Abstract
Oxidative stress is elevated in human obesity and several animal models. Oxidative stress, through the damaging effects of oxygen radicals, may contribute to obesity‐associated conditions. These include elevated blood pressure, lipids, glucose, and insulin resistance, all of which are present in the spontaneously hypertensive obese (SHROB/Kol) rat model of prediabetes. In the present study, SHROB (N=27) were compared to lean SHR/Kol (N=11) littermates. Oxidative stress was measured by assay of peroxides in plasma and the lipid fraction of kidney and liver tissue. Plasma and organ lipid peroxides were increased up to 3‐fold in untreated SHROB rats relative to lean SHR littermates. The activity in the liver cytosol of the protective enzyme superoxide dismutase was not different (SHROB: 63±5 vs SHR: 53±7 U/mg protein). Another protective enzyme, catalase, was also unchanged in the liver cytosol (SHROB: 95±6 vs SHR: 93±13 U/mg protein). Thus, the enzymes responsible for breaking down superoxide and hydrogen peroxide fail to up‐regulate in response to increased oxidative stress in SHROB. Subsequent oxidative damage may contribute to insulin resistance in the liver and renal and hepatic dysfunction.
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