1. Investigación
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Search Results
- Vitamin E Reduces Adipose Tissue Fibrosis, Inflammation, and Oxidative Stress and Improves Metabolic Profile in Obesity
2015-07-06 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 (n510) fed chow diet (10% kcal from fat), obese group (O, n512) 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, n512). 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.
- Comparative responsiveness to prolonged hyperinsulinemia between adipos-tissue and mammary-gland lipoprotein lipase activities in pregnant rats.
1996-09-19T15:40:25Z Plasma-triglyceride levels were higher in pregnant than in virgin rats. The glucose infusion did not modify this parameter, probably because ef the changes in LPL activity in other tissues which are known to occur in the opposite direction to those observed in this study for adipose tissue and mammary gland. The present results support the notion that the insulin resistant condition which normally occurs during late gestation is responsible for the decreased LPL acti11ity in adipose tissue, but that the mammary gland remains sensitive to insulin and so maternal hyperinsulinemia would contribute to the induction of LPL activity in this organ prior to parturition.