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Molecular, Genetic, and Biochemical Nutrition Commons™
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Full-Text Articles in Molecular, Genetic, and Biochemical Nutrition
Effects Of Vagotomy And Fenugreek On Hyperlipidemia And Insulin Resistance, Rituraj Khound
Effects Of Vagotomy And Fenugreek On Hyperlipidemia And Insulin Resistance, Rituraj Khound
Department of Nutrition and Health Sciences: Dissertations, Theses, and Student Research
Hyperlipidemia is the impairment of lipid metabolism marked by abnormally high levels of lipid in circulation. This has been implicated in a number of metabolic diseases including diabetes, cardiovascular diseases, and nonalcoholic fatty liver disease. Insulin resistance is the impairment of insulin action, which leads to several diseases such as obesity and type 2 diabetes. New clinical and therapeutic approaches are warranted for the prevention and treatment of hyperlipidemia and insulin resistance. In our study, we investigated the mechanism underlying the effect of complete disruption of the sub-diaphragmatic vagus nerve (vagotomy) on hyperlipidemia and insulin sensitivity. We observed that vagotomy …
Attenuation Of Mtorc1-Driven Secretion Of Lipoproteins And Triacylglycerides By Short Chain Fatty Acids: Mechanistic Insight Into The Pathogenesis Of Hypertriglyceridemia, Joseph L. Roberts
Attenuation Of Mtorc1-Driven Secretion Of Lipoproteins And Triacylglycerides By Short Chain Fatty Acids: Mechanistic Insight Into The Pathogenesis Of Hypertriglyceridemia, Joseph L. Roberts
Department of Nutrition and Health Sciences: Dissertations, Theses, and Student Research
The mechanistic target of rapamycin complex 1 (mTORC1) is a serine/threonine kinase that drives several anabolic processes including lipid synthesis, protein synthesis, and adipogenesis. mTORC1 is highly active in the livers of obese rodents, in overnutrition, and is implicated in the development of obesity related metabolic disorders, including the overproduction of atherogenic lipoproteins. Direct inhibition of mTORC1 is not a viable treatment strategy because it prevents feedback inhibition of the insulin-signaling cascade, leading to increased lipid synthesis and secretion of lipoproteins. Thus, therapeutic approaches that drive catabolic pathways are considered promising mechanisms for overcoming mTORC1-driven anabolism. Human liver HepG2 cells …