We aimed to investigate the relationship of total adiponectin, high-molecular-weight (HMW) adiponectin, and leptin with the development and improvement of non-alcoholic fatty liver (NAFL) independent of sex and weight change over a maximum of 8.5 years.
<b>Methods:</b> A total of 203 children and adolescents aged 5-18 years were enrolled, and their anthropometric data, body composition, liver ultrasound score for NAFLD (range, 0-6), biochemical test results, and FGF-21, leptin, and adiponectin levels were analyzed.
The present review will discuss the modulation of bodily processes by the circadian rhythm with specific attention to the regulation of NAFLD by leptin and related hormones.<b>Areas covered</b>: PubMed/MEDLINE was searched for articles related to concomitant occurrence of NAFLD and T2DM between January 1995 and September 2019.
Low vitamin D level was associated with metabolic syndrome and high leptin level in subjects with nonalcoholic fatty liver disease: a community-based study.
Leptin is a vital biomarker of non-alcoholic fatty liver (NAFLD), and its evaluation of the concentration level in vivo is of great significance to NAFLD diagnosis.
Cases with NAFLD were more obese (BMI 31.0 ± 4.4 vs. 24.1 ± 2.8 kg/m, P < 0.001) and had significantly increased levels of sCD14, sCD163 and higher leptin to adiponectin ratio vs. HIV-positive controls.
The activation of iNOS by leptin is necessary for the synthesis and secretion of TNC in hepatocytes, suggesting an important role of this alarmin in the development of NAFLD.
Some adipokines, such as adiponectin and leptin, have been reported to be involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), while the association of adipsin and visfatin with NAFLD still remains unclear.
Obese people with healthy livers are characterized by intact glucose homoeostasis, lower pro-inflammatory cytokine levels, and higher adiponectin and leptin concentrations compared with obese people with NAFLD.
Serum levels of leptin, macrophage migration inhibitory factor (MIF), interleukin-6 (IL-6), high sensitive C-reactive protein (Hs-CRP), and tumor necrosis factor alpha (TNF-α) were significantly higher, and adiponectin levels were significantly lower in OSA with NAFLD subjects.
Extending the studies, we hypothesized that high circulatory leptin in NAFLD causes renal mesangial cell activation and tubular inflammation via a NOX2 dependent pathway that upregulates proinflammatory miR21.
Leptin-deficient (<i>ob/ob</i>) obese mice with NAFLD were treated with metformin, and signaling pathways were compared with non-metformin treated mice.
Conflicting evidence concerning leptin, an adipocyte-derived hormone, in atherogenesis and non-alcoholic fatty liver disease (NAFLD) has been reported.
Few studies have focused on the effects of a soy containing diet on inflammation and serum leptin level among patients with nonalcoholic fatty liver disease (NAFLD).
Patients with steatosis had higher tumour necrosis factor-α levels and those with NASH or a combination of liver damage types had raised leptin levels after adjustment for age, sex and BMI.We concluded that NAFLD is highly prevalent in COPD and might contribute to cardiometabolic comorbidities.
This study was designed to evaluate the pro-inflammatory and pro-oxidant effects of leptin and linoleic acid on immune cells from patients with NAFLD and to corroborate the modulatory effects of curcumin and its preventive properties against the progression of NAFLD using a high-fat diet (HFD)-induced NAFLD/nonalcoholic steatohepatitis mouse model.