Brain Insulin Resistance Is Related to Carbohydrate Consumption and the Presence of Carbonylated Proteins, While Peripheral Insulin Resistance Is Linked to Fat Consumption and the Presence of Malondialdehyde

Consumption of high fat (HFD) or carbohydrates (LFD) diets are related to insu-lin resistance; however, central and peripheral alterations can occur independently. The timeline of insulin resistance was determined taking in consideration the role of diet on oxidative damage. Background/Objectives: The aim to this study was to ascertain whether HFD or LFD induces peripheral insulin resistance (PIR) before brain insulin re-sistance (BIR), and whether the timing of these alterations correlates with heightened oxi-dative damage markers in plasma, adipose tissue and cerebral cortex. Methodology and results: 3-month-old C57BL/6 male mice were fed with either HFD, LFD, or standard diet for 1, 2, or 3 months. Glucose and insulin tolerance test were performed to determine PIR, and hypothalamic thermogenic response to insulin was used to determine BIR status. For oxidative damage, levels of malondialdehyde (MDA), protein carbonyl group (PCO), and the enzymatic activity of glutathione peroxidase (GSH-Px) were evaluated in plasma, white adipose tissue, brown fat and brain cortex. PIR occurred at 3 months of HFD how-ever MDA levels in the white adipose tissue increased at 2 months. BIR occurred at 1 and 2 months of LFD but the enzymatic activity of GSH-Px was lower at one month and the amount of PCO increased at 2 months. Conclusion: The use of HFD or LFD at different duration can influence the establishment of PIR or BIR, and oxidative damage in the fat tissue and cerebral cortex can play an important role.