Abstract
Abnormal fat deposition has been identified as an i mportant mechanism of obesity-associated with insulin resistance. Literature data also indicate that exer cise can improve insulin action. The heme pathway enzyme δAminolevulinate Dehydratase (δ-ALA-D) is a good marker for oxidative stress and t his sulfhydryl enzyme is inhibited in such oxidative pathologies diabetes. T he aim of this study was to evaluate the effects of physical exercise in mice fed high sucrose (20% in drinking water), on aspects of insulin resistance, profile o f oxidative status in different tissues and influence on δ-ALA-D activity. Glucose (p<0.003), insulin (p<0.01) plasma levels and abdominal fat index (p<0.001) were signi ficantly higher in mice fed the sucrose in the wate r when compared to control group. Not have difference on t hese parameters between exercised mice fed the sucrose and control group. Hepatic, ALA-D activity and TBARS from liver, kidney and brain, of sucrose fed animals with and without exercise were not different than t hat of control group. The results of the present st udy possibly indicate that the sucrose administration i n the water, cause marked insulin resistance and th at the physical exercise showed efficient in increase insu lin sensibility in mice with insulin resistance.
Highlights
Marked hyperinsulinemia, glucose intolerance, dyslipidemia and central adiposity (Henriksen, 2002) and Insulin resistance of skeletal muscle glucose transport represents a major defect in the normal maintenance of euglycemia (Henriksen, 2002)
The aim of this study was to evaluate the effects of physical exercise in mice fed high sucrose (20% in drinking water), on aspects of insulin resistance, profile of oxidative status in different tissues and influence on δ-Aminolevulinic Acid (ALA)-D activity
The results of the present study possibly indicate that the sucrose administration in the water, cause marked insulin resistance and that the physical exercise showed efficient in increase insulin sensibility in mice with insulin resistance
Summary
Marked hyperinsulinemia, glucose intolerance, dyslipidemia and central adiposity (Henriksen, 2002) and Insulin resistance of skeletal muscle glucose transport represents a major defect in the normal maintenance of euglycemia (Henriksen, 2002). Elevated levels of circulating glucose can produce to as “syndrome X” or the “insulin resistance syndrome” permanent chemical alterations in proteins and increase (Henriksen, 2002; Reaven, 1993). The link among these lipid peroxidation in a variety of experimental models of disorders has been attributed to hyperinsulinemia, a hyperglycemia (Folmer et al, 2002). The deleterious effects of hyperglycemia on the properties of physiologically abundant proteins such as hemoglobin, albumin and collagen have been investigated (Soares et al, 2006)
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