1789-P: Advanced Age in Spontaneously Hypertensive Rats Induces Prediabetes by Alterations in Pancreatic Islets



Introduction and Objective: In the last decades, the increase in life expectancy has led to a demographic transition into an older adult population. Chronic affections like type-2 diabetes and hypertension increase their incidence in adults. Combined with the aging process, the onset of diabetes or hypertension is exacerbated, however there are few evidences regarding their interaction. The senescence of endocrine pancreatic cells induces morpho-physiological changes that contribute to dysregulation of glycaemia, and hypertension could contribute with other factors, including a proinflammatory environment, accumulation of non-enzymatically modified proteins, leading to increased apoptosis and oxidative stress. The objective of our research is to evaluate some physiological, histological and gene expression alterations in pancreatic islets, studied from 24-month-old spontaneously hypertensive rats (SHR).Methods: We maintained SHR and Wistar-Kyoto rats as control group, until 2 years-old. Fasting glycaemia, hypertension, glucose tolerance test and serum insulin were determinated. Pancreatic islets were isolated to analyze histological modifications and changes in gene expression.Results: Hypertension was sustained in old SHR, with increased insulin resistance and the area under the curve of glucose tolerance test. Islets from SHR presented a significant decrease on glucagon expression and content, but increase of insulin and PDX-1 expression, without histological alterations.Conclusion: Hypertension and aging exacerbate alterations in pancreatic islets, leading to glucose intolerance and prediabetic state

Disclosure

A. Vilches-Flores: None. D. Cabeza: None.

Funding

UNAM DGAPA-PAPIIT IN214424



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