Study summary · research use only
AMP-activated protein kinase agonist dose dependently improves function and reduces apoptosis in glucotoxic beta-cells without changing triglyceride levels
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat cell-line study, the authors tested the AMPK agonist AICAR (5-aminoimidazole-4-carboxamide ribonucleoside) in glucotoxic insulinoma INS-1E beta-cells cultured at 27 mM glucose. Impaired glucose-stimulated insulin secretion and elevated apoptosis after prolonged high-glucose culture were assessed with 0.3 or 1 mM AICAR included during culture. The abstract reports that glucose-induced impairment of insulin release was reverted by 0.3 but not 1 mM AICAR, which did not affect insulin content, and that the glucose-induced rise in triglyceride content was not altered by either AICAR concentration. Inclusion of 1 but not 0.3 mM AICAR induced phosphorylation of AMPK and acyl-CoA carboxylase, paralleled by a reduced number of apoptotic cells and lowered CHOP expression. The authors conclude AICAR dose-dependently altered beta-cell function and apoptosis without changing triglyceride levels.
Abstract
Prolonged hyperglycaemia leads to impaired glucose-stimulated insulin secretion (GSIS) and apoptosis in insulin-producing beta-cells. The detrimental effects have been connected with glucose-induced lipid accumulation in the beta-cell. AMP-activated protein kinase (AMPK) agonist, 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), promotes utilization of nutrient stores for energy production. It was tested how impaired GSIS and elevated apoptosis observed in insulinoma (INS)-1E cells after prolonged culture at 27 mM glucose were affected by the inclusion of 0.3 or 1 mM AICAR during culture. Glucose-induced impairment of insulin release was reverted by the inclusion of 0.3 but not 1 mM AICAR, which did not affect insulin content. The glucose-induced rise in triglyceride (TG) content observed in the cells cultured at 27 mM glucose was not altered by the inclusion of either 0.3 or 1 mM AICAR. Inclusion of 1 but not 0.3 mM AICAR during culture induced phosphorylation of AMPK and its downstream target acyl-CoA carboxylase. Phosphorylation was paralleled by reduced number of apoptotic cells and lowered expression of pro-apoptotic C/EBP homologous protein (CHOP). In conclusion, AICAR dose dependently improves beta-cell function and reduces apoptosis in beta-cells exposed to prolonged hyperglycaemia without changing TG levels.
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