Agata Maria Rabuazzo

TL;DR: In pancreatic beta cells from type 2 diabetic subjects, the impaired secretory response to glucose is associated with a marked alteration of mitochondrial function and morphology, which leads to lower ATP, decreased ATP/ADP ratio, with consequent reduction of insulin release.

TL;DR: Results indicate that alanine aminotransferase, triglyceride and serum tumour necrosis factor-alpha levels, as well as fatty liver improved after polyunsaturated fatty acid administration.

TL;DR: The data indicate that chronic exposure to elevated FFA or glucose levels increases apoptosis in rat pancreatic islets and these cytotoxic effects could be mediated by oxidative stress.

TL;DR: Gl glucose-induced impairment of insulin secretion is associated with altered mitochondrial function, which results in impaired glucose oxidation, overexpression of the UCP-2 protein, and a consequent decrease of ATP production in rat pancreatic islets, mediated by the PPAR-gamma pathway.

TL;DR: The data show that metformin is able to restore the intracellular abnormalities of glucose and FFA metabolism and to restore a normal secretory pattern in rat pancreatic islets whose secretory function has been impaired by chronic exposure to elevated FFA or glucose levels, raising the possibility that, in diabetic patients, met formin (in addition to its peripheral effects) may have a direct beneficial effect on the beta-cell secretoryfunction.