White- and Brown-Rice Supplementation Improves Insulin Tolerance, Brown Fat Activation, Energy Expenditure, and Changes the Gut Microflora in Diet-Induced Obesity

Abstract

Increased consumption of white rice (WR) with parallel decreased use of brown rice (BR) have been associated with increased prevalence of type 2 diabetes (T2DM), suggesting WR may elevate the risk of T2DM. To test whether WR or BR have differential effects on glucose metabolism in diet-induced obesity, C57BL/6 mice were fed 6 different diets: control diet (CD, 10%), high fat diet (HFD, 46%) and CD and HFD with either WR or BR. Diets with WR or BR were controlled with comparable carbohydrate and protein contents. After 18 weeks, the median weights of HFD mice were greater (36%) than those on CD. Surprisingly, adding WR or BR to HFD decreased weight gains equally by 53% with parallel reduction of abdominal, visceral, subcutaneous, and total fat vs. HFD. Activity and food intake did not change among mice on HFD. However, HFD decreased heat, VO2, and VCO2 production vs. CD which were normalized by adding WR or BR, per indirect calorimetry with metabolic cages. Intraperitoneal glucose tolerance test on HFD were improved by either WR or BR, although mice on BR+HFD exhibited greater improvements than mice on WR+HFD (P<0.05). Adding WR or BR to HFD decreased HFD-induced elevations of plasma leptin and MCP-1 levels. HFD decreased brown fat tissue mass and markers, UCP-1 and PGC1α vs. CD mice which improved when WR or BR was added to HFD. Gut microbiota composition, assessed by 16S rRNA sequencing and metagenomic analysis, showed clear differences between HFD vs. CD or vs. the addition of BR or WR. The ratio of Firmicutes to Bacteroidetes was increased significantly in HFD vs. CD diet, which has been associated with obesity and metabolic syndrome, but decreased by the addition of WR (63%) or BR (81%). Thus, BR and, surprisingly, WR may activate BAT, increase energy expenditure to reduce body weight and improve insulin sensitivity while on HFD, possibly by altering gut microbiome, indicating that common substances may exist in BR and WR to lower the risks for T2DM. Disclosure H. Yokomizo: None. A. Ishikado: Employee; Self; Sunstar Inc.. Employee; Spouse/Partner; Sunstar Inc.. T. Shinjo: None. K. Park: None. Y. Maeda: None. I. Wu: None. D.M. Pober: None. S. Devkota: None. M. Matsumoto: Employee; Self; Sunstar Inc.. A. Kostic: None. G.L. King: Research Support; Self; Sanofi-Aventis.