Abstract

An enhanced oxidative stress status has been documented in obese patients and animal models, and a depletion of the antioxidant mechanisms in these conditions is a common feature. Therefore, we have tested the hypothesis that food supplementation with an antioxidant molecule such as vitamin C could prevent fat deposition induced by a high-fat diet in rodents. Ascorbic acid dietary supplementation reduced body weight and the retroperitoneal and subcutaneous fat depots in cafeteria diet-induced obese rats, without affecting food intake. Microarray technology has been applied in rat subcutaneous fat to assess the molecular mechanisms underlying the depletion of fat stores induced by ascorbic acid. Thus, expression of genes involved in cell proliferation, regulation of transcription, and host response are upregulated while a number of genes participating in lipid metabolism, cell adhesion, differentiation, and steroidogenesis (such as steroidogenic acute regulatory protein and hydroxysteroid 11-beta dehydrogenase 2) are downregulated. These data provide new insights to understand that not only calories count in weight gain, but also that the antioxidant status and other mechanisms affecting energy conversion efficiency could participate in energy homeostasis, in which glucocorticoids could be involved.