Endocrine Abstracts

Lipid sensing by pancreatic beta cells is co-ordinated through the expression and activity of peroxisome proliferator-activated receptors (PPARs). Through their action to lower triacylglycerol delivery to peripheral tissues, PPARalpha activators also oppose insulin resistance by relieving inhibition of insulin-stimulated glucose disposal. Mid to late pregnancy is an insulin-resistant state associated with hypertriglyceridaemia. We investigated regulatory interactions between P...

Activation of PPARalpha pharmacologically by WY14,643 enhances insulin sensitivity in insulin-resistant high-fat-fed rats. PPARalpha is expressed in pancreatic islets, where it affects genes involved in lipid metabolism. We investigated effects of PPARalpha activation by WY14,643 on glucose-stimulated insulin secretion (GSIS) in a rat model of high-fat feeding in which insulin resistance is observed in conjunction with compensatory insulin hypersecretion. To identify persisten...

Peroxisome proliferator-activated receptor (PPAR) alpha is one of three PPARs (alpha, beta (delta) and gamma), which are distinguished by distinct lipid and eicosanoid ligands. All three PPARs are present in pancreatic islets. PPARalpha expression and/or activity is important in the regulation of tissue triacylglycerol (TAG) content and fatty acid oxidation (FAO). PPARalpha binds the hypolipidaemic fibrates and promotes FA-mediated up-regulation of FAO. Surplus FA normally up-...

Insulin resistance is an established consequence of glucocorticoid excess. In rats, administration of the synthetic glucocorticoid dexamethasone decreases the sensitivity of glucose oxidation to insulin in soleus muscle strips, but sensitivity of lactate formation is unimpaired. In rats, cortisol impairs pyruvate tolerance and, in man, dexamethasone decreases whole-body glucose oxidation. The present study explored possible mechanisms that might underlie these effects. Activat...