Increased oxidative stress and the apoptosis of regulatory T cells in obese mice but not resistant mice in response to a high-fat diet

• DIO mice experience higher body weight, energy intake and plasma lipids than DR mice.
• HFD increase the production of proinflammatory cytokine in DIO mice but not DR mice.
• HFD decrease Tregs production in DIO mice but not DR mice.
• Increased oxidative stress subject Tregs to apoptosis in DIO mice but not DR mice.

High fat feeding induces a variety of obese and lean phenotypes in inbred rodents. Obesity is a pro-inflammatory state, and regulatory T cells (Tregs) are essential negative regulators of inflammation. We aimed to determine the involvement of Tregs in the mice susceptible or resistant to high-fat diet (HFD). In the study, diet-induced obese (DIO) mice experienced significant increases in weight gain, energy intake, fat masses, plasma lipid and proinflammatory cytokines in comparison with control and diet-resistant (DR) mice. Also, Tregs production decreased in DIO mice. HFD diminished mitochondrial transmembrane potential (MTP) in the spleen Tregs of DIO mice and reinforced apoptosis compared with that in DR mice. Moreover, HFD significantly decreased antioxidant enzymes expressions and increased reactive oxygen species (ROS) productions in the Tregs of DIO mice, but not in those of DR mice, which should provide valuable evidence for unraveling the pathogenesis of inflammation found in this obese mice model.