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The prevalence of obesity and related consequences, including insulin resistance and Alzheimer's-like neuropathology, has increased dramatically. Contributing to this prevalence is the shift in lifestyle preference away from wholesome foods and exercise to the Western-style diet and sedentarism. Despite advances in drug development, a healthy diet and regular exercise remain the most effective approaches to mitigating the unwanted sequelae of diet-induced obesity on brain health. In this study, we used the high-fat high-sugar (HFHS) mouse model of neurodegeneration to examine the effects of exercise training (HFHS+Ex), genistein treatment (HFHS+Gen), and combination treatment (HFHS+Ex+Gen) on proteins relating to neurodegeneration in the brain of male mice. After a period of 12 weeks, as expected, HFHS feeding increased body weight, adipose tissue weight, and systemic plasma inflammation (TNF-α) compared to lean mice fed a standard diet. HFHS feeding also increased protein expression of brain markers of insulin resistance (pGSK-3β, p-IR), apoptosis (caspase 3), early neurofibrillary tangles (CP13), and amyloid-beta precursor (CT20). Compared to HFHS mice, Ex decreased body weight, plasma TNF-α, and expression of pGSK-3β, caspase 3, CP13, amyloid-β precursor (22c11), and ADAM10. Treatment with Gen was equally protective on these markers and decreased the expression of p-IR. Combination treatment with Ex and Gen afforded the greatest overall benefits, and this group exhibited the greatest reduction in body and adipose tissue weight and all brain markers, except for 22c11 and ADAM10, which were decreased compared to mice fed an HFHS diet. In addition, levels of 4G8, which detects protein levels of amyloid-β, were decreased with combination treatment. Our results indicate that exercise training, genistein supplementation, or combination treatment provide varying degrees of neuroprotection from HFHS feeding-induced Alzheimer's pathology. Future perspectives could include evaluating moderate exercise regimens in combination with dietary supplementation with genistein in humans to determine whether the same benefits translate clinically. [ABSTRACT FROM AUTHOR]

Skeletal muscle is composed of bundles of muscle fibers with distinctive characteristics. Oxidative muscle fiber types contain higher mitochondrial content, relying primarily on oxidative phosphorylation for ATP generation. Notably, as a result of obesity, or following prolonged exposure to a high-fat diet, skeletal muscle undergoes a shift in fiber type toward a glycolytic type. Mitochondria are highly dynamic organelles, constantly undergoing mitochondrial biogenesis and dynamic processes. Our study aims to explore the impact of obesity on skeletal muscle mitochondrial biogenesis and dynamics and also ascertain whether the skeletal muscle fiber type shift occurs from the aberrant mitochondrial machinery. Furthermore, we investigated the impact of exercise in preserving the oxidative muscle fiber types despite obesity. Mice were subjected to a normal standard chow and water or high-fat diet with sugar water (HFS) with or without exercise training. After 12 weeks of treatment, the HFS diet resulted in a noteworthy reduction in the markers of mitochondrial content, which was recovered by exercise training. Furthermore, higher mitochondrial biogenesis markers were observed in the exercised group with a subsequent increase in the mitochondrial fission marker. In conclusion, these findings imply a beneficial impact of moderate-intensity exercise on the preservation of oxidative capacity in the muscle of obese mouse models. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is an inflammatory disease causing more than three million deaths annually around the world. Previous studies have shown an increased incidence of COPD among smokers. Studies also have shown antioxidant nutrients such as carotenoids, have been associated with lower rates of COPD. To investigate if the consumption of carotenoids and carotenoid-rich foods is associated with higher pulmonary function. Data were taken from the Atherosclerosis Risk in Communities (ARIC) study, which included approximately 15,000 individuals aged 45-64 years at baseline. Dietary intake of carotenoids and carotenoid-rich foods were assessed by food frequency questionnaire. Total carotenoid intake was calculated by summing five specific carotenoids: α-carotene, β-carotene, β-cryptoxanthin, lycopene, and lutein/zeaxanthin. Pulmonary function was evaluated as the ratio of forced expiratory volume in one second [FEV1] and forced vital capacity [FVC]. Linear regression analysis was used to assess the association between the intakes of carotenoids and carotenoid-rich foods and pulmonary function. Significance level was p < 0.05. A positive association between the total carotenoid intake with pulmonary function was only marginally significant; however, α-carotene, β-carotene, and β-cryptoxanthin were each positively associated (p = 0.001, p = 0.003, p = 0.007, respectively) with FEV1/FVC ratio in study participants. Food sources of these pro-vitamin A carotenes were also positively associated (p = 0.008) with FEV1/FVC ratio. This study suggests a possible role for the provitamin A carotenes, and their associated foods in improved pulmonary health. [ABSTRACT FROM AUTHOR]