The Effects of Exercise Training on Glucose Homeostasis and Muscle Metabolism in Type 1 Diabetic Female Mice

Although exercise training is an important recommendation for the management of type 1 diabetes (T1D), most of the available research studies predominantly focus on male subjects. Given the importance of sex as a biological variable, additional studies are required to improve the knowledge gap regarding sex differences in T1D research. Therefore, the purpose of this study was to examine the role of exercise training in mediating changes in glucose homeostasis and skeletal muscle metabolism in T1D female mice. Female mice were injected with streptozotocin (STZ) to induce T1D. Two weeks after STZ injection, control (CON) and STZ mice were exercise trained on a treadmill for 4 weeks. Aerobic exercise training failed to improve glucose tolerance, prevent the decrease in body weight and adipose tissue mass, or attenuate muscle atrophy in T1D female mice. However, insulin sensitivity was improved in T1D female mice after exercise training. Aerobic exercise training maintained skeletal muscle triglyceride content but did not prevent depletion of skeletal muscle or liver glycogen in T1D mice. Gene expression analysis suggested that T1D resulted in decreased glucose transport, decreased ketone body oxidation, and increased fatty acid metabolism in the skeletal muscle, which was not altered by exercise training. These data demonstrate that 4 weeks of aerobic exercise training of a moderate intensity is insufficient to counteract the negative effects of T1D in female mice, but does lead to an improvement in insulin sensitivity

Oxidative Stress is Not Increased in Male Mice Hearts Fed a High Saturated or High Unsaturated Fat Diet

High fat, low carb diets are becoming increasingly popular in the United States as part of new weight loss strategies. Although research supports short-term weight loss on these diets, much is unknown about the long-term effects. High consumption of fat has been suggested to increase oxidative stress, an imbalance between the production of reactive oxygen species and antioxidants. The purpose of these preliminary studies was to evaluate the effects of three high fat diets on measures of oxidative stress in the hearts of mice. Hearts were obtained from male mice fed a high saturated fat (HSF) or high unsaturated fat (HUF) diet for 12 weeks. Lipid peroxidation, aconitase activity, and protein carbonylation were not significantly different in HSF or HUF hearts as compared to hearts from control mice fed a low-fat diet. Interestingly, protein carbonylation was significantly increased in the hearts of female mice fed a ketogenic diet (KD) for 5 weeks but not in male hearts fed a KD for 6 weeks following 12 weeks of HUF. These findings highlight some potentially important sex differences. Future studies are needed to further investigate whether the KD affects oxidative stress differently in males and females

The Effects of the Ketogenic Diet on Oxidative Stress in Heart, Liver, and Muscle: A Review of Literature

In the United States, fad diets are becoming increasingly popular as a dietary strategy to combat the growing incidence of chronic diseases, such as obesity, diabetes, and cardiovascular disease. The ketogenic diet, a diet that that consists of high fat and low carbohydrate content, has gained widespread mainstream media attention as a formula to improve weight loss as well as enhance exercise performance. Although research supports a positive effect on obesity in the short-term, there are a number of health concerns regarding long-term consumption of the diet. Research suggests that consumption of diets high in fat content can increase oxidative stress, which is an imbalance between the production of reactive oxygen species (ROS) and antioxidant capacity. Since increased oxidative stress has been associated with several chronic diseases, such as obesity and heart disease, the consumption of the ketogenic diet may facilitate disease progression. In research studies, oxidative stress is typically measured via assessment of ROS (e.g., superoxide and hydrogen peroxide) and/or antioxidant enzymes (e.g. superoxide dismutase, glutathione peroxidase, catalase). In addition, cellular measures of lipid peroxidation, protein carbonylation, or the ratio of reduced to oxidized glutathione are used as markers of oxidative stress. In this review article, we will discuss the measurements of these commonly used indicators of oxidative stress. In addition, we will review previously conducted studies in which the ketogenic diet was employed in an effort to determine if the ketogenic diet contributes to elevated oxidative stress in the heart and other organs

The Effects of the Ketogenic Diet on Oxidative Stress in Heart, Liver, and Muscle: A Review of Literature

In the United States, fad diets are becoming increasingly popular as a dietary strategy to combat the growing incidence of chronic diseases, such as obesity, diabetes, and cardiovascular disease. The ketogenic diet, a diet that that consists of high fat and low carbohydrate content, has gained widespread mainstream media attention as a formula to improve weight loss as well as enhance exercise performance. Although research supports a positive effect on obesity in the short-term, there are a number of health concerns regarding long-term consumption of the diet. Research suggests that consumption of diets high in fat content can increase oxidative stress, which is an imbalance between the production of reactive oxygen species (ROS) and antioxidant capacity. Since increased oxidative stress has been associated with several chronic diseases, such as obesity and heart disease, the consumption of the ketogenic diet may facilitate disease progression. In research studies, oxidative stress is typically measured via assessment of ROS (e.g., superoxide and hydrogen peroxide) and/or antioxidant enzymes (e.g. superoxide dismutase, glutathione peroxidase, catalase). In addition, cellular measures of lipid peroxidation, protein carbonylation, or the ratio of reduced to oxidized glutathione are used as markers of oxidative stress. In this review article, we will discuss the measurements of these commonly used indicators of oxidative stress. In addition, we will review previously conducted studies in which the ketogenic diet was employed in an effort to determine if the ketogenic diet contributes to elevated oxidative stress in the heart and other organs