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Long-Term Consumption of High-Fat-High-Fructose (HFHF) Diet Decreased Insulin Sensitivity and Damaged the Islets of Langerhans on Sprague Dawley Rats

type 2 diabetes HFHF diet insulin sensitivity pancreatic beta cells langerhans

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Obesity is linked to the rising incidence of type 2 diabetes, with excessive dietary fat intake being one of the primary causes. The development of fat animal models is discovered to be a standard experimental strategy based on the replication of human behavior in food consumption. Therefore, the purpose of this study is to investigate how long-term HFHF diet consumption affects the indicators of diabetes mellitus in Sprague Dawley (SD) rats, such as insulin sensitivity by measuring the HOMA-IR, counting beta cells and analyzing the histology of the pancreas. This experiment was conducted within normal and HFHF groups, with each group consisting of 18 male SD rats. The normal groups had a modified AIN-93 M, while the HFHF group received a high-fat diet with 30% fructose-based water. The feed and beverage intakes were monitored every 24 hours to calculate daily caloric consumption (energy intake) for 17 weeks. The results demonstrated a significant difference between the normal and HFHF groups in the HOMA-IR levels (insulin sensitivity) and number of pancreatic beta cells (P<0.05). This implied that following 17 weeks of HFHF intake, the HOMA-IR level of insulin sensitivity was reduced. However, the islet of Langerhans in pancreatic histopathology seemed damaged in the HFHF rats, as evidenced by the changes in its shape and lower beta cell number.  Consuming the HFHF diet over an extended period increased glucose levels, decreased insulin sensitivity levels, and damaged pancreatic histopathology.