Westside PUFAs
Member
- Joined
- Feb 4, 2015
- Messages
- 1,972
"Numerous other inflammatory mediators are produced and potentially secreted into the circulation by adipose tissue (Table 2). Among these, adiponectin (81), resistin (20), acylation-stimulating protein (82), and components of the renin-angiotensin system (83) may be the most important in contributing to chronic inflammation, insulin resistance, and cardiovascular disease risk."
"Chronic inflammation is a common feature of the metabolic syndrome, and inflammatory signals may originate within visceral adipose tissue as this fat depot expands in response to chronic positive energy balance. Both adipocytes and macrophages within fat secrete numerous hormones and cytokines that may contribute to the characteristic pathophysiologic changes seen in the metabolic syndrome, and local inflammation within adipose tissue may be the sentinel event that causes systemic insulin resistance and systemic inflammation, two of the cardinal features of the metabolic syndrome. The inciting event that causes adipose tissue to become inflamed as it expands remains unknown but will likely have a significant genetic component potentially accounting for some of the variance in metabolic risk between equivalently obese individuals. The contribution of individual cytokines in causing the pathophysiologic features of the metabolic syndrome remains controversial; however; that the metabolic alterations triggered by acute inflammation mimic the metabolic syndrome in many ways suggests that circulating cytokines, whether they are derived from adipose tissue or peripheral blood immune cells, may have similar metabolic effects on muscle, liver, and endothelium while potentially having differential effects on immune function. In addition, adipose tissue-derived cytokines, such as IL-6 and leptin, may also participate directly in endothelial cell activation and inflammation in the vascular bed, both changes that could contribute to the progression of atherosclerosis. Recognition of the interaction between adipocytes and macrophages within fat exposes a new paradigm whereby adipocyte-derived factors modulate local immune responses and macrophage-derived cytokines alter adipocyte differentiation and metabolic responses. As future studies continue to provide new information regarding links between inflammation and metabolism, the potential to identify new therapeutic options for the treatment of the metabolic syndrome remains high, encouraging the global effort to reduce the morbidity associated with this highly prevalent disease."
http://jasn.asnjournals.org/content/15/11/2792.full#ref
"Chronic inflammation is a common feature of the metabolic syndrome, and inflammatory signals may originate within visceral adipose tissue as this fat depot expands in response to chronic positive energy balance. Both adipocytes and macrophages within fat secrete numerous hormones and cytokines that may contribute to the characteristic pathophysiologic changes seen in the metabolic syndrome, and local inflammation within adipose tissue may be the sentinel event that causes systemic insulin resistance and systemic inflammation, two of the cardinal features of the metabolic syndrome. The inciting event that causes adipose tissue to become inflamed as it expands remains unknown but will likely have a significant genetic component potentially accounting for some of the variance in metabolic risk between equivalently obese individuals. The contribution of individual cytokines in causing the pathophysiologic features of the metabolic syndrome remains controversial; however; that the metabolic alterations triggered by acute inflammation mimic the metabolic syndrome in many ways suggests that circulating cytokines, whether they are derived from adipose tissue or peripheral blood immune cells, may have similar metabolic effects on muscle, liver, and endothelium while potentially having differential effects on immune function. In addition, adipose tissue-derived cytokines, such as IL-6 and leptin, may also participate directly in endothelial cell activation and inflammation in the vascular bed, both changes that could contribute to the progression of atherosclerosis. Recognition of the interaction between adipocytes and macrophages within fat exposes a new paradigm whereby adipocyte-derived factors modulate local immune responses and macrophage-derived cytokines alter adipocyte differentiation and metabolic responses. As future studies continue to provide new information regarding links between inflammation and metabolism, the potential to identify new therapeutic options for the treatment of the metabolic syndrome remains high, encouraging the global effort to reduce the morbidity associated with this highly prevalent disease."
http://jasn.asnjournals.org/content/15/11/2792.full#ref
