Effects of lifestyle intervention on soluble CD163, a macrophage activation marker, in patients with non-alcoholic fatty liver disease

Abstract

Objective: Liver macrophages play an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Soluble CD163 (sCD163), a macrophage-specific biomarker, reflects disease activity in the range of liver diseases. The impact of lifestyle intervention on sCD163 in adult NAFLD patients has not been investigated.

Material and methods: We assessed 126 NAFLD patients participating in a lifestyle intervention study for sCD163 concentrations at baseline, after the three-month intervention period, and at long-term follow-up after 12 and 24 months.

Results: The median sCD163 concentration at baseline was 2.59 mg/L (IQR = 1.78–3.63 mg/L). There was a significant decrease in sCD163 from baseline to three months follow-up (−0.64 mg/L, p < .001) with no difference between the four study groups (p = .6). At 12 and 24 months follow-up, the sCD163 concentrations had returned to baseline level (p = .3 and p = .1). Baseline sCD163 correlated with liver biomarkers and metabolic variables. There was a significantly greater decrease in sCD163 in patients who had a decrease in alanine aminotransferase (ALT) compared with patients with unchanged or increased ALT (−0.76 mg/L vs. −0.41 mg/L, p = .02), and in patients with a decrease in HOMA-IR compared with individuals with no decrease (−0.86 mg/L vs. −0.55 mg/L, p = .03).

Conclusion: sCD163 is associated with markers of liver necro-inflammation and glucose homoeostasis in NAFLD. Participation in a lifestyle intervention programme resulted in a significant reduction in sCD163. Our data support the utility of sCD163 as a biomarker for monitoring the efficacy of therapeutic interventions in NAFLD.

Keywords:

• Macrophages
• non-alcoholic fatty liver disease
• obesity
• exercise
• CD163
• weight loss

Acknowledgments

We would like to thank all the patients for their participation in this study. We thank laboratory technician Kirsten Bank Petersen for excellent technical assistance.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

Jacob George is supported by the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney; a National Health and Medical Research Council of Australia (NHMRC) Programme Grant (1053206) and Project grants (APP1107178 and APP1108422) and the Danish Council for Strategic Research Funding (TRAIN 10-092797).