LAUSR

Objectives As birds are a natural model of diabetes, the objective of this study was to test the hypothesis that feeding adult mourning doves, Zenaida macroura, a high fat diet (60% calories from fat; HF) or refined carbohydrate diet (white bread: WB) for four weeks results in diabetes-like pathologies including hyperglycemia and altered metabolic profiles. Methods Separate cohorts of doves were captured for each feeding trial and were acclimated for one week to their respective study diets; cohort 1: WB (n = 6) vs nutritionally-balanced seeds (n = 6), and cohort 2: HF (n = 4) vs control (n = 6). The WB study mimicked natural feeding options for wild birds whereas the HF study used experimental diets. Four weeks later, birds were euthanized with an overdose of sodium pentobarbital and we collected cardiac blood, liver, kidney (HF study only), and pectoralis muscle for metabolomic analyses and biochemical assays. Results Pathway analysis of metabolic concentrations revealed only two pathways that were significantly altered (p < 0.05) and concurrently highly impacted (scale: 0-1; > 0.60) by the HF diet consumption: ubiquinone and other terpenoid-quinone biosynthesis (plasma and pectoralis muscle) and alanine, aspartate, and glutamate metabolism (plasma and kidney; p < 0.05). Only three low impact pathways were significantly affected by the WB diet consumption: glutathione metabolism and histidine metabolism (liver), and glyoxylate and dicarboxylate metabolism (pectoralis muscle; p < 0.05). Further, consumption neither of the HF nor of the WB diet altered plasma uric acid, insulin, pectoralis muscle, liver triglycerides, or body mass (only measured in HF study) significantly, but liver glycogen concentrations were 2.12-fold higher in WB than control doves (p < 0.015). Lastly, blood glucose concentrations did not differ between WB or HF birds and control birds. Conclusions Contrary to our hypothesis, consumption of a WB or HF diet for four weeks did not induce symptoms of diabetes in doves. Further elucidating the apparent avian resistance to diet-induced metabolic complications may help develop novel therapeutic agents for mammalian diabetes. Funding Sources ASU School of Life Sciences/Office of Knowledge Enterprise Development - Research Investment Initiative, a summer research fellowship from the American Physiology Society, and the Center of Evolution and Medicine Graduate Fellow Award.