Filtering by
- All Subjects: Obesity
- Creators: School of Life Sciences
- Member of: Theses and Dissertations
In 2017-2018, the results showed that 0.5% menthol (n=4) suppressed weight gain more effectively than both the baseline chow diet (n=4, p=0.022) and the HFD (n=4, p=0.027). Again in 2018-2020, the 0.5% menthol (n=6) showed promising results, showing significant suppression of weight gain when compared to chow (n=13, p=0.022). Unfortunately, the difference in weight gain in 1% menthol (n=6) was inconclusive when comparing to both chow and HFD. Although 1% menthol was inconclusive in its efficacy in suppressing weight regain, the promising results on 0.5% menthol show that menthol has the potential to be an effective treatment to both prevent rapid weight gain and maintain weight loss from caloric restriction.
body weight. Microarray analysis identified 53 probe sets significantly altered post- ω-3PUFA, with APOE being one of the most upregulated genes. High dose of long chain ω-3PUFA supplementation modulates significant changes in plasma fatty acid profile, AT and systemic inflammation. These findings associate with significant improvement of insulin-stimulated glucose disposal. Unbiased microarray analysis of Sc fat biopsy identified APOE as the most differentially regulated gene after ω-3PUFA 22 supplementation. We speculate that ω-3PUFA increases macrophage-derived APOE mRNA levels with anti-inflammatory properties.
According to the CDC, obesity has increased from 30.5% to 42.4% over the past 18 years. Western diets (WDs) consist of large portions in high fats, high carbohydrates, excess sugar and high-glycemic foods that can cause metabolic complications and mitochondrial dysfunction. Diet-induced obesity can lead to changes in muscle metabolism and muscle fiber phenotypes, which in turn lead to metabolic complications. Muscle fiber phenotype is determined protein isoform-content of myosin heavy chain (MHC). Regular exercise alters mitochondrial content and fat oxidation and shifts MHC proportions under healthy circumstances. However, diet and exercise-driven fiber type shifts in diet-induced obesity are less understood. We designed our experiment to better understand the impact of diet and/ or exercise on fiber type content of gastrocnemius muscle in diet-induced obese mice. Exercise and genistein may be used as a treatment strategy to restore the MHC proportions in obese subjects to that of the lean subjects. We hypothesized that genistein and exercise would have the greatest MHC I change in muscle fiber phenotype of mouse gastrocnemius muscles. Further, we also hypothesized that a standard diet would reverse the expected increase in fast fiber phenotype (MHC IIb). Lastly, we also hypothesized that exercise would also reduce the abundance of MHC IIb. Gastrocnemius muscles were collected from mice, homogenized, run through gel electrophoresis and stained to give muscle fiber proportions. Paired sample t-tests were conducted for differences between the MHC isoforms compared to the lean (LN) and high-fat diet (HFD) control groups. The results showed that genistein and exercise significantly increased the abundance of MHC I muscle fibers (19%, p<0.05). Additionally, diet and exercise restored the muscle fiber phenotype to that of lean control. As expected, HFD obese mice exhibited elevated fast twitch fibers compared to only 3% slow twitch fibers. These findings show the potential for exercise and supplementation of genistein as a strategy to combat diet induced obesity. Future research should aim to understand the mechanisms that genistein acts on to make these changes, and aim to replicate these data in humans with obesity.