Patients with nonalcoholic fatty liver disease display increased serum resistin levels and decreased adiponectin levels

Jiang, Lingling; Li, Lin; Hong, Xiao-fei; Li, Youming; Zhang, Bing-Ling

doi:10.1097/meg.0b013e328317f4b5

Cited by 34 publications

(30 citation statements)

References 31 publications

(36 reference statements)

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“…However, we did not see decreased serum adiponectin or an increase in other proinflammatory cytokines levels in our study. Resistin has been shown to be elevated in NAFLD subjects and is associated with increased insulin resistance and NF-kB activation (48, 49). Moreover, our novel hepatic transcriptome profiling results implicate activation of the MAPK and NF-kB inflammatory pathways.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D Deficiency Is Associated With Increased Risk of Non-alcoholic Steatohepatitis in Adults With Non-alcoholic Fatty Liver Disease: Possible Role for MAPK and NF-κB?

Nelson

Roth²,

Wilson

et al. 2016

American Journal of Gastroenterology

109

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Objective To determine the relationship of serum vitamin D deficiency to histologic features of NAFLD, and associated demographic, clinical, laboratory, and transcriptomic data in the well characterized NASH CRN cohort. Methods Serum vitamin D 25(OH)D (VD) was quantified by liquid chromatography-tandem mass spectrometry in 190 adults (>18 yrs) with biopsy-proven NAFLD. Subjects were categorized according to their level of VD as either sufficient (>30ng/ml), insufficient (≥20≤30ng/ml), or deficient (VDD; <20 ng/ml). Multivariable logistic regression was used to investigate the association of VDD and the presence of definite nonalcoholic steatohepatitis (NASH) and individual histological features of NAFLD after adjusting for age, sex, race, BMI, ALT, and diabetes status. Hepatic transcriptomic data was compared between VDD and non-VDD subjects. Results VDD was present in 55% of subjects and was independently associated with definitive NASH (OR 3.15, 95% CI 1.62–6.15, p=0.001), increased lobular inflammation (OR=1.98, 95%CI, 1.08–3.61, p=0.026), more ballooning (OR=2.38, 95%CI, 1.32–4.30, p=0.004), and the presence of fibrosis (OR=2.32, 95%CI, 1.13–4.77, p=0.022). There was a significant inverse relationship between lower levels of serum resistin and increased VD level category (p=0.013). The KRT10, SEMA3B, SNORD3C, ARSD, and IGKV4-1 genes were differentially expressed (FDR<0.05) between VDD and non-VDD subjects. Gene ontology and pathway analysis suggest activation of the MAPK and NF-kB pathways in VDD NAFLD subjects. Conclusions VDD is prevalent among U.S. adult NAFLD patients and is independently associated with a definitive diagnosis of NASH and increased histological severity. Novel associations in pro-inflammatory pathways were identified that suggest the mechanism for VDD in the pathogenesis of NASH and support dietary and/or lifestyle modifications to increase vitamin D levels in these patients.

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Section: Discussionmentioning

confidence: 99%

Vitamin D Deficiency Is Associated With Increased Risk of Non-alcoholic Steatohepatitis in Adults With Non-alcoholic Fatty Liver Disease: Possible Role for MAPK and NF-κB?

Nelson

Roth²,

Wilson

et al. 2016

American Journal of Gastroenterology

109

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“…It is accepted that obesity, particularly central obesity is a risk factor strongly associated with NAFLD [17-19]. About half of the literatures support the notion that serum resistin increases are accountable for the obesity and insulin resistance [20-23], while the other half showed the opposite: resistin is downregulated in obese subjects and resistin had no correlation with insulin resistance [8,10,24]. Resistin is primarily secreted by monocytes or macrophages in humans [25-27].…”

Section: Discussionmentioning

confidence: 99%

The relationship between hepatic resistin overexpression and inflammation in patients with nonalcoholic steatohepatitis

et al. 2014

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BackgroundThe relationship between resistin and non-alcoholic steatohepatitis (NASH) is not clear, some studies claimed that serum resistin levels were associated with neither the presence of NASH nor its severity, others declared that serum resistin was related with inflammation and fibrosis in NASH. Our animal study verified that the distribution of resistin in the liver is correlated with inflammation in NASH. However, there is no pertinent study in humans.MethodsThirty patients with NASH, 28 simple steatosis, and 43 controls were recruited. Blood was collected for resistin, liver chemistries, fasting insulin and some metabolic parameters. Liver histology was scored according to NAFLD activity scoring system. Hepatic resistin expression was examined by real-time polymerase chain reaction, immunohistochemistry. Resistin protein expression was confirmed by western blotting in 13 patients with concomitant NAFLD and gallstone.ResultsSerum resistin was significantly elevated in both NASH and simple steatotic subjects compared with controls (all P < 0.05). Hepatic resistin was significantly increased in NASH patients in both mRNA and protein levels than those in simple steatosis and control subjects (all P < 0.05). Both serum and hepatic resistin had a correlation with obesity, but not with insulin resistance. The distribution of resistin positive cells was predominantly in perisinusoidal cells (such as Kupffer cells and hepatic stellate cells) in human NASH. Multivariate analysis revealed that waist-hip ratio, higher serum triglyceride, and hyperresistinemia were independent factors related to higher grade of steatosis; whereas hepatic resistin and serum cytokeratin predict NASH and severity of liver fibrosis.ConclusionsHepatic resistin overexpression in NASH patients is associated with the severity of liver inflammation and fibrosis. Liver-derived resistin may be involved in the pathogenesis of human NASH.

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“…In a second study, visceral adipose tissue expression of resistin was unchanged but serum levels of the adipocytokine were higher in patients with NASH [147]. Increased levels of resistin in NAFLD patients was shown also by other authors [106]. Moreover, among NASH patients, those with advanced fibrosis have been shown to have higher circulating resistin compared to those with less extensive fibrosis [146].…”

Section: Resistinmentioning

confidence: 53%

“…Numerous studies showed lower serum adiponectin concentrations in NAFLD patients when compared to matched controls [102][103][104][105][106] but the correlation between plasma levels of the adipocytokine and the severity of liver damage is still controversial. In one report, plasma adiponectin negatively correlated with steatosis and necroinflammation but not with the severity of fibrosis, which was predicted only by insulin resistance [102].…”

Section: Adiponectin: Clinical Correlationmentioning

confidence: 99%

Role of Adipocytokines in Hepatic Fibrosis

Bertolani¹,

Marra²

2010

CPD

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Hepatic fibrosis is a dynamic process whereby the liver responds to conditions of persistent damage. This leads to deposition of fibrillar extracellular matrix, altered hepatocyte regeneration, deranged microvascular architecture and cirrhosis. Accumulating data demonstrate that obesity and insulin resistance are associated with a more severe and faster progression of the fibrogenic process indifferent chronic liver diseases, and attention has focused on possible links between the adipose tissue and liver repair.ADIPOCYTOKINEs are cytokines secreted primarily by adipose tissue, they are relevant for adipose tissue physiology and metabolism.Alterations in the adipocytokine pattern are involved in different obesity-related diseases, such as hypertension, atherosclerosis and type II diabetes mellitus (T2DM).Numerous recent studies have analyzed the role played by adipocytokines in the process of hepatic 'wound healing' and fibrogenesis. In particular, data have accumulated on the role of adiponectin and leptin. This review summarizes the more significant and recent findings concerning the role played by different adipocytokines in hepatic fibrogenesis, discussing the actions of adipocytokines on the biology of liver cells, and their effects in different animal models. The variations in the circulating levels and intrahepatic expression of different adipocytokines in patients with fibrogenic liver diseases are also discussed.

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Patients with nonalcoholic fatty liver disease display increased serum resistin levels and decreased adiponectin levels

Cited by 34 publications

References 31 publications

Vitamin D Deficiency Is Associated With Increased Risk of Non-alcoholic Steatohepatitis in Adults With Non-alcoholic Fatty Liver Disease: Possible Role for MAPK and NF-κB?

Vitamin D Deficiency Is Associated With Increased Risk of Non-alcoholic Steatohepatitis in Adults With Non-alcoholic Fatty Liver Disease: Possible Role for MAPK and NF-κB?

The relationship between hepatic resistin overexpression and inflammation in patients with nonalcoholic steatohepatitis

Role of Adipocytokines in Hepatic Fibrosis

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