Insulin-secreting beta-cell dysfunction induced by human lipoproteins

Oxidative stress and AMPK are both involved in decreased glucose-stimulated insulin secretion (GSIS) following PGC-1α overexpression [control MIN6 cells (Ad-GFP, white bars)

In intact INS-1 cells stimulated with methyl succinate, the blunted in- sulin secretion correlated with an inhibited increase in [Ca 21 ] m upon a second exposure.. In contrast,

KO of IL-1Ra in b cells of normal and obese mice led to diminished glucose- stimulated insulin secretion in vivo and in vitro, to impaired glucose tolerance in obese mice, to

F IG. Induction of WT-HNF1␣ and DN-HNF1␣ regulates the HNF1␣ mRNA expression and HNF1␣ promoter luciferase activity through altered HNF4 ␣ binding. A, for EMSA, the

The beta-cell mitochondria are known to generate metabolic coupling factors, or messengers, that mediate plasma membrane depolarization and the increase in cytosolic Ca(2+),

Although intracellular glutamate potentiates insulin secretion, extracellular glutamate may activate ionotropic receptors.. As a consequence of such activation, insulin exocytosis

In parallel, CART silencing decreased synthesis of insulin and expression of genes encoding proteins important for exocytosis, glucose sensing, and insulin processing, likely as

Adenoviral overexpression of Pax4 caused a 3.5-fold increase in -cell proliferation with a concomitant 1.9-, 4-, and 5-fold increase in Bcl-xL (antiapoptotic), c-myc, and Id2