Changes of function and metabolism of the pancreatic B-cell caused by amino acids and related compounds.
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.
D000596:Amino Acids / Q000502:physiology*; D000598:Amino Acids, Cyclic; D000818:Animals; D002208:Caproates / Q000502:physiology; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D007515:Islets of Langerhans / Q000378:metabolism* / Q000502:physiology; D007651:Keto Acids / Q000502:physiology*; D007930:Leucine / Q000502:physiology*; D051379:Mice
D000596:Amino Acids; D000598:Amino Acids, Cyclic; D002208:Caproates; D007328:Insulin; D007651:Keto Acids; C006504:2-aminobicyclo(2,2,1)heptane-2-carboxylic acid; C013082:alpha-ketoisocaproic acid; D007930:Leucine