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Volume 8 Journal of Obesity &Weight Loss Therapy Obesity Summit 2018
July 10-11, 2018
July 10-11, 2018 Bangkok, Thailand
19th World Obesity Congress
Disease mechanisms and dietary intervention for obesity and T2DM
Shaodong Guo
Texas A&M University, USA
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 (IRS 1, 2) and subsequent Akt→Fo xo1 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
fork head/winged-helix transcription component Foxo1.
Biography
Shaodong Guo is an Associate Professor in the Department of Nutrition and Food Science at Texas A&M University College. He has received his PhD in Physiology
from Peking University, China. Later, he has completed his Postdoctoral research training in Genetics, Biochemistry and Medicine in the Chinese Academy of
Sciences, the University of Illinois at Chicago and Harvard University, respectively. He was an Instructor in Medicine at Children’s Hospital Boston and Harvard
Medical School for two years prior to joining the Faculty at Texas A&M Health Science Center. Currently, he serves as a Senior Editor for the Journal of Endocrinology
and Journal of Molecular Endocrinology, two major official journals of Endocrine Society of Europe, UK and Australia and he is the author of the textbook chapter
for metabolic syndrome and published by Springer in 2016. His lab research focuses on insulin/glucagon and estrogen signal transduction, insulin resistance, gene
transcriptional control of nutrient homeostasis and cardiac dysfunction in diabetes. He is a recipient of ADA Junior Faculty Award, Career Development Award and
Richard R Lee Award. His work has been published in several journals including the JBC, Endocrinology, Hypertension, Diabetes, Circulation Research, AJP, MCB
and Nature Medicine, receiving more than 5,000 citations from the Google Scholar.
Shaodong Guo, J Obes Weight Loss Ther 2018, Volume 8
DOI: 10.4172/2165-7904-C4-066