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ARS Home » Southeast Area » Little Rock, Arkansas » Arkansas Children's Nutrition Center » Research » Publications at this Location » Publication #249737
Title: Carbohydrate-responsive gene expression in adipose tissue of rats

Author
item SHANKAR, KARTIK - Arkansas Children'S Nutrition Research Center (ACNC)
item HARRELL, AMANDA - Arkansas Children'S Nutrition Research Center (ACNC)
item KANG, PING - Arkansas Children'S Nutrition Research Center (ACNC)
item SINGHAL, ROHIT - Arkansas Children'S Nutrition Research Center (ACNC)
item RONIS, MARTIN - Arkansas Children'S Nutrition Research Center (ACNC)
item Badger, Thomas

Submitted to: Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/2/2009
Publication Date: 2/1/2010
Citation: Shankar, K., Harrell, A., Kang, P., Singhal, R., Ronis, M.J., Badger, T.M. 2010. Carbohydrate-responsive gene expression in adipose tissue of rats. Endocrinology. 151(1):153-164.

Interpretive Summary: As obesity continues to be one of the most important public health issues, the understanding of the how composition of our diets affects our ability to gain weight is becoming increasingly important. Our studies showed that diets high in either carbohydrates or high in fat, led to greater body weight gain and greater body fat accumulation. Our results also showed that carbohydrates caused specific genes to be turned on and others to be turned off in the fat tissue. Furthermore, we learned that the high level of carbohydrates actually regulated genes that control: 1) conversion of carbohydrates into fat (a process known as lipid biosynthesis) and 2) breakdown of carbohydrates (a process known as glycolysis).

Technical Abstract: Although obesity is often associated with high fat diets, it can develop from a variety of meal patterns. Excessive intake of simple carbohydrates is one consistent eating behavior leading to obesity. However, the impact of over-consumption of diets with high carbohydrate-to-fat ratios (C/F) on body composition and global adipose tissue gene expression remains unclear. We employed total enteral nutrition (TEN) to evaluate the effects of caloric intake and C/F on body weight gain and development of obesity. Female Sprague-Dawley rats were fed diets with either low C/F (LC) or high C/F (HC), (reflecting an 18-fold increase in C/F), at two levels of caloric intake; 187 kcal/kg3/4/d or 220 kcal/kg3/4/d (15 % excess) for 4 wk. At the end of the study period, rats fed HC diets had about 20 % higher BW at either caloric intake compared to rats fed LC diets (P < 0.05). Body composition (assessed by NMR, CT and adipose tissue weights) revealed higher percent fat mass (P < 0.05) in HC rats. Obesity was associated with increased serum resistin, leptin, fasting hyperinsulinemia, and insulin resistance following an oral glucose challenge (P < 0.05). Microarray analyses of adipose tissues revealed HC diets led to changes in 270 and 464 transcripts at 187 and 220 Kcal/kg3/4/d intakes. Genes regulating glucose transport, glycolysis, fatty acid, and triglyceride biosynthesis, desaturation and elongation, adipogenesis, and adipokines were affected by HC diets. These results suggest that C/F and interactions with excessive caloric intake per se may regulate body composition and play important roles in the development of obesity and metabolic syndrome.