Key result
Adipose tissue inflammation linked to obesity complications including insulin resistance and T2D.
Why the study?
Chronic low-grade adipose tissue inflammation impairs insulin signaling and increases the risk of insulin resistance and type 2 diabetes, warranting an updated clinical perspective on obesity-associated complications in humans.
This review highlights the systemic nature of adipose tissue inflammation in obesity and its role in impairing insulin signaling and increasing the risk of type 2 diabetes.
Answers are grounded in this paper and cite their sources.
Adipose inflammation links obesity to metabolic risk; leaves open whether targeting it improves clinical outcomes.
Obesity is characterized by a state of chronic low-grade inflammation due to increased immune cells, specifically infiltrated macrophages into adipose tissue, which in turn secrete a range of proinflammatory mediators. This nonselective low-grade inflammation of adipose tissue is systemic in nature and can impair insulin signaling pathways, thus, increasing the risk of developing insulin resistance and type 2 diabetes. The aim of this review is to provide an update on clinical studies examining the role of adipose tissue in the development of obesity-associated complications in humans. We will discuss adipose tissue inflammation during different scenarios of energy imbalance and metabolic dysfunction including obesity and overfeeding, weight loss by calorie restriction or bariatric surgery, and conditions of insulin resistance (diabetes, polycystic ovarian syndrome).
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Tam et al. (2013) conducted a review in Obesity and metabolic dysfunction. Adipose tissue inflammation was evaluated. This review discusses the role of adipose tissue inflammation in the development of obesity-associated complications, including insulin resistance and type 2 diabetes, across various clinical scenarios.
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