![]() IL-6 signaling involves activation of either a membrane-bound receptor (classical) or formation of a signaling complex with a soluble (s)IL-6 receptor found in circulation (trans-signaling). Interleukin-6 (IL-6) is an inflammatory cytokine closely associated with metabolic disease ( 5, 6), has both pro- and anti-inflammatory properties, and may play a role in the progression of NAFLD to NASH ( 7, 8). Liver inflammation plays a key role in the transition of simple steatosis to steatohepatitis. ![]() These data suggest that hyperglycemia and hyperlipidemia can directly impact IL-6 trans-signaling and that this may be linked to enhanced severity of NAFLD in patients with concomitant diabetes. Monocyte activation was associated with reduced sIL-6R secretion. Plasma sgp130 strongly correlated with liver stiffness and was significantly increased in subjects with F4 fibrosis stage. In line with this, plasma sgp130 in both patient cohorts positively correlated with HbA 1c, and subjects with diabetes had higher circulating levels of IL-6 and trans-signaling coreceptors. We found that exposure of stellate cells to high glucose and palmitate increased IL-6 and soluble gp130 (sgp130) secretion. Associations with liver pathology were investigated in two patient cohorts: 1) biopsy-confirmed steatohepatitis and 2) class 3 obesity. ![]() ![]() Secretion patterns were investigated with use of human hepatocyte, stellate, and monocyte cell lines. We investigated whether secretion of IL-6 trans-signaling coreceptors are altered in NAFLD by diabetes and whether this might associate with the severity of fatty liver disease. Interleukin-6 (IL-6) is involved in both diseases, interacting with both membrane-bound (classical) and circulating (trans-signaling) soluble receptors. Many people living with diabetes also have nonalcoholic fatty liver disease (NAFLD). ![]()
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