Key result
A high-fructose diet increased triglyceride content and adipocyte hypertrophy in visceral adipose depots of male Wistar rats, which was prevented by vitamin A deficiency.
Why the study?
To test the hypothesis that vitamin A and/or its metabolic pathways are involved in high-fructose-mediated alterations in adipose tissue biology.
Vitamin A and its metabolic pathway are essential for high-fructose-induced triglyceride accumulation and adipocyte hypertrophy in visceral white adipose tissue in a rat model.
Answers are grounded in this paper and cite their sources.
Vitamin A deficiency may blunt fructose-driven visceral adiposity in rats; leaves open human relevance and requires prospective study.
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 STUDY: Here, 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.
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Reddy et al. (2019) studied High-fructose-induced triglyceride accumulation. High-fructose diet vs. Control diet was evaluated on Triglyceride content in visceral adipose depot (p=≤ .01). A high-fructose diet increased triglyceride content and adipocyte hypertrophy in visceral adipose depots of male Wistar rats, which was prevented by vitamin A deficiency.
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