In mouse pancreatic islets the kinetics of insulin secretion and O2 uptake in response to the non-metabolizable leucine analogue (+/-)-BCH (2-endo- aminonorbornane −2-carboxylic acid) were compared. In addition, the fuel-mobilizing effect of (+/-)-BCH was studied with a mitochondrial fraction from islets. (1) Within 2 min 20 mM-(+/-)-BCH markedly enhanced insulin release or O2 consumption by islets respiring in the absence of exogenous fuels. During prolonged exposure to 20 mM-(+/-)-BCH secretion declined more rapidly than O2 uptake. (2) L-Glutamine (10 mM) prevented the decrease of both insulin release and O2 uptake of islets exposed to 20mM-(+/-)-BCH. During the second phase of insulin release in response to 20 mM-(+/-)-BCH + 10 mM-L-glutamine, kinetics of secretion and respiration correlated closely. (3) Initial peaks were consistently seen in the (+/-)-BCH-induced secretory profiles, but never in the respiratory profiles. (4) In contrast with L-glycerol 3-phosphate, L-malate or pyruvate, L-glutamine or L-glutamate maintained low rates of oxidative phosphorylation in B-cell mitochondria. The effects of L-glutamine or L-glutamate were potentiated severalfold by (+/-)-BCH. (5) The effects of other branched-chain amino acids on oxidative phosphorylation resembled their effects on insulin release, redox state of nicotinamide nucleotides and glutamate dehydrogenase activity. (6) The results support the view that (+/-)-BCH stimulates insulin secretion via a primary enhancement of hydrogen supply to the respiratory chain of B-cell mitochondria.
The ultrastructural study of a skin biopsy in a patient afflicted with hereditary sensory neuropathy type IV (congenital insensitivity to pain with anhidrosis) did not reveal any unmyelinated axons or axonal terminals around eccrine sweat glands but only processes, partially covered by a basement membrane and therefore resembling Schwann cell processes. The absence of such unmyelinated axons in close proximity to eccrine sweat glands where they normally occur appears to be the morphological equivalent to the anhidrosis and also corresponds to the deficiency of unmyelinated axons in the sural nerve of the same patient, as previously reported.
1The effects of clonidine, yohimbine, corynanthine and prazosin on glucose-induced insulin secretion by incubated or perifused mouse pancreatic islets were investigated. 2 Clonidine (0.1 pM) inhibited glucose-induced insulin secretion alone and in the presence of yohimbine (0.1 pM), corynanthine (10 pM) or prazosin (1 pM).3 In higher concentrations, yohimbine (1-10 pM) antagonized the inhibitory effect of clonidine (0.1 pM) upon glucose-induced insulin secretion by incubated islets and by perifused islets. 4 The results support the view that adrenergic inhibition of insulin secretion is mediated by cz2-adrenoceptors on pancreatic 1-cells.
3-Phenylpyruvate evoked a monophasic insulin release from perifused mouse islets. L-Phenylalanine was not an insulin secretagogue and was oxidized by islets at a very low rate, suggesting that 3-phenylpyruvate does not trigger insulin release by enhancing production of reducing equivalents. Moreover, allosteric activation of glutamate dehydrogenase does not play a role in 3-phenylpyruvate-induced insulin secretion.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.