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About the Authors:
Dmitry Grapov
Affiliations Department of Nutrition, University of California Davis, Davis, California, United States of America, Obesity and Metabolism Research Unit, United States Department of Agriculture - Agricultural Research Service - Western Human Nutrition Research Center, Davis, California, United States of America
Sean H. Adams
Affiliations Department of Nutrition, University of California Davis, Davis, California, United States of America, Obesity and Metabolism Research Unit, United States Department of Agriculture - Agricultural Research Service - Western Human Nutrition Research Center, Davis, California, United States of America
Theresa L. Pedersen
Affiliation: Obesity and Metabolism Research Unit, United States Department of Agriculture - Agricultural Research Service - Western Human Nutrition Research Center, Davis, California, United States of America
W. Timothy Garvey
Affiliation: Department of Nutrition Sciences, University of Alabama at Birmingham and Birmingham VA Medical Center, Birmingham, Alabama, United States of America
John W. Newman
* E-mail: [email protected]
Affiliations Department of Nutrition, University of California Davis, Davis, California, United States of America, Obesity and Metabolism Research Unit, United States Department of Agriculture - Agricultural Research Service - Western Human Nutrition Research Center, Davis, California, United States of America
Introduction
Obesity is a risk factor for the development of Type 2 diabetes, a disease which chronically increases circulating non-esterified fatty acids (NEFA) [1], dampens the pulsatile secretion of insulin [2], [3], and diminishes tissue glucose uptake while promoting hepatic glucose output [2], [4], [5]. Peripheral insulin resistance and fuel partitioning in type 2 diabetes are well-studied with respect to glucose, yet impacts on many metabolic domains remain to be assessed. Investigations of diabetes employing global metabolomics in plasma have reported changes in numerous metabolites including lipids, carbohydrates and amino acids, highlighting the fact that type 2 diabetes elicits broad perturbations of energy metabolism [6]–[8]. For example, diabetes increases circulating medium- and long-chain acylcarnitines [6] and branched-chain amino acids [7], [9], suggesting broad dysfunctions in fuel catabolism and mitochondrial function [6]. In contrast, studies addressing the impact of diabetes on circulating levels of low abundance signaling lipids including oxylipins (OxL) and endocannabinoids (eCBs) are less common. Here, we quantified many of these potent mediators along with NEFA to assess the covariant behavior of these molecules in obese diabetic and non-diabetic cohorts.
OxL and eCBs are structurally diverse...