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Stress-induced impairments in subcutaneous WAT function contribute to the development of visceral obesity. Exposure to acute stress alters local WAT IL-1β content in a depot specific manner. This depot specific response, when repeated, may lead to a maladaptive shift in the milieu of inflammatory proteins found within subcutaneous adipose tissue such that its ability to properly function becomes impaired. Consequently, circulating lipids are shunted towards to visceral adipose resulting in the development of visceral obesity as marked by a maladaptive shift in body fat distribution or an increase in the ratio of visceral to non-visceral fat mass.