AI Article Synopsis
- High fructose intake is linked to serious metabolic issues, including insulin insensitivity and the rise of metabolic syndrome (MS), affecting about 25% of adults globally.
- A study on rats highlighted that infliximab, a TNF-α antagonist, was administered after fructose-induced MS was established, revealing mixed results in managing symptoms.
- While infliximab reduced triglyceride levels and increased HDL cholesterol, it did not improve body weight, blood glucose, hypertension, or malondialdehyde levels in the rats.
Article Abstract
Public health issues have been raised regarding fructose toxicity and its serious metabolic disorders. Deleterious effects of high fructose intake on insulin sensitivity, body weight, lipid homeostasis have been identified. The new millennium has witnessed the emergence of a modern epidemic, the metabolic syndrome (MS), in approximately 25% of the world's adult population. The current study aimed to investigate the effect of the TNF-α antagonist infliximab on fructose-induced MS in rats. Rats were administered fructose (10%) in drinking water for 12 weeks to induce the experimental MS model. infliximab (5 mg/kg) was injected once weekly intraperitoneally starting on the 13th week for 4 weeks. Increase in body weight, blood glucose level, serum triglycerides (TGs), adiponectin level and blood pressure were present in MS rats. They also prompted increases in serum of leptin, TNF-α, and malondialdehyde (MDA) levels. Treatment with infliximab did not affect body weight, hyperglycemia or hypertension, but decreased serum TGs and increased serum HDL-c levels. Infliximab also decreased adiponectin levels. Surprisingly, infliximab increased MDA above its value in the MS group. These results reflect the fact that infliximab affects the manifestations of MS in rats. Though infliximab reduced TGs, increased HDL-c levels, reversed adiponectin resistance occurred by fructose, the drug failed to combat MS-mediated hyperglycemia, hypertension, and elevated MDA above the insult.
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| http://dx.doi.org/10.1177/0960327120969960 | DOI Listing |
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