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Shaodong Guo

Shaodong Guo

Associate Professor, Department of Nutrition and Food Sciences, Texas A&M University, Texas, U.S.A.

Title: Disease Mechanisms and Dietary Intervention for Obesity and T2DM

Biography

Biography: Shaodong Guo

Abstract

Insulin resistance serves as the major mechanism for the development of obesity, which is pandemic in population worldwide over the past decades, largely owing to over nutrition. Excess energy stores in the adipose tissue and other organs as lipids, promoting lipotoxicity and metabolic inflammation, activating intracellular protein kinases to impair insulin signaling components, and resulting in insulin resistance. Insulin resistance is the key etiologic illness that defines “metabolic syndrome”, a set of interrelated disorders/issues, inclusive of obesity, hyperglycemia, dyslipidemia, and hypertension. Following insulin resistance, a lot of patients with the metabolic syndrome sooner or later developed pancreatic β-cell failure, which triggers the onset of type 2 diabetes mellitus (T2DM) and its complications. Our cell- and animal-based totally studies demonstrate that insulin and its signaling cascades generally control cell growth, metabolism and survival through activation of mitogen-activated protein kinases (MAPKs) and phosphotidylinositide-3-kinase (PI3K), of which activation of PI-3K-associated with insulin receptor substrate-1 and -2 (IRS1, 2) and subsequent Akt→Foxo1 phosphorylation cascade has a central function in control of nutrient homeostasis and organ survival. Inactivation of Akt and activation of Foxo1, through suppression IRS1 and IRS2 in a variety of organs following over nutrition, lipotoxicity, and inflammation may form a fundamental mechanism for insulin resistance in humans. This seminar discusses the premise of insulin signaling, resistance, and how excess nutrients and lipid signaling from obesity promotes infection and insulin resistance, selling organ failure with emphasis on the IRS and the forkhead/winged-helix transcription component Foxo1