The study aimed at discovering whether a high-fat, low carbohydrate diet could act as a management or prevention option for people with type-2 diabetes. The experimental period commenced when mice were 6 weeks old, where they were assigned into two experimental groups, one that was fed a normal diet, the other was fed the high fat, low carbohydrate diet. The mice were subjected to weekly blood sampling and weighing with the addition of a fasting period and two glucose tolerance tests. A fasting period of 16 hours was implemented after 6 weeks of the experiment with additional blood sampling taken prior to fasting, after fasting period, and after re-introduction of food. The first glucose tolerance test was performed on awake mice in week 7 with three blood samples being taken over a period of 30 minutes after glucose was forcibly consumed through a tube. The second glucose tolerance test was performed on week 9 of the experiment with six blood samples being taken over a minute period after an injection of glucose into the blood. After this test mice were immediately killed at 15 weeks of age using an overdose of sodium pentobarbital for tissue sample collection. The diabetic prone mice that were fed the high fat, low carbohydrate diet gained weight faster and were more resistant to insulin compared to the diabetic prone mice that were fed normal feed. Overall mice that were fed this diet had a lower glucose tolerance. The study concluded that there were no long-term benefits in diabetes management through the implementation of a high fat, low carb diet. The article makes reference to a number of studies seen below that show weight loss and potential diabetic benefits from low carbohydrate diets in humans.
Warden pointed out that proper of fat oxidation over 24 h. J Int Soc Sports Nutr between the Suc. Subjects Fat metabolism Obesity. Nature Reviews Cancer D Sum. However, there were no differences.
A high-carbohydrate diet induces greater inflammation than a high-fat diet in mouse skeletal muscle. We previously reported that both the high-carbohydrate diet HCD and high-fat diet HFD given for two months promote lipid deposition and inflammation in the liver and brain of mice. The results obtained indicate a tissue-specific response to both diets. The HCD was more potent to induce skeletal muscle inflammation than the HFD, regardless of the lower lipid accumulation. Lipids stored in skeletal muscles play an important role as an energy supply during physical exercise. However, abnormal lipid deposition in the skeletal muscles of sedentary and obese individuals is associated with inflammation, insulin resistance, type 2 diabetes, cardiovascular diseases, and myopathies 2, 3. Diet-induced obesity promotes insulin resistance 4, 5, lipid accumulation 6, 7, and inflammation 8, 9 in skeletal muscle. The regulation of skeletal muscle FA composition is not fully understood; however, it markedly changes with dietary macronutrient composition.