Abstract
Adipose tissue plays essential roles in maintaining lipid and glucose homeostasis. To date several types of adipose tissue have been identified, namely white, brown, and beige, that reside in various specific anatomical locations throughout the body. The cellular composition, secretome, and location of these adipose depots define their function in health and metabolic disease. In obesity, adipose tissue becomes dysfunctional, promoting a pro-inflammatory, hyperlipidemic and insulin resistant environment that contributes to type 2 diabetes mellitus (T2DM). Concurrently, similar features that result from adipose tissue dysfunction also promote cardiovascular disease (CVD) by mechanisms that can be augmented by T2DM. The mechanisms by which dysfunctional adipose tissue simultaneously promote T2DM and CVD, focusing on adipose tissue depot-specific adipokines, inflammatory profiles, and metabolism, will be the focus of this review. The impact that various T2DM and CVD treatment strategies have on adipose tissue function and body weight also will be discussed.
Highlights
Obesity has reached epidemic proportions, with over 60% of the US population classified as overweight or obese [1]
Visceral adiposity is associated with insulin resistance, a predisposition to diabetes, local and systemic inflammation, dyslipidemia [characterized by hypertriglyceridemia, a preponderance of small, dense low-density lipoprotein (LDL) particles and reduced high-density lipoprotein (HDL)cholesterol levels], insulin resistance, dysglycemia [a broad term that refers to an abnormality in blood sugar stability], adipose tissue and systemic inflammation, hypertension, a thrombogenic profile and non-alcoholic fatty liver disease (NAFLD) [194]
Abundant evidence indicates that adiposity and adipose tissue inflammation are associated with insulin resistance, which refers to a reduced response to binding of insulin to its receptor in peripheral tissues such as adipose tissue and skeletal muscle
Summary
Obesity has reached epidemic proportions, with over 60% of the US population classified as overweight or obese (defined by a body mass index ≥ 25 or 30 kg/m2, respectively) [1]. While much recent research has aimed to delineate the precise cause(s) of obesity-associated T2DM, the primary mechanism is believed to be insulin resistance that derives from white adipose tissue, liver, and/or skeletal muscle, accompanied by impaired insulin secretion by pancreatic βcells [6]. Both obesity and T2DM increase the risk of cardiovascular disease (CVD), increasing morbidity and mortality by greater than 2-fold [7,8,9,10]. The complex and interrelated associations between obesity, diabetes, and CVD will be explored in greater detail
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