Abstract
One of the pathologic hallmarks of obesity is macrophage infiltration of adipose tissue that has been confirmed as source of multipotent adult stem cells. Stem cell growth factor-beta (SCGF-β) shows activity on granulocyte/macrophage progenitor cells in combination with granulocyte macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF). Obesity-associated inflammation induces insulin resistance (IR), which is central to nonalcoholic fatty liver disease (NAFLD) or hepatic steatosis (HS). We searched for relationship between levels of SCGF-β and those of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-β (TNF-β), interleukin-12p40 (IL-12p40), interleukin-10 (IL-10), ferritin, GM-CSF and M-CSF and between SCGF-β concentrations and IR in obese patients with HS. Eighty obese patients were retrospectively studied. Serum cytokines levels were appreciated by magnetic bead-based multiplex immunoassays. IR was evaluated by homeostatic model assessment (HOMA), HOMA-derived β-cell function (HOMA-B%), quantitative insulin sensitivity check Index (QUICKI) and single point insulin sensitivity estimator (SPISE). HS and spleen volume were assessed by ultrasonography (US). SCGF-β and IL-6 levels predicted HOMA values (p = 0.032 and 0.041, respectively) only in males. In male patients, CRP and IL-6 levels (p = 0.007) predicted SCGF-β concentrations (p = 0.03 and 0.007, respectively), which in turn predicted HS at US, p = 0.037. SCGF-β levels were linked to IR and HS severity with the mediation role of CRP. IL-10 levels negatively predicted SCGF-β concentrations (p = 0.033). M-CSF levels predicted serum concentration of both TNF-β and IL-12p40 (p = 0.00), but did not predict serum IL-10 (p = 0.30). Prediction of HOMA values by SCGF-β levels, likely mediated by markers of inflammation, characterizes this study, shedding some light on mechanisms inducing/worsening IR of male patients with obesity-related NAFLD.
Highlights
Macrophages are key mediators of obesity-induced insulin resistance (IR)
We aimed at finding associations between SCGF-β levels and some molecules promoting or suppressing inflammatory responses in obese patients suffering from nonalcoholic fatty liver disease (NAFLD) or hepatic steatosis (HS)
IR may depend on excessive fat volume, while inflammation may depend on local secretion of inflammatory molecules [22,24]
Summary
Macrophages are key mediators of obesity-induced insulin resistance (IR). This phenomenon is due to direct and paracrine signals from M1 classically-activated-macrophages while M2 alternatively-activated-macrophages fail to generate these effects [1,2,3]. Several studies emphasize the role of C-reactive protein (CRP) in promoting differentiation toward a pro-inflammatory M1 phenotype [4]. In this sense, chronic low-grade inflammation is revealed by high levels of serum. Little is known about the possible role played by SCGF-β in the metabolic derangement of obesity and its complications. With this in mind, we aimed at finding associations between SCGF-β levels and some molecules promoting or suppressing inflammatory responses in obese patients suffering from NAFLD or hepatic steatosis (HS).
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