Abstract
Obesity and aging are risk factors for diabetes. Here we investigated effects of aging, obesity and fasting on central and peripheral glucose tolerance and on glucose-sensing neuronal function in the arcuate nucleus of rats, with a view to providing insight into central mechanisms regulating glucose homeostasis and how they change or are subject to dysfunction with aging and obesity. We show that following a glucose load, central glucose tolerance at the level of the cerebrospinal fluid (CSF) and plasma is significantly reduced in rats maintained on high fat diet (HFD). With aging, up to 2 years, central glucose tolerance was impaired in an age-dependent manner whilst peripheral glucose tolerance remained unaffected. Aging-induced peripheral glucose intolerance was improved by a 24 hour fast, whilst central glucose tolerance was not corrected. Pre-wean, immature animals have elevated basal plasma glucose levels and a delayed increase in central glucose levels following peripheral glucose injection compared to mature animals. Electrophysiological recording techniques revealed an energy-status-dependent role for glucose excited, inhibited and adapting neurons along with glucose-induced changes in synaptic transmission. We conclude that aging affects central whilst HFD profoundly affects central and peripheral glucose tolerance, and glucose-sensing neurons adapt function in an energy-status-dependent manner.
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