Visceral abdominal fat accumulation predicts the conversion of metabolically healthy obese subjects to an unhealthy phenotype.
BACKGROUND
A proportion of obese subjects appear metabolically healthy (MHO) but little is known about the natural history of MHO and factors predicting its future conversion to metabolically unhealthy obese (MUO).


OBJECTIVE
The aim was to determine prospectively the frequency of conversion of MHO to MUO and the clinical variables that independently predicted this conversion, with a particular focus on the role of body composition.


METHODS
We identified 85 Japanese Americans with MHO (56 men, 29 women), aged 34-73 years (mean age 49.8 years) who were followed at 2.5, 5 and 10 years after enrollment with measurements of metabolic characteristics, lifestyle and abdominal and thigh fat areas measured by computed tomography. Obesity was defined using the Asian body mass index criterion of ⩾25 kg m(-2). Metabolically healthy was defined as the presence of ⩽2 of 5 metabolic syndrome components proposed by the National Cholesterol Education Program Adult Treatment Panel III, while metabolically unhealthy was defined as ⩾3 components.


RESULTS
Over 10 years of follow-up, 55 MHO individuals (64.7%) converted to MUO. Statistically significant univariate predictors of conversion included dyslipidemia, greater insulin resistance and greater visceral abdominal (VAT) and subcutaneous abdominal fat area (SAT). In multivariate analysis, VAT (odds ratio per 1-s.d. increment (95% confidence interval) 2.04 (1.11-3.72), P=0.021), high-density lipoprotein (HDL) cholesterol (0.24 (0.11-0.53), P<0.001), fasting plasma insulin (2.45 (1.07-5.62), P=0.034) and female sex (5.37 (1.14-25.27), P=0.033) were significantly associated with future conversion to MUO. However, SAT was not an independent predictor for future conversion to MUO.


CONCLUSIONS
In this population, MHO was a transient state, with nearly two-thirds developing MUO over 10 years, with higher conversion to MUO independently associated with VAT, female sex, higher fasting insulin level and lower baseline HDL cholesterol level.
Seattle Epidemiologic Research and Information Center, VA Puget Sound Health Care System, Seattle, WA, USA.|Division of Endocrinology and Metabolism, Department of Medicine, Kyung Hee University School of Medicine, Kyung Hee University Hospital at Gangdong, Seoul, Korea.
Y-C
YC
Hwang
Department of Preventive Medicine and Environmental Health, Graduate School of Medicine, Osaka City University, Osaka, Japan.
T
T
Hayashi
Department of Medicine, University of Washington School of Medicine, Seattle, WA, USA.
W Y
WY
Fujimoto
Department of Medicine, University of Washington School of Medicine, Seattle, WA, USA.|Hospital and Specialty Medicine Service, VA Puget Sound Health Care System, Seattle, WA, USA.
S E
SE
Kahn
Department of Anthropology, University of Washington, Seattle, WA, USA.
D L
DL
Leonetti
Department of Medicine, University of Washington School of Medicine, Seattle, WA, USA.
M J
MJ
McNeely
Seattle Epidemiologic Research and Information Center, VA Puget Sound Health Care System, Seattle, WA, USA.|Department of Medicine, University of Washington School of Medicine, Seattle, WA, USA.
E J
EJ
Boyko
D050154:Adiposity; D000328:Adult; D000368:Aged; D001213:Asian / Q000706:statistics & numerical data*; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition; D015992:Body Mass Index; D008076:Cholesterol, HDL / Q000097:blood; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D050152:Intra-Abdominal Fat / Q000378:metabolism*; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000453:epidemiology* / Q000378:metabolism*; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism*; D010641:Phenotype; D011446:Prospective Studies; D014481:United States / Q000453:epidemiology
D001786:Blood Glucose; D008076:Cholesterol, HDL; D008077:Lipoproteins, LDL