Vitamin A and its metabolic pathway play a determinant role in high‐fructose‐induced triglyceride accumulation of the visceral adipose depot of male Wistar rats

Here, we tested a hypothesis that vitamin A and/or its metabolic pathways are involved in the high‐fructose‐mediated alteration in adipose tissue biology. For this purpose, weanling male Wistar rats were provided with one of the following diets: control (C), control with vitamin A deficiency (C‐VAD), high fructose (HFr), and HFr with VAD (HFr‐VAD) for 16 weeks, except that half of the C‐VAD diet‐fed rats were shifted to HFr diet (C‐VAD(s)HFr), after 8‐week period. Compared with control, feeding of HFr diet significantly increased the triglyceride content (P ≤ .01) and thus adipocyte size (hypertrophy) (P ≤ .001) in visceral adipose depot; retroperitoneal white adipose tissue (RPWAT) and these changes were corroborated with de novo lipogenesis, as evidenced by the increased glycerol‐3‐phosphate dehydrogenase activity (P ≤ .01) and up‐regulation of lipogenic pathway transcripts, fructose transporter, and aldehyde dehydrogenase 1 A1. On the contrary, the absence of vitamin A in the HFr diet (HFr‐VAD) failed to exert these changes; however, it induced adipocyte hyperplasia. Further, vitamin A deficiency‐mediated changes were reversed by replenishment, as evident from the group that was shifted from C‐VAD to HFr diet. In conclusion, vitamin A and its metabolic pathway play a key determinant role in the high‐fructose‐induced triglyceride accumulation and adipocyte hypertrophy of visceral white adipose depot.Significance of the studyHere, we report the metabolic impact of high‐fructose feeding under vitamin A–sufficient and vitamin A–deficient conditions. Feeding of high‐fructose diet induced triglyceride accumulation and adipocyte hypertrophy of the visceral white adipose depots. These changes corroborated with augmented expression of vitamin A and lipid metabolic pathway genes. Contrarily, absence of vitamin A in the high‐fructose diet did not elicit such responses, while vitamin A replenishment reversed the changes exerted by vitamin A deficiency. To our knowledge, this is the first study to report the role of vitamin A and its metabolic pathway in the high‐fructose‐induced triglyceride synthesis and its accumulation in visceral adipose depot and thus provide a new insight and scope to understand these nutrients interaction in clinical conditions.