Chronic dietary vitamin A supplementation regulates obesity in an obese mutant WNIN/Ob rat model

Abstract

Objective: To understand the possible role of chronic dietary high vitamin A supplementation in body weight regulation and obesity using a novel WNIN/Ob obese rat model developed at the National Centre for Laboratory Animal Sciences of National Institute of Nutrition, India.

Research methods and procedures: Thirty-six 7-month-old male rats of lean, carrier, and obese phenotypes were broadly divided into two groups; each group was subdivided into three subgroups consisting of six lean, six carrier, and six obese rats and received diets containing either 2.6 or 129 mg vitamin A/kg of diet for 2 months. Body weight gain, food intake, and weights of various organs were recorded. Adiposity index and BMI were calculated. Serum and liver retinol and brown adipose tissue (BAT)-uncoupling protein1 (UCP1) mRNA expression levels were quantified.

Results: Chronic feeding of high but non-toxic doses of vitamin A through diet significantly reduced (P < or = 0.05) body weight gain, adiposity index, and retroperitoneal white adipose tissue mass (without affecting food intake) in obese rats compared with their lean and carrier counterparts. In general, vitamin A treatment significantly improved hepatic retinol stores (P < or = 0.05) in all phenotypes without affecting serum free retinol levels. However, augmented BAT-UCP1 expression was observed only in carrier and obese rats (whose basal expression was low).

Discussion: Our data suggest that chronic dietary vitamin A supplementation at high doses effectively regulates obesity in obese phenotype of the WNIN/Ob strain, possibly through up-regulation of the BAT-UCP1 gene and associated adipose tissue loss. However, in vitamin A-supplemented lean and carrier rats, changes in adiposity could not be related to BAT-UCP1 expression levels.