American journal of physiology. Endocrinology and metabolism
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Am. J. Physiol. Endocrinol. Metab. · Sep 2008
ReviewWhy are we shaped differently, and why does it matter?
Body fat distribution is an important predictor of metabolic abnormalities in obese humans. Dysregulation of free fatty acid (FFA) release, especially from upper body subcutaneous adipose tissue, appears to contribute substantially to these metabolic disturbances. ⋯ Regional variations in the storage of fatty acids, both meal derived and direct reuptake, and storage of circulating FFAs that may help to explain why some depots expand at the expense of others have been reported. We review the quantitative data on regional lipolysis, meal, and FFA storage in adults to provide an overview of fat balance differences in adults with different fat distribution patterns.
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Am. J. Physiol. Endocrinol. Metab. · Sep 2008
Adiponectin deficiency promotes endothelial activation and profoundly exacerbates sepsis-related mortality.
Sepsis is a multifactorial, and often fatal, disorder typically characterized by widespread inflammation and immune activation with resultant endothelial activation. In the present study, we postulated that the adipokine adiponectin serves as a critical modulator of survival and endothelial activation in sepsis. To this aim, we evaluated both loss-of-function (adiponectin gene-deficient mice) and subsequent gain-of-function (recombinant adiponectin reconstitution) strategies in two well-established inflammatory models, cecal ligation perforation (CLP) and thioglyocollate-induced peritonitis. ⋯ Importantly, all of these effects were blunted by recombinant total adiponectin administration given 3 days prior to thioglycollate challenge. The protective effects of adiponectin were ascribed largely to higher-order adiponectin oligomers, since administration of recombinant C39A trimeric adiponectin did not attenuate endothelial adhesion molecule expression in thioglycollate-challenged Adipoq(-/-) mice. These data suggest a critical role of adiponectin as a modulator of survival and endothelial inflammation in experimental sepsis and a potential mechanistic link between adiposity and increased sepsis.