Soluble CD163 correlates with lipid metabolic adaptations in human type 1 diabetes patients during ketoacidosis.

Research paper by Mads M Svart, Nikolaj N Rittig, Niels N Møller, Holger J HJ Møller, Henning H Gronbaek

Indexed on: 29 May '18Published on: 29 May '18Published in: Journal of Diabetes Investigation


Diabetic ketoacidosis (DKA) is associated with inflammation and increased lipolysis. The macrophage activation marker soluble CD163 (sCD163) is associated with obesity, non-alcoholic fatty liver disease, and type-2 diabetes. We aimed to investigate whether sCD163 correlates with, key elements of lipolysis in type-1 diabetes (DM1) patients during mild diabetic ketoacidosis. We investigated nine patients with DM1 twice during: (i) euglycaemic control conditions (CTR) and a bolus of saline and (ii) hyperglycaemic ketotic conditions (KET) induced by lipopolysaccharide (LPS) administration combined with insulin deprivation. Blood samples, indirect calorimetry, palmitate tracer, and adipose tissue biopsies were used to investigate lipid metabolism. We observed a significant increase in plasma sCD163 levels following LPS exposure (p<0.001). Concentrations of sCD163 were positively correlated with plasma concentrations of (free fatty acids (FFA), palmitate rate of appearance (R ), and lipid oxidation rates and negatively correlated to the expression of G0/G1 switch 2 gene (G0S2) mRNA content in adipose tissue (p<0.01, all). Further, sCD163 levels correlated positively with plasma peak concentrations of cortisol, glucagon, tumor necrosis factor alfa (TNF-α), interleukin (IL)-6, and IL-10 (p<0.01, all). Data on lipolysis and inflammation has previously been published. Macrophage activation assessed by sCD163 may play an important role in DKA, as it correlates strongly with important components of lipid metabolism including FFA, palmitate, lipid oxidation, G0S2, and proinflammatory cytokines during initial steps of DKA. These results are novel and add important knowledge to the field of DKA. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.