Eugene F. Du Toit

TL;DR: It is proposed that dyslipidaemia may be a mechanism for the activation of inflammatory/stress‐activated signalling pathways in obesity and type II diabetes, which will lead to apoptosis and atrophy in skeletal muscle.

TL;DR: In this article, the effects of chronic melatonin administration on the development of metabolic syndrome as well as ischemia-reperfusion injury in a rat model of diet-induced obesity (DIO) were investigated.

TL;DR: The precise roles and utility of this GPCR family in healthy and diseased human myocardium, and in mediating central and peripheral survival responses, warrant further investigation, as do the putative negative influences of ageing, IHD co‐morbidities, and relevant drugs on opioid receptor signalling and protective responses.

TL;DR: In obesity, the impact of an increased susceptibility of the myocardium to ischemic-reperfusion injury on myocardial injury is likely to be overshadowed by the comparatively greater roles played by predicted increases in circulating insulin and fatty acids found in vivo.

TL;DR: It is concluded that NO is a trigger for classic preconditioning, cGMP generation plays an important role in its protection, and attenuation of p38 MAPK during sustained ischemia accompanies NO preconditionsing and may mediate cardiac protection.