FOXO1 is downregulated in obese mice subjected to short-term strength training.

Obesity is a worldwide health problem and is directly associated with insulin resistance and type 2 diabetes. The liver is an important organ for the control of healthy glycemic levels, since insulin resistance in this organ reduces phosphorylation of forkhead box protein 1 (FOXO1) protein, leading to higher hepatic glucose production (HGP) and fasting hyperglycemia. Aerobic physical training is known as an important strategy in increasing the insulin action in the liver by increasing FOXO1 phosphorylation and reducing gluconeogenesis. However, little is known about the effects of strength training in this context. This study aimed to investigate the effects of short-term strength training on hepatic insulin sensitivity and glycogen synthase kinase-3ß (GSK3ß) and FOXO1 phosphorylation in obese (OB) mice. To achieve this goal, OB Swiss mice performed the strength training protocol (one daily session for 15 days). Short-term strength training increased the phosphorylation of protein kinase B and GSK3ß in the liver after insulin stimulus and improved the control of HGP during the pyruvate tolerance test. On the other hand, sedentary OB animals reduced FOXO1 phosphorylation and increased the levels of nuclear FOXO1 in the liver, increasing the phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) content. The bioinformatics analysis also showed positive correlations between hepatic FOXO1 levels and gluconeogenic genes, reinforcing our findings. However, strength-trained animals reverted to this scenario, regardless of body adiposity changes. In conclusion, short-term strength training is an efficient strategy to enhance the insulin action in the liver of OB mice, contributing to glycemic control by reducing the activity of hepatic FOXO1 and lowering PEPCK and G6Pase contents.

Exercise alters the mitochondrial proteostasis and induces the mitonuclear imbalance and UPRmt in the hypothalamus of mice.

The maintenance of mitochondrial activity in hypothalamic neurons is determinant to the control of energy homeostasis in mammals. Disturbs in the mitochondrial proteostasis can trigger the mitonuclear imbalance and mitochondrial unfolded protein response (UPRmt) to guarantee the mitochondrial integrity and function. However, the role of mitonuclear imbalance and UPRmt in hypothalamic cells are unclear. Combining the transcriptomic analyses from BXD mice database and in vivo experiments, we demonstrated that physical training alters the mitochondrial proteostasis in the hypothalamus of C57BL/6J mice. This physical training elicited the mitonuclear protein imbalance, increasing the mtCO-1/Atp5a ratio, which was accompanied by high levels of UPRmt markers in the hypothalamus. Also, physical training increased the maximum mitochondrial respiratory capacity in the brain. Interestingly, the transcriptomic analysis across several strains of the isogenic BXD mice revealed that hypothalamic mitochondrial DNA-encoded genes were negatively correlated with body weight and several genes related to the orexigenic response. As expected, physical training reduced body weight and food intake. Interestingly, we found an abundance of mt-CO1, a mitochondrial DNA-encoded protein, in NPY-producing neurons in the lateral hypothalamus nucleus of exercised mice. Collectively, our data demonstrated that physical training altered the mitochondrial proteostasis and induced the mitonuclear protein imbalance and UPRmt in hypothalamic cells.

Effects of baru almond oil (Dipteryx alata Vog.) supplementation on body composition, inflammation, oxidative stress, lipid profile, and plasma fatty acids of hemodialysis patients: A randomized, double-blind, placebo-controlled clinical trial.

BACKGROUND: The consumption of nuts and edible seeds is associated with the improvement of the metabolic profile and reduction of cardiovascular diseases. However, the effects of its subproducts, such as oil, are still poorly studied. This study aimed to evaluate the effect of the baru almond oil supplementation on inflammation, oxidative stress, body composition, lipid profile, and plasma fatty acids of hemodialysis patients. METHODS: In a randomized, double-blind, 12-week placebo-controlled clinical study, hemodialysis patients were supplemented with 5 g of baru oil (BG, n = 17) or 5 g of mineral oil (placebo, BP, n = 12). Body composition, renal function, ultra-sensitive C-reactive protein (us-CRP), oxidative stress, plasma fatty acids, and lipid profile were analysed before and after the intervention. RESULTS: Patients were aged 50.5 ±â€¯2.2 years and the average time of dialyses was 52,1 ±â€¯42,6 months. The BG decreased us-CRP concentration compared to PG (-1.2 ±â€¯0.2 vs. + 0.8 ±â€¯0.2 mg / L,d = 0.88; p =  0.01). Baru almond oil supplementation was not effective in improving body composition, lipid profile, and oxidative stress. CONCLUSION: Baru almond oil supplementation decreased us-CRP concentration in patients with chronic kidney disease under hemodialysis treatment.