Abdominal Adipose Tissue: Early Metabolic Dysfunction Associated to Insulin Resistance and Oxidative Stress Induced by an Unbalanced Diet

Jul 16, 2008Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme

Early Metabolic Problems in Belly Fat Linked to Insulin Resistance and Oxidative Stress from an Unbalanced Diet

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Abstract

Rats fed a fructose-rich diet exhibited significantly higher plasma levels of glucose, triglycerides, and insulin.

Early changes in the lipid composition of abdominal adipose tissue included increased saturated fats relative to unsaturated fats.
Higher levels of oxidative stress markers, such as lipid peroxidation, were observed in the adipose tissue of rats on the fructose-rich diet.
Antioxidant enzyme activity decreased in the adipose tissue, while levels of certain antioxidants were also reduced.
Incubated adipose tissue from fructose-fed rats released higher amounts of free fatty acids with altered fatty acid ratios.
These metabolic changes may contribute to the development of insulin resistance and oxidative stress, potentially leading to pancreatic dysfunction.

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The possible contribution of early changes in lipid composition, function, and antioxidant status of abdominal adipose tissue (AAT) induced by a fructose-rich diet (FRD) to the development of insulin resistance (IR) and oxidative stress (OS) was studied. Wistar rats were fed with a commercial diet with (FRD) or without 10% fructose in the drinking water for 3 weeks. The glucose (G), triglyceride (TG), and insulin (I) plasma levels, and the activity of antioxidant enzymes, lyposoluble antioxidants, total glutathione (GSH), lipid peroxidation as TBARS, fatty acid (FA) composition of AAT-TG as well as their release by incubated pieces of AAT were measured. Rats fed with a FRD have significantly higher plasma levels of G, TG, and I. Their AAT showed a marked increase in content and ratios of saturated to monounsaturated and polyunsaturated FAs, TBARS, and catalase, GSH-transferase and GSH-reductase, together with a decrease in superoxide dismutase and GSH-peroxidase activity, and total GSH, alpha-tocopherol, beta-carotene and lycopene content. Incubated AAT from FRD released in vitro higher amount of free fatty acids (FFAs) with higher ratios of saturated to monounsaturated and polyunsaturated FAs. Our data suggest that FRD induced an early prooxidative state and metabolic dysfunction in AAT that would favor the overall development of IR and OS and further development of pancreatic beta-cell failure; therefore, its early control would represent an appropriate strategy to prevent alterations such as the development of type 2 diabetes.

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