Erythrocyte sodium-lithium countertransport activity is inversely correlated to adiponectin, retinol binding protein 4 and body height

Abstract

Background. We have previously described that the sodium/lithium countertransport (SLC) in the erythrocyte cell membrane is closely linked to obesity and insulin resistance. Adiponectin and retinol-binding protein 4 (RBP-4) are believed to affect obesity and insulin resistance. In the present study, we aimed to further characterize the relationship between SLC, inflammatory markers, adiponectin and RBP-4. Methods. We included 93 clinically healthy 58-year-old men selected to display variations in insulin sensitivity. High sensitivity C-reactive protein (hs-CRP), TNF-alpha, soluble TNF-alpha-receptors (sTNFR) 1 and 2, IL-6 and RBP-4 were measured using antibody-based techniques. Adiponectin was determined by a radioimmunoassay kit. The lithium concentration in the special flux medium was measured by atomic absorption spectrophotometry. Results. In univariate analyses, SLC correlated negatively with RBP-4 (r_s = −0.256, p = −0.017) and to adiponectin (r_s = −0.316, p = 0.003) and positively with TNF-alpha (r_s = 0.346, p = 0.001) and hs-CRP (r_s = 0.288, p = 0.005). There were no statistically significant correlations with sTNFR 1 or 2 or IL-6. SLC was negatively associated to body height (r_s = −0.256, p = 0.013). Conclusions. We are the first to report that SLC correlates negatively with adiponectin and RBP-4. This finding is intriguing, as adiponectin is anti-inflammatory and anti-diabetic whereas RBP-4 supposedly decreases insulin sensitivity. We also observed a negative association between SLC activity and body height indicating that SLC activity is not primarily influenced by fat mass. The positive association of SLC with markers of inflammatory activity such as TNF-alpha and hs-CRP is in line with the proposed link between inflammation and insulin resistance.

Key Words::

• Sodium-lithium countertransport
• inflammation
• TNF
• RBP-4
• adiponectin
• obesity
• height

Acknowledgements

This work was supported by grants from the Swedish Foundation for Strategic Research, the Swedish Heart-Lung Foundation, The Swedish Medical Research Council (12270, 10880) and AstraZeneca, Mölndal, Sweden. We thank Project Assistant Marie-Louise Ekholm and laboratory technologist Carita Fagerlund for excellent research assistance.

Declaration of interest: The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.