Abstract
Currently, increasing prevalence of obesity and type 2 diabetes (DM2) correlates with disruption of circadian rhythm caused by higher exposure of light at night (LAN), due to restriction of sleep, shift work, jet lag and artificial light in houses, streets and work and leisure environments. Moreover, exposure LAN when diet associated with altered nutrient supply, such as high fat (HFD), triggers more marked changes in lipid and glucose homeostasis accelerating the development of obesityIn this context, the microRNA (miRNA) represents an emerging class of regulators of energy homeostasis, which can to be modulated by light and circadian rhythm. The microRNAs are small no-coding RNA, which act in the control of gene expression, pos-transcriptional level, leading to inhibition or reduction of protein synthesis. In patophysiological states, such as malnutrition, obesity and DM2 the mechanisms of synthesis and maturation of microRNA are changed, fact that favors to progression these diseases.Over years, our research group has characterized the pancreatic function in protein-malnourished mice. These animals show lower glucose stimulated insulin secretion and other insulinotropic agents, as well as higher glucose tolerance and insulin peripheral sensibility. Moreover, malnourished mice exhibit alteration in clock genes expression and pattern circadian of insulin secretion. We believe, these circadian changes predispose, protein-malnutrition mice, to be more susceptible to metabolic changes induced to exposure light continues. Thus we aim to assess the effects of exposure the LAN on function ²-pancreatic and peripheral tissues in the control of glucose homeostasis in malnourished mice. Furthermore, we propose to determine a possible role of miRNA as mediators of changes in insulin secretion in this experimental model. (AU)
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