Abstract

The difference between metabolically healthy obesity (MHO) and metabolically unhealthy obesity (MUO) phenotypes might be partly attributable to genetic traits modulating body fat distribution and other obesity-related metabolic traits, specifically with regard to LEPR rs8179183 in Korean women with obesity. A total of 177 females with obesity participated in the study and were grouped by genotype (GC or GG) and metabolic health status (MHO and MUO). Between the MHO and MUO groups, significant differences were found in waist circumference, waist-to-hip ratio, lipid profiles, glucose-related markers, biomarkers of liver health, adiponectin, oxidative stress markers, whole fat area (WFA), and subcutaneous fat area (SFA) at the level of the L1 vertebra, and WFA and visceral fat area (VFA) at the level of the L4 vertebra. Lipid profiles, glucose-related markers, adipokines, oxidative stress markers, and WFA and VFA at the L4 level were significantly different between the GC and GG genotypes. Notably, the individuals with the MUO phenotype and the GG genotype had the least favorable values of glucose-related markers, lipid profiles, adipokines, oxidative stress markers, and regional fat distribution. These observations suggest that the development of obesity-related metabolic traits is highly associated not only with the rs8179183 genotype but also with metabolic status in Korean females with obesity.

Highlights

  • Obesity-related disease complications reduce life quality and expectancy and increase health-care costs

  • Genome-wide association studies have identified a set of loci harboring genes possibly controlling both the distribution of extra body fat and the metabolic profile associated with excess adiposity (i.e., metabolically healthy obesity (MHO) or metabolically unhealthy obesity (MUO))

  • Through DEXA and CT measurements, we found that whole fat area (WFA) and subcutaneous fat area (SFA) at the L1 level and WFA and visceral fat area (VFA) at the L4 level were significantly increased in the MUO group

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Summary

Introduction

Obesity-related disease complications reduce life quality and expectancy and increase health-care costs. Some studies have suggested that obesity does not always accompany metabolic abnormalities and an increased risk of cardiometabolic complications. Because of the lack of generally accepted criteria to identify metabolically healthy obesity (MHO), its prevalence varies widely among studies. The prognostic value of MHO is hotly debated, because it tends to shift progressively toward metabolically unhealthy obesity (MUO) [1]. Genome-wide association studies have identified a set of loci harboring genes possibly controlling both the distribution of extra body fat and the metabolic profile associated with excess adiposity (i.e., MHO or MUO). Ten more genetic variants have been associated with a reduced

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