MHO or MUO? White adipose tissue remodeling

Abstract

SummaryIn this review, we delve into the intricate relationship between white adipose tissue (WAT) remodeling and metabolic aspects in obesity, with a specific focus on individuals with metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO). WAT is a highly heterogeneous, plastic, and dynamically secreting endocrine and immune organ. WAT remodeling plays a crucial role in metabolic health, involving expansion mode, microenvironment, phenotype, and distribution. In individuals with MHO, WAT remodeling is beneficial, reducing ectopic fat deposition and insulin resistance (IR) through mechanisms like increased adipocyte hyperplasia, anti‐inflammatory microenvironment, appropriate extracellular matrix (ECM) remodeling, appropriate vascularization, enhanced WAT browning, and subcutaneous adipose tissue (SWAT) deposition. Conversely, for those with MUO, WAT remodeling leads to ectopic fat deposition and IR, causing metabolic dysregulation. This process involves adipocyte hypertrophy, disrupted vascularization, heightened pro‐inflammatory microenvironment, enhanced brown adipose tissue (BAT) whitening, and accumulation of visceral adipose tissue (VWAT) deposition. The review underscores the pivotal importance of intervening in WAT remodeling to hinder the transition from MHO to MUO. This insight is valuable for tailoring personalized and effective management strategies for patients with obesity in clinical practice.

Adipocyte‐specific FAK deletion promotes pancreatic β‐cell apoptosis via adipose inflammatory response to exacerbate diabetes mellitus

“… 22 Adipose tissue metabolism disorders have effects on glycolipid metabolism, cytokine and adipokine secretion. 23 Disorders of glycolipid metabolism and abnormal secretion of lipokines induce systemic inflammation, suggesting that inflammatory cytokines of WAT may be an important regulator for metabolic diseases. It is reported that inflammatory cytokines exacerbate diabetes mellitus by disrupting pancreatic β‐cell survival.…”

Impaired Remodeling of White Adipose Tissue in Obesity and Aging: From Defective Adipogenesis to Adipose Organ Dysfunction

“…Adipocyte size varies according to several factors, including sex and fat depot (lower in vWAT than in sWAT in women, but not in It is worth noting that the adipogenic capacity of sWAT is not only limited but also extremely variable among individuals, as shown by the existence of persons with obesity either with or without insulin resistance and components of the metabolic syndrome, including impaired glucose regulation, atherogenic dyslipidemia, and hypertension, despite the same body mass index (BMI). In addition to these two obese phenotypes, which are called metabolic unhealthy obese (MUO) and metabolic healthy obese (MHO), respectively [17,18], there are also lean phenotypes characterized by the presence or absence of metabolic derangement, i.e., the metabolic unhealthy normal weight (MUNW), also called metabolically obese normal weight [MONW], and the metabolic healthy normal weight (MHNW), respectively [19]. This indicates that it is not just a matter of absolute quantity of fat and shifts the focus on sWAT dysfunction and remodeling of fat depots, which is dependent on the individual capacity to expand and accommodate the surplus of energy [20].…”