Literature DB >> 7005061

Changes of function and metabolism of the pancreatic B-cell caused by amino acids and related compounds.

U Panten, S Holze, S Lenzen.   

Abstract

Evidence is presented that, to explain the insulin releasing capacity of L-leucine, b-BCH or alpha-ketoisocaproate (KIC), the following alternatives must be considered: 1. Interaction of the unchanged molecules with specific B-cell membrane receptors triggers insulin release. Stimulation of metabolism is a consequence of these events. 2. Primary enhancement of intramitochondrial hydrogen production triggers insulin secretion which could modulate metabolism. 3. Combination of mechanism 1 and 2: a) Additive effects of 1 and 2. b) Potentiation of 1 by 2. c) Potentiation of 2 by 1. 4. Different control of first phase or second phase of insulin release by 1, 2, or 3.

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Year:  1980        PMID: 7005061

Source DB:  PubMed          Journal:  Horm Metab Res Suppl        ISSN: 0170-5903


  3 in total

1.  Regulation of insulin secretion by energy metabolism in pancreatic B-cell mitochondria. Studies with a non-metabolizable leucine analogue.

Authors:  U Panten; S Zielmann; J Langer; B J Zünkler; S Lenzen
Journal:  Biochem J       Date:  1984-04-01       Impact factor: 3.857

2.  Mechanism of 3-phenylpyruvate-induced insulin release from isolated pancreatic islets.

Authors:  U Panten; J Langer
Journal:  Biochem J       Date:  1981-08-15       Impact factor: 3.857

3.  Effects of ketone bodies on insulin release and islet-cell metabolism in the rat.

Authors:  T J Biden; K W Taylor
Journal:  Biochem J       Date:  1983-05-15       Impact factor: 3.857

  3 in total

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