Adipose Tissue Distribution, Inflammation and Its Metabolic Consequences, Including Diabetes and Cardiovascular Disease

Figure 1. Metabolically healthy obesity (MHO) vs. metabolically unhealthy obesity (MUHO). In comparison with lean metabolically healthy subjects, those with MHO have increased adiposity and BMI, but with reduced systemic inflammation and retained insulin sensitivity, thus defining them as not having metabolic syndrome (MetS). MHO subjects have elevated subcutaneous white adipose tissue (WAT) levels, without excessive accumulation of visceral fat. Their adipokine profile is similar to lean subjects, but with increased leptin, resistin, and FGF21, and decreased adiponectin, which limits their risk of developing type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD) in the short term. By contrast, those with MUHO exhibit elevated insulin resistance and systemic inflammation in addition to increased adiposity and BMI over lean controls, contributing to MetS. MUHO individuals have excess subcutaneous and intra-abdominal adipose tissue, with increased hepatic fat and fat distributed amongst other visceral organs. This leads to a dysfunctional adipokine profile, characterized by reduced adiponectin and omentin, with further elevated leptin, resistin, FGF21, and cytokines when compared…

Figure 2. Adipose depots and ectopic fat sites and their features that contribute to type 2 diabetes mellitus (T2DM) or cardiovascular disease (CVD). Features of intra-abdominal white adipose tissue (WAT), subcutaneous fat, hepatic fat, heart and arterial fat (inclusive of epicardial, pericardial, and perivascular fat), pancreatic fat, skeletal muscle fat, brown adipose tissue, and a dysbiotic gut that contribute to either T2DM or CVD. Arrows indicate changes in comparison with subjects without T2DM or CVD. The T2DM treatment strategies that have been reported to improve each adipose depot feature are listed under “treatments.” Treatments: weight loss due to lifestyle changes (L); weight loss due to bariatric surgery (B); metformin (M); GLP-1 receptor agonists (G); SGLT-2 inhibitors (S); thiazolidinediones (TZDs, T); anti-inflammatory approaches (AI); microbiome modulation with pre- or pro-biotics (P).