FRIDAY, June 5 (HealthDay News) -- Mice lacking receptors for a major inflammatory cytokine that is a major inhibitor of insulin sensitivity, tumor necrosis factor, still become obese after being fed a high-fat and high-sugar diet, but are not protected against obesity-associated insulin resistance, according to a study published online May 28 in Endocrinology.
To investigate the role of tumor necrosis factor receptors (TNFRs) in metabolism, Nathalie Pamir, Ph.D., and colleagues from the University of Washington in Seattle fed normal mice or mice lacking both TNFRs either a normal diet or a high-fat and high-sucrose diet starting at 4 weeks of age.
The researchers found that mice lacking both TNFRs were 10 percent heavier and 18 percent fatter than normal mice at 4 weeks of age, and were 26 percent heavier and 50 percent fatter after 14 weeks of eating a high-fat and high-sucrose diet. Mice lacking both receptors had a lower metabolic rate (oxygen consumption compared with carbon dioxide production, locomotor activity); obese mice lacking both receptors were markedly insulin resistant; and mice lacking both receptors and fed a high-fat and high-sucrose diet had greater macrophage infiltration in their adipose tissue (predominantly anti-inflammatory macrophages).
"TNFRs play a physiological role to limit body weight and adiposity by modestly increasing metabolic rate and fatty acid oxidation, and they are required for obesity-induced activation of adipose tissue macrophages," Pamir and colleagues conclude. "Despite these effects, TNFRs are not required for obesity-induced insulin resistance."
Abstract
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