title: Overnutrition, mTOR signaling, and cardiovascular diseases.
abstract: The prevalence of obesity and associated medical disorders has increased dramatically in the United States and throughout much of the world in the past decade. Obesity, induced by excess intake of carbohydrates and fats, is a major cause of Type 2 diabetes, hypertension, and the cardiorenal metabolic syndrome. There is emerging evidence that excessive nutrient intake promotes signaling through the mammalian target of rapamycin (mTOR), which, in turn, may lead to alterations of cellular metabolic signaling leading to insulin resistance and obesity-related diseases, such as diabetes, cardiovascular and kidney disease, as well as cancer. While the pivotal role of mTOR signaling in regulating metabolic stress, autophagy, and adaptive immune responses has received increasing attention, there remain many gaps in our knowledge regarding this important nutrient sensor. For example, the precise cellular signaling mechanisms linking excessive nutrient intake and enhanced mTOR signaling with increased cardiovascular and kidney disease, as well as cancer, are not well understood. In this review, we focus on the effects that the interaction between excess intake of nutrients and enhanced mTOR signaling have on the promotion of obesity-associated diseases and potential therapeutic strategies involving targeting mTOR signaling.
authors.affiliation: Divisions of Endocrinology, Diabetes, Hypertension and Metabolism, Diabetes Cardiovascular Center, University of Missouri School of Medicine, Columbia, Missouri; Harry S. Truman Memorial Veterans Hospital, University of Missouri School of Medicine, Columbia, Missouri; and.
authors.forename: Guanghong
authors.initials: G
authors.lastname: Jia
authors.affiliation: Divisions of Endocrinology, Diabetes, Hypertension and Metabolism, Diabetes Cardiovascular Center, University of Missouri School of Medicine, Columbia, Missouri; Harry S. Truman Memorial Veterans Hospital, University of Missouri School of Medicine, Columbia, Missouri; and.
authors.forename: Annayya R
authors.initials: AR
authors.lastname: Aroor
authors.affiliation: Departments of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, Missouri; Harry S. Truman Memorial Veterans Hospital, University of Missouri School of Medicine, Columbia, Missouri; and Dalton Cardiovascular Research Center, University of Missouri School of Medicine, Columbia, Missouri.
authors.forename: Luis A
authors.initials: LA
authors.lastname: Martinez-Lemus
authors.affiliation: Divisions of Endocrinology, Diabetes, Hypertension and Metabolism, Diabetes Cardiovascular Center, University of Missouri School of Medicine, Columbia, Missouri; Departments of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, Missouri; Harry S. Truman Memorial Veterans Hospital, University of Missouri School of Medicine, Columbia, Missouri; and Dalton Cardiovascular Research Center, University of Missouri School of Medicine, Columbia, Missouri sowersj@health.missouri.edu.
authors.forename: James R
authors.initials: JR
authors.lastname: Sowers
mesh_terms: D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control; D002149:Energy Intake; D004734:Energy Metabolism; D006801:Humans; D007333:Insulin Resistance; D058990:Molecular Targeted Therapy; D009765:Obesity / Q000150:complications* / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology; D019893:Ribosomal Protein S6 Kinases / Q000378:metabolism; D012307:Risk Factors; D015398:Signal Transduction / Q000187:drug effects; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism*
chemical_list: D019893:Ribosomal Protein S6 Kinases; D058570:TOR Serine-Threonine Kinases
keywords: cardiorenal metabolic syndrome; cardiovascular disease; insulin resistance; mammalian target of rapamycin; obesity