Open AccessFructose‐Fed Rhesus Monkeys: A Nonhuman Primate Model of Insulin Resistance, Metabolic Syndrome, and Type 2 Diabetes
Author(s) -
Bremer Andrew A.,
Stanhope Kimber L.,
Graham James L.,
Cummings Bethany P.,
Wang Wenli,
Saville Benjamin R.,
Havel Peter J.
Publication year - 2011
Publication title -
clinical and translational science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.303
H-Index - 44
eISSN - 1752-8062
pISSN - 1752-8054
DOI - 10.1111/j.1752-8062.2011.00298.x
Subject(s) - insulin resistance , metabolic syndrome , fructose , primate , type 2 diabetes , dyslipidemia , diabetes mellitus , insulin , endocrinology , medicine , biology , obesity , physiology , neuroscience , biochemistry
Abstract The incidence of insulin resistance has increased dramatically over the past several years, and we and others have proposed that this increase may at least in part be attributable to increased dietary fructose consumption. However, a major limitation to the study of diet‐induced insulin resistance is the lack of relevant animal models. Numerous studies, mostly in rodents, have demonstrated that diets high in fructose induce insulin resistance; however, important metabolic differences exist between rodents and primates. Thus, the results of metabolic studies performed in primates are substantively more translatable to human physiology, underscoring the importance of establishing nonhuman primate models of common metabolic conditions. In this report, we demonstrate that a high‐fructose diet in rhesus monkeys produces insulin resistance and many features of the metabolic syndrome, including central obesity, dyslipidemia, and inflammation within a short period of time; moreover, a subset of monkeys developed type 2 diabetes. Given the rapidity with which the metabolic changes occur, and the ability to control for many factors that cannot be controlled for in humans, fructose feeding in rhesus monkeys represents a practical and efficient model system in which to investigate the pathogenesis, prevention, and treatment of diet‐induced insulin resistance and its related comorbidities. Clin Trans Sci 2011; Volume 4: 243–252