Abstract
NH4+ caused a dose-related, rapid, and reversible inhibition of glucose-stimulated insulin release by isolated rat islets. It also inhibited glyceraldehyde-, Ba2+-, and sulfonylurea-stimulated insulun secretion. NH4+ failed to affect glucose utilization and oxidation, glucose-stimulated proinsulin biosynthesis, the concentration of ATP, AD, and AMP, and the intracellular pH. NH4+ also failed to affect the ability of theophylline and cytochalasin B to augment glucose-induced insulin release. However, in the presence and absence of glucose, accumulation of NH4+ in islet cells was associated with a fall in the concentration of NADH and HADPH and a concomitant alteration of 86Rb+ and 45Ca2+ (or 133Ba2+) handling. These findings suggest that reduced pyridine nucleotides, generated by the metabolism of endogenous of exogenous nutrients, may modulate ionophoretic processes in the islet cells and by doing so, affect the net uptake of Ca2+ and subsequent release of insulin.
MeSH Terms
Ammonia/pharmacology
Animals
Cations/metabolism
Female
Glucose/antagonists & inhibitors,metabolism
Glyceraldehyde/antagonists & inhibitors
Hydrogen-Ion Concentration
Insulin/metabolism
Insulin Secretion
Islets of Langerhans/drug effects,metabolism
Proinsulin/biosynthesis
Pyridines/metabolism
Rats
Water/metabolism
Chemicals
Cations
Insulin
Pyridines
Water
Glyceraldehyde
Ammonia
Proinsulin
Glucose
Authors & Affiliations
8 authors, click to expand affiliations / ORCID
Sener A
Hutton J C
Kawazu S
Boschero A C
Somers G
Devis G
Herchuelz A
Malaisse W J
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