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Glucagon

Glucagon is a 29-amino acid polypeptide acting as an important hormone in carbohydrate metabolism. The polypeptide has a molecular weight of 3485 daltons and was discovered in 1923 by Kimball and Murlin. more...

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Gamma-hydroxybutyrate

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Its primary structure is: NH₂-His-Ser-Gln-Gly-Thr-Phe- Thr-Ser-Asp-Tyr-Ser-Lys-Tyr-Leu-Asp-Ser- Arg-Arg-Ala-Gln-Asp-Phe-Val-Gln-Trp-Leu- Met-Asn-Thr-COOH

History

In the 1920s, Kimball and Murlin studied pancreatic extracts and found an additional substance with hyperglycemic properties. Glucagon was sequenced in the late-1950s, but a more complete understanding of its role in physiology and disease was not established until the 1970s, when a specific radioimmunoassay was developed.

Physiology

The hormone is synthesized and secreted from alpha cells of the Islets of Langerhans, which are located in the pancreas. The alpha cells are located in the outer rim of the islet.

Regulation

Stimulus for increased secretion of glucagon

Decreased plasma glucose
Increased catecholamines
Increased plasma amino acids (to protect from hypoglycemia if an all protein meal consumed)
Sympathetic nervous system

Stimulus for decreased secretion of glucagon

Somatostatin
Insulin

Function

Glucagon helps maintain the level of glucose in the blood by binding to specific receptors on hepatocytes, causing the liver to release glucose - stored in the form of glycogen - through a process known as glycogenolysis. As these stores become depleted, glucagon then encourages the liver to synthesize additional glucose by gluconeogenesis. This glucose is released into the bloodstream. Both of these mechanisms lead to glucose release by the liver, preventing the development of hypoglycemia.

Increased free fatty acids and ketoacids into the blood
Increased urea production

Mechanism of action

Acts via cAMP generation

Pathology

Abnormally-elevated levels of glucagon may be caused by pancreatic cancers such as glucagonoma, symptoms of which include necrolytic migratory erythema (NME).

Pharmacological application of glucagon

An injectable form of glucagon is essential first aid in cases of severe hypoglycemia. The glucagon is given by intramuscular injection, and quickly raises blood glucose levels. It works only if there is glycogen stored in liver cells, and it won't work again until those stores are replenished.

Glucagon has also inotropic properties. Although its use is impracticable in heart failure, it has some value in treatment of myocardial depression secondary to betablocker overdose. However there have been no clinical controlled trial on the use of glucagon.

Media

Read more at Wikipedia.org

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Comparative effects of glucagon-like peptide-2, growth hormone, keratinocyte growth factor in rats after massive small bowel resection
From JPEN: Journal of Parenteral and Enteral Nutrition, 1/1/04 by Washizawa, N

Background: Exogenous administration of selected growth factors exert gut-trophic effects and may improve mucosal redox status. However, little comparative data on effects of specific growth factors after small bowel resection (SBR) are available. We hypothesized that an analog of glucagon-like peptide-2 (GLP-2) would exert superior gut-trophic effects after SBR than either growth hormone (GH) or keratinocyte growth factor (KGF) and that KGF would have the more potent effect on mucosal glutathione (GSH) redox status.

Methods: Thirty-seven male rats underwent small bowel transeclion with s.c. saline (TxS; n=7) or 80% SBR with either s.c. saline (RxS, n=7), GLP-2 (RxGLP-2, 0.2mg/kg/d, n=8), KGF (RxKGF, 3.0mg/kg/d, n=7) or GH (RxGH, 3.0mg/kg/d, n=8). all rats were pair-fed standard diet to intake of RxS rats. After 7 days, DNA content was measured in full-thickness jejunum, ileum, and colon. Villus height in small bowel segments and crypt depth in all gut segments were measured and total mucosal thickness calculated. Mucosal expression of goblet cells and the cyloprotective trefoil peptide TFF3 were determined by morphology and Western blotting, respectively. The ratio of mucosal GSH to glutathione disulfide (GSSG) was determined as an index of redox status.

Results: SBR (RxS) increased small bowel and colonie mucosal growth indices versus control (TxS) and oxidized ileal and colonie mucosal GSFI redox (Tables 1, 2, and 3). SBR did not affect gut goblet cell number or TFF3 expression. GLP-2 increased jejunal villus height, total mucosal thickness and DNA content compared to RxS, RxGH or RxKGF (Tables 1 and 2). Growth indices in ileum were similar in the GLP-2, GH and KGF groups, while in colon, GH and KGF modestly increased mucosal crypt depth vs RxS (Tables 1 and 2). hi jejunual mucosa, GLP-2 upregulated the GSH/GSSG ratio vs RxS, while KGF had an intermediate effect, hi both ileum and colon, GLP-2 (but not GH or KGF), prevented the SBR-induced decline in the mucosal GSF1/GSSG ratio (Table 3). Goblet cell number and TFF 3 expression in small bowel and colon were unaffected by GLP-2 or GH, but were markedly upregulated by KGF in all gut segments.

Conclusions: GLP-2 exerts superior effects on adaptive jejunal growth and small bowel and colonie GSH redox status compared to GH or KGF after massive SBR in rats. Both GFI and KGF increase colonie mucosal growth in this model. KGF has potent trophic effects on gut mucosal goblet cells and TFF3 expression after SBR that are not shared by GLP-2 or GH.

N. Washizawa, MD1; L. H. Gu, MD1; L. Gu1; K. P. Openo, MPH2; D. P. Jones, MD2; T. R. Ziegler, MD1; 1 Department of Medicine, Emory University, Atlanta, Georgia; 2Biochemistry, Emory University, Atlanta, Georgia.

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