cannot be abolished by injection of common substrates of gluconeogenesis but the combination fructose plus glucagon plus NAD is highly effective.
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PMID:Disturbances in the glucose metabolism in intestinal ischemia shock. 724 66

Intestinal ischaemia and reperfusion cause changes in cardiovascular and pulmonary function. In a rat model, the plasma concentrations of atrial natriuretic peptide (ANP) and pancreatic glucagon rose on reperfusion after 20 min of intestinal ischaemia, coinciding with significant arterial hypotension: mean(s.e.m.) ANP 79(13) versus control 36(4) fmol ml-1 (P < 0.01); and mean(s.e.m.) glucagon 22(2) versus control 10(1) fmol ml-1 (P < 0.001). Glucagon was also released on reperfusion after 5 min of ischaemia: mean(s.e.m.) 18(2) fmol ml-1 (P < 0.001 versus control). In a second experiment, pretreatment of rats with allopurinol did not prevent arterial hypotension but abolished ANP release (mean(s.e.m.) 36(2)fmol ml-1 versus no pretreatment 70(7) fmol ml-1, P < 0.05), while glucagon release was unaffected. The release of ANP, but not that of glucagon, is therefore mediated by oxygen free radicals and may signify cardiac and/or pulmonary injury or dysfunction. The actions of these peptides may be relevant in the pathophysiological perturbation of intestinal ischaemia-reperfusion.
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PMID:Atrial natriuretic peptide and glucagon release in experimental intestinal ischaemia and reperfusion. 820 37

Intestinal ischemia, also called mesenteric ischemia, is a severe gastrointestinal and vascular medical emergency caused by a sudden decrease of blood flow through the mesenteric vessels. It generates hypoperfusion of intestinal tissues and can rapidly progress to intestinal wall infarction, systemic inflammation or even death if not treated in time. The mortality of this condition is still considerably high despite all the medical advances of the past few years. This is partially due to the difficulty of diagnosing early stage mesenteric ischemia. Indeed, a speedy and correct diagnosis is decisive for suitable medical care. However, early symptoms are unspecific and conventional clinical markers are neither specific nor sensitive enough. In the last few years, significant clinical and preclinical efforts have been made to find biomarkers which could predict gastrointestinal damage before it becomes irreversible. Here, the gut-derived hormone glucagon-like peptide-1 (GLP-1) is described as a potential early biomarker of this severe condition. Indeed, GLP-1 plasma levels rise rapidly in both mice and humans with intestinal ischemia. This discovery could counter the cruel lack of clinical biomarkers available to diagnose and therefore manage intestinal ischemia efficiently in the early stages. GLP-1 could thus become part of a panel of biomarkers for intestinal ischemia and could help to reduce the associated high mortality rates.
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PMID:Could glucagon-like peptide-1 be a potential biomarker of early-stage intestinal ischemia? 3044 82