Objective: To test whether enhancing the capability of adipose tissue to store lipids using antioxidant supplementation may prevent the lipotoxic effects and improve the metabolic profile of long-term obesity. Methods: C57BL/6J mice were randomized into three experimental groups for 28 weeks: control group (n 5 10) fed chow diet (10% kcal from fat), obese group (O, n 5 12) fed high-fat (HF) diet (45% kcal from fat), and obese group fed HF diet and supplemented twice a week with 150 mg of a-tocopherol (vitamin E) by oral gavage (OE, n 5 12). Results: HF diet resulted in an obese phenotype with a marked insulin resistance, hypertriglyceridemia, and hepatic steatosis in O mice. Histological analysis of obese visceral adipose tissue (VAT) revealed smaller adipocytes surrounded by a fibrotic extracellular matrix and an increased macrophage infiltration, with the consequent release of proinflammatory cytokines. Vitamin E supplementation decreased oxidative stress and reduced collagen deposition in the VAT of OE mice, allowing a further expansion of the adipocytes and increasing the storage capability. As a result, circulating cytokines were reduced and hepatic steasosis, hypertriglyceridemia, and insulin sensitivity were improved. Conclusions: Our results suggest that oxidative stress is implicated in extracellular matrix remodeling and may play an important role in metabolic regulation.

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Lipid oxidation products (LOPs), generated in culinary oils during episodes of thermal stressing can give rise to cellular damage. The aims of this study were to determine whether orally-administered, LOP-containing thermally-stressed safflower oil exerts teratogenic actions in rats, and whether this effect could be prevented by co-administration of alpha-tocopherol (alpha-TOH). Safflower oil was heated for a period of 20 min according to standard frying practices and stored at -20 degrees C under N2. Four experimental groups of pregnant Wistar rats were employed; two received 0.30 ml of pre-heated oil (HO), one of which was also supplemented with 150 mg of alpha-TOH (HOE), and two served as controls, one treated with the non-heated oil (O) and the other without any treatment (C). The oil was administered daily by gavage from day 1 of pregnancy to day 11.5, when the animals were killed and the embryos examined. LOPs and alpha-TOH were determined both in the heated and non-heated oils. The percentage of embryo malformations and reabsorptions were determined in the above four experimental groups. Heating the oil substantially increased its concentration of LOPs and decreased its alpha-TOH content. The percentage of embryo malformations in the HO group was 21.73%, compared with 5.6 and 7% in the O and C groups, respectively. Supplementation of the pre-heated oil with alpha-TOH was found to decrease the percentage of malformations to 7%. The results obtained from these investigations indicate that LOPs detectable at millimolar levels in the heated cooking oils administered (e.g. saturated and alpha,beta-unsaturated aldehydes, and/or their conjugated hydroperoxydiene precursors) exert potent teratogenic actions in experimental animals which are at least partially circumventable by co-administration of the chain-breaking antioxidant alpha-TOH. Plausible mechanisms for these processes and their health relevance to humans regarding diet and methods of frying/cooking are discussed.

Water-soluble aldehydes, extracted from thermally oxidized culinary oil, increase the expression of CD36. This effect is partially decreased by the presence of alpha-tocopherol.