Long-term consumption of high-fat fructose diet increased the pancreatic-derived factor level and impaired glucose and lipid metabolisms in male rats

High-fat fructose diet (HFFr) consumption leads to inflammatory response and adverse metabolic consequences. Evaluating the changes in pancreatic-derived factor (PANDER) as one of the inflammatory metabolites, due to its regulatory role in glucose metabolism, could provide insight into the glucose homeostasis mechanisms.

Dams and their pups were randomly assigned to a standard diet (StD) and HFFr groups. After weaning, the male Wistar offspring were allocated to StD, StD-DMSO (Vehicle: V), StD-4-phenyl butyric acid (Drug: D), HFFrD, HFFrD-V and HFFrD-D groups, while they were on their diet for five weeks and treated for ten days. At the end of the procedure, the plasma glucose, insulin and PANDER levels, atherogenic indices and pancreatic PANDER content were determined.

HFFrD intake increased plasma glucose level and homeostasis model assessment of insulin resistance. Also, atherogenic indices were elevated through the increase of cholesterol and low-density lipoprotein and the decrease of high-density lipoprotein (HDL) in HFFrD group. An increase in both plasma and pancreatic PANDER levels was observed in the HFFrD group. The drug decreased the plasma and pancreatic PANDER levels along with plasma glucose, cholesterol and the ratio of cholesterol to HDL levels in the HFFrD group.

Since long-term HFFrD intake led to hyperglycemia, insulin resistance and dyslipidemia with an increase in plasma and pancreatic PANDER levels, and on the other hand, 4-phenyl butyric acid administration decreased PANDER levels as well as plasma glucose and cholesterol concentrations, PANDER increment may be the cause of glucose and lipid disturbances.