Because of its thermogenic property in response to cold and overnutrition, brown adipose tissue in adult humans has become an attractive therapeutic target for treatment of obesity, atherosclerosis and other metabolic syndromes. It is unknow if fructose impacts adipogenesis, metabolism and functions of brown adipocytes. To address the question, we isolate brown preadipocyte from newborn mouse pups, immortalized the cells, and differentiated cells in culture medium with different sugars (1g/L glucose, 1g/L glucose plus 1g/L fructose, 1g/L fructose). Fructose plus glucose increased expression of adipogenesis markers including PPAR-γ, UCP-1 and C/EBP1. Fructose alone decreased adipogenesis proteins. Moreover, fructose alone increased CD36 but decreased FABP4 expression, suggesting cells need to uptake more fatty acid in compromise of carbon shortage from glucose, but fatty acid could not be effectively transported to organelles such as mitochondria, ER or Golgi because of lack of FABP4. In contrast, Fructose plus glucose increased FABP4 although it did not change of CD36, suggesting fatty acid could effectively be trafficked to organelles. Fructose plus glucose did not change phosphorylation of p38-MAPK but enhanced the phosphorylation of Erk at Thr202 and Tyr204. As to Akt, the site of Ser473 phosphorylation decreased, not at Thr308. Our data indicates physiological level of fructose together with glucose promotes brown adipogenesis, enhances thermogenic protein UCP-1, facilitates fatty acid transport and metabolisms in differentiated mouse brown adipocytes.

Disclosure

X. Wu: None. S.A.A. Elsaid: None. S. Tee: None.

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