Adipose tissue remodeling (adipocyte proliferation, triglyceride (TG) turnover, and flux of extracellular matrix proteins) is a dynamic process that helps maintain adipose tissue health and metabolic function. We hypothesized that adipose tissue remodeling would be decreased in people with metabolically unhealthy obesity (MUO), defined as having prediabetes and nonalcoholic fatty liver disease, compared to those who are metabolically healthy and normal weight (MHNW).


The incorporation of deuterium in DNA, glycerol, and collagen was assessed in subcutaneous abdominal adipose tissue biopsy samples obtained in 11 MHNW and 20 MUO participants after they ingested deuterated water (D2O) daily for 3-5 wks to assess rates of adipocyte proliferation and adipose tissue TG, collagen 1a1 (COL1a1) and collagen 1a2 (COL1a2) synthesis.


Compared with the MHNW group, all markers of adipose tissue remodeling were greater in people with MUO: i) adipocyte proliferation rate: 2.2±0.2 %/wk vs. 1.0±0.2 %/wk, P=0.002); ii) adipose tissue TG synthesis rate: 77.7±7.4 cm3/week vs. 18.9±3.1 cm3/week, P<0.001); and iii) adipose tissue COL1a1 (6.8±0.4 %/wk vs. 4.8±0.4 %/wk) and COL1a2 rates (5.1±0.3 %/wk vs. 3.8±0.4 %/wk) synthesis rates (both P<0.05 vs. MHNW).


In contrast with our hypothesis, people with MUO have evidence of markedly increased adipose tissue remodeling compared with those who are MHNW. Our study is unable to determine whether increased adipose tissue remodeling is an adaptive response to, or a cause of, metabolic dysfunction in people with MUO.