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Abstract
Background: Recent pieces of research point to a link between basal metabolic rate (BMR) and non-alcoholic fatty liver disease (NAFLD) or hepatic steatosis (HS). The spleen in obese patients is associated with the cardiovascular system. Enlargement of the spleen is suggestive of nonalcoholic steatohepatitis (NASH). Patients with NASH present an increase in growth factor (HGF) as well as those with advanced heart failure. Interleukin-16 and interleukin-12p40 levels were found to correlate significantly with BMI, and waist circumference. Aim: We tried to find a relationship between BMR, spleen length and HGF. Methods: We analysed retrospective data from 80 obese patients with NAFLD. We evaluated indices of indirect calorimetry by the bioimpendance analysis; carotid intima-media thickness (IMT), spleen length (SLD) and HS by ultrasonography; serum HGF, IL-16, IL-12p40 and IL-6 concentrations by a magnetic bead-based multiplex immunoassays and the severity of NAFLD by BARD score > 2. Results: HGF levels of the obese were higher than those of controls, p < 0.001. At linear regression, BMR was foreseen by spleen length (p < 0.001), which was predicted by HGF (p = 0.04). BMR was predicted by IL-16 (p = 0.005), which predicted HGF, p = 0.034. Only fat mass, among other factors, predicted early atherosclerosis, p = 0.017; IL-12p40 did not predict IMT, HGF and BMR (p = 0.57, 0.09 and 0.59, respectively). The BARD score > 2 was negatively predicted by BMR and FFM (p =0.032 and 0.031, respectively), at the logistic regression. Interesting findings at the extended regression (mediation effect) were: IL-16 was likely causal in predicting BMR by HGF levels; HGF was influential in predicting BMR by SLD level. HS was predicted by SLD in males (p = 0.014), of advanced age (p < 0.001) and by BMR (p < 0.001). IL-6 concentrations, but not BMR were influential in the prediction of HS by SLD. Conclusion: These data reinforce the concept that the immune system is a sensor of the metabolic state, showing a link between HGF levels and BMR, which is mediated by IL-16 (cytokine inducing a cascade of inflammatory factors), and ascertaining the influential effect of the spleen, as main immune organ.
Highlights
There is a wide consensus about the immune system as a sensor of the metabolic state [1]
In this context, increased basal metabolic rate (BMR) may be a clue of metabolic syndrome (MS) when dealing with hepatic steatosis (HS) or nonalcoholic fatty liver disease (NAFLD) patients [6]
The core findings of this research could be summarised in: (j) Hepatic growth factor (HGF) levels of the obese were higher than those of controls; BMR was foreseen by spleen length, which in turn was predicted by HGF; BMR was predicted by IL-16, which predicted HGF; fat mass (FM) predicted early atherosclerosis; IL-12p40 did not predict intima-media thickness (IMT), HGF and BMR
Summary
There is a wide consensus about the immune system as a sensor of the metabolic state [1]. RMR has been substituted by the more precise basal metabolic rate (BMR), which depends on body composition as expressed by fat-free mass (FFM) and fat mass (FM) [4,5] In this context, increased BMR may be a clue of MS when dealing with hepatic steatosis (HS) or nonalcoholic fatty liver disease (NAFLD) patients [6]. Conclusion: These data reinforce the concept that the immune system is a sensor of the metabolic state, showing a link between HGF levels and BMR, which is mediated by IL-16 (cytokine inducing a cascade of inflammatory factors), and ascertaining the influential effect of the spleen, as main immune organ
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