Nonalcoholic fatty liver disease (NAFLD) without insulin resistance: Is it different?

Singh, Shivaram Prasad; Misra, Bijay; Kar, Sanjib; Panigrahi, Manas; Misra, Debasis; Bhuyan, Pallavi; Pattnaik, Kaumudee; Meher, Chudamani; Agrawal, Omprakash; Rout, Niranjan; Swain, Manorama

doi:10.1016/j.clinre.2014.08.014

Cited by 26 publications

(22 citation statements)

References 29 publications

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“…Understanding the mechanisms by which simple fatty liver develops into NASH is critical. Several risk factors (such as LPS, oxidative stress and inflammatory cytokines) are likely to provide a "second hit", which may contribute to the transformation process from simple steatosis to NASH [4, 5, 17]. Several studies have demonstrated that immune disorders, such as an imbalance of anti-inflammatory cytokines and pro-inflammatory cytokines, are involved in liver inflammation [18, 19].…”

Section: Discussionmentioning

confidence: 99%

“…The mechanisms mediating these liver disorders,from simple liver steatosis to NASH,remain unclear. Lipopolysaccharide (LPS), oxidative stress, cytokines and other pro-inflammatory mediators may be involved in imposing a ‘second hit’ during the transitional process [4, 5]. Hepatic inflammation is one of the most pronounced features of NASH, and hepatic immune responses play critical roles in the pathogenesis of NASH and other progressive diseases [5, 6].…”

Section: Introductionmentioning

confidence: 99%

“…Lipopolysaccharide (LPS), oxidative stress, cytokines and other pro-inflammatory mediators may be involved in imposing a ‘second hit’ during the transitional process [4, 5]. Hepatic inflammation is one of the most pronounced features of NASH, and hepatic immune responses play critical roles in the pathogenesis of NASH and other progressive diseases [5, 6]. It is believed that an imbalance between anti-inflammatory T helper type 2 (Th2) cytokines and pro-inflammatory Th1 cytokines is responsible for the development of NASH [6, 7].…”

Section: Introductionmentioning

confidence: 99%

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The imbalance of Th17/Treg cells is involved in the progression of nonalcoholic fatty liver disease in mice

Xie

et al. 2017

BMC Immunol

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BackgroundNon-alcoholic fatty liver disease (NAFLD) is a common, chronic liver disease worldwide. Recent studies have shown that T helper (Th) 17 and regulatory T (Treg) cells play critical roles in various disorders of liver inflammation. Here, we explored the value of polyene phosphatidylcholine capsules (PPC) for regulating the imbalance of Th17/Treg cells in the pathogenesis of mice with NAFLD.MethodsC57BL/6 mice were randomly divided into three groups as follows:normal diet (ND), high-fat diet (HF),and HF plus PPC(HF + PPC). The frequencies of splenic Th17 and Treg cells were measured by flow cytometry, and their related cytokines were analyzed by CBA and real-time PCR.ResultsAt the end of 24 weeks, mice in the HF group had a higher frequency of intrahepatic Th17 cells,and a lower proportion of Treg cells compared with the ND group. The levels of Th17 cell-related cytokines (IL-6, IL-17 and IL-23) in serum and in liver tisse were increased,and the hepatic mRNA levels of RORγt, STAT3 and IL-6 were also increased. By contrast,the FoxP3 mRNA level was decreased in the HF group. Moreover, significant pathological and biochemical changes in the liver, as well as serum biochemical changes, were found in mice with NAFLD. Interestingly, following treatment with PPC, the levels of liver inflammation,frequencies of Th17/Treg cells and associated cytokines,and biochemical data were significantly altered.ConclusionThese findings demonstrate a critical role for PPC in partially attenuating liver inflammatory responses in mice with NAFLD that involves the imbalance of Treg/Th17 cells and associated cytokines.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The imbalance of Th17/Treg cells is involved in the progression of nonalcoholic fatty liver disease in mice

Xie

et al. 2017

BMC Immunol

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“…71,72 However, in contrast, a recent study from India has shown that 50% of Indian subjects with NAFLD did not have insulin resistance and one third of these patients had significant fibrosis. 73 The lack of insulin resistance may be associated with less severe disease in lean Indian fatty liver subjects. 69 In contrast, other studies from India found the prevalence of insulin resistance in around 97.5% subjects with NAFLD.…”

Section: Insulin Resistancementioning

confidence: 99%

The Riddle of Nonalcoholic Fatty Liver Disease: Progression From Nonalcoholic Fatty Liver to Nonalcoholic Steatohepatitis

Sharma

Mitnala

Vishnubhotla

et al. 2015

Journal of Clinical and Experimental Hepatology

128

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Nonalcoholic fatty liver (NAFL) is an emerging global epidemic which progresses to nonalcoholic steatohepatitis (NASH) and cirrhosis in a subset of subjects. Various reviews have focused on the etiology, epidemiology, pathogenesis and treatment of NAFLD. This review highlights specifically the triggers implicated in disease progression from NAFL to NASH. The integrating role of genes, dietary factors, innate immunity, cytokines and gut microbiome have been discussed. ( J CLIN EXP HEPATOL 2015;5:147-158)

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“…Lean-NAFLD patients were 43% in non-IR group, while this value decreased up to 25% in those with IR. 39 Lastly, in Caucasian European patients, differential lipid profile was found according to BMI. 40 Our findings were in concordance because IR was found significantly higher in obese-NAFLD patients.…”

Section: Discussionmentioning

confidence: 96%

Oxidized low‐density lipoprotein antibodies/high‐density lipoprotein cholesterol ratio is linked to advanced non‐alcoholic fatty liver disease lean patients

Ampuero

Ranchal

Gallego‐Durán

et al. 2016

J of Gastro and Hepatol

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Nonalcoholic fatty liver disease (NAFLD) without insulin resistance: Is it different?

Cited by 26 publications

References 29 publications

The imbalance of Th17/Treg cells is involved in the progression of nonalcoholic fatty liver disease in mice

The imbalance of Th17/Treg cells is involved in the progression of nonalcoholic fatty liver disease in mice

The Riddle of Nonalcoholic Fatty Liver Disease: Progression From Nonalcoholic Fatty Liver to Nonalcoholic Steatohepatitis

Oxidized low‐density lipoprotein antibodies/high‐density lipoprotein cholesterol ratio is linked to advanced non‐alcoholic fatty liver disease lean patients

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