Abstract
BackgroundRecent findings have established an association between obesity and immune dysfunction. However, most of the studies investigating the effects of obesity on immune function have been carried out in genetically obese rodent models. Since human obesity is mostly due to intake of a high fat diet and decreased energy expenditure, we asked whether immunological defects also occur in diet-induced obesity. Specifically, we focused on the function of monocytes and macrophages, as these cells are thought to be involved in the low-grade inflammation present in obesity.MethodsMale Sprague-Dawley rats were fed a high-fat or a standard chow diet for either 2 or 10 weeks. At the end of the intervention period animals were anaesthetised, blood collected for determination of plasma mediator concentrations and lipopolysaccharide (LPS) stimulated production of TNF-α by monocytes. LPS stimulated production of TNF-α in alveolar macrophages was also determined.ResultsHigh-fat feeding for either 2 or 10 weeks resulted in significant increases in fat mass and serum leptin. Although increased serum leptin has previously been linked to modulation of innate immunity, we found no significant difference in the LPS stimulated production of TNF-α by either blood monocytes or alveolar macrophages between the dietary groups. Furthermore, we failed to find a significant increase in circulating TNF-α concentrations in obese animals, as reported for genetically obese animals.ConclusionOur data suggest that defects in innate immune function observed in genetically obese animals are not mimicked by dietary obesity, and may more likely reflect the gross abnormality in leptin function of these models. Further work is required delineate the effects of dietary obesity on inflammatory state and immune function.
Highlights
Recent findings have established an association between obesity and immune dysfunction
Since specific gene defects only account for a small proportion of obesity in humans [7,35], this study was designed to investigate whether the functional defects in the monocyte/macrophage system described in genetically obese animal models are present in an animal model of diet-induced obesity, that more closely resembles human obesity
The absence of any significant effects of diet-induced obesity on critical functional parameters of the monocyte/macrophage system used here raises the important question as to whether the changes in the production of pro-inflammatory cytokines observed in genetically obese animals result from the complex
Summary
Recent findings have established an association between obesity and immune dysfunction. It has been reported that obese individuals have a higher incidence and severity of infectious diseases [4] These defects include disturbances in macrophage mediated phagocytosis and pro-inflammatory cytokine production [5] as well as increased sensitivity to endotoxin-induced lethality [6]. With leptin resembling several aspects of a cytokine and exerting various immunological functions [reviewed by [8]], it is unclear whether these models examine the effects of obesity in general or rather the effects of a defective leptin system on immune function. This question needs to be addressed by investigating immune function in diet-induced models of obesity
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