Sugar, Uric Acid, and the Etiology of Diabetes and Obesity

Richard J. Johnson; Takahiko Nakagawa; L. Gabriela Sanchez-Lozada; Mohamed Shafiu; Shikha Sundaram; Myphuong Le; Takuji Ishimoto; Yuri Y. Sautin; Miguel A. Lanaspa


Diabetes. 2013;62(10):3307-3315. 

In This Article

Fructose-Induced Metabolic Syndrome Does Not Require Increased Energy Intake

The ability for fructose (and sucrose, which contains fructose) to stimulate food intake and to lower metabolism provides a mechanism for how a high fructose intake may encourage weight gain and visceral fat accumulation. However, fructose or sucrose also alters fat stores and metabolism independent of excessive energy intake. Although weight gain is largely controlled by overall energy intake, other features of metabolic syndrome can occur independent of weight gain. For example, rats fed fructose develop fatty liver, hypertriglyceridemia, and insulin resistance when compared with rats fed isocaloric glucose or starch-enriched diets.[4,5] Indeed, hypertriglyceridemia, fatty liver, and type 2 diabetes can be induced in metabolic syndrome–prone rats with caloric restriction provided the diet is high (40%) in sucrose (which contains fructose).[5] A recent epidemiological analysis in humans also found an association of diabetes prevalence with sugar availability that was independent of total energy intake.[13]