Circulating white blood cell count and measures of adipose tissue inflammation predict higher 24-h energy expenditure

Energy expenditure (EE) and measures of inflammation increase with adiposity, and this obesity-induced chronic and subclinical inflammation was extensively reported to be a cause of insulin resistance. However, whether subclinical inflammation has a role in increasing EE, which may be at the cost of developing insulin resistance, is not clear.

We investigated the association between circulating white blood cell count (WBC) in a population of Native Americans (n=243) with measurement of EE in a respiratory chamber, and in a subset of the same population (n=34), with gene expression measures of inflammation in subcutaneous abdominal adipose tissue (SAAT). All subjects were healthy on oral glucose tolerance test. Statistically, nonnormally distributed variables were logarithmically transformed before analyses to approximate normal distributions.

WBC was associated with 24-h EE adjusted for age, sex, fat-free mass, and fat mass (r=0.13, P=0.04). In SAAT, tumor necrosis factor-alpha (TNF-alpha), shown as log10-transformed TNF-alpha (r=0.36, P=0.05), and plasminogen activator inhibitor-1 (PAI-1), shown as log10-transformed PAI-1 (lPAI-1; r=0.41, P=0.02), expressions were also positively correlated with adjusted 24-h EE. lPAI-1 was also correlated with adjusted sleep EE (r=0.34, P=0.07).

In conclusion, circulating markers of inflammation (WBC) and markers of inflammation within adipose tissue (TNF-alpha and PAI-1) are positively associated with EE, indicating a role of chronic subclinical inflammation in the regulation of metabolic rate.