Intermuscular adipose tissue is associated with monocyte chemoattractant protein-1, independent of visceral adipose tissue.

OBJECTIVES: Emerging evidence suggests that intermuscular adipose tissue is a risk factor for insulin resistance, but the underlying mechanism still remains unclear. We investigated whether the levels of leptin, adiponectin, and monocyte chemoattractant protein-1 are associated with intermuscular adipose tissue in obese subjects. DESIGN AND METHODS: A cross-sectional study was performed on 77 obese Korean women. Areas of visceral adipose tissue, subcutaneous adipose tissue, and intermuscular adipose tissue were measured by computed tomography scan, and serum concentrations of adipokines were measured by enzyme-linked immunosorbent assays. Correlation between the levels of adipokines and the fat areas was assessed using Pearson correlation and covariate-adjusted multivariable regression. RESULTS: Leptin was positively correlated with subcutaneous adipose tissue (r=0.452, P<0.001), fasting insulin (r=0.403, P<0.001), and homeostasis model assessment of insulin resistance (r=0.360, P=0.001), whereas monocyte chemoattractant protein-1 was positively correlated with intermuscular adipose tissue (r=0.483, P<0.001). After adjustment for age, height, and other body composition metrics, leptin was still related to subcutaneous adipose tissue (ß=0.390, P=0.001). Monocyte chemoattractant protein-1 was associated with intermuscular adipose tissue (ß=0.433, P=0.001) after adjustment for visceral adipose tissue. CONCLUSIONS: Intermuscular adipose tissue was correlated with monocyte chemoattractant protein-1, suggesting its role in the development of insulin resistance.

Prediction of prevalent but not incident non-alcoholic fatty liver disease by levels of serum testosterone.

BACKGROUND AND AIMS: The association between testosterone level and development of non-alcoholic fatty liver disease (NAFLD) is not well known. We examined the relationship of total testosterone level with development and regression of NAFLD. METHODS: Among the men who had undergone repeated liver ultrasonography in 2 years or more at a health promotion center, subjects with available serum testosterone level at baseline were included in the study. Alcohol consumers (> 20 g/day) were excluded from the study. RESULTS: Among the 1944 men, 44.3% of subjects were diagnosed with NAFLD. Higher level of testosterone significantly lowered the prevalence of fatty liver (odds ratios per SD increase, 0.686 and 0.795 at baseline and follow-up, respectively). During the median 4.2 years follow-up, 22.4% of subjects in the normal group developed fatty liver, and 21.0% of subjects in the NAFLD group recovered at the follow-up. In longitudinal analyses, higher level of testosterone was significantly associated with the development or regression of fatty liver, before adjustment for obesity and metabolic parameters. However, in the full-adjusted model, testosterone level did not influence the development or regression of fatty liver. CONCLUSIONS: Although testosterone level was significantly low in the subjects with NAFLD in cross-sectional analyses, baseline testosterone level did not independently influence the development or regression of fatty liver at the median 4.2 years follow-up. Obesity and metabolic parameters may play key roles in the link between testosterone level and NAFLD.