Non-alcoholic fatty liver disease in 2016

Townsend, Sarah; Newsome, Philip N.

doi:10.1093/bmb/ldw031

Cited by 68 publications

(58 citation statements)

References 85 publications

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“…The worldwide prevalence of NAFLD is on the rise, and it is rapidly becoming the most common cause of chronic liver disease affecting 25% of the world's population (Chalasani et al, 2018;Charlton et al, 2011;Townsend & Newsome, 2016). The characteristics of metabolic syndrome (Mets) are not only very common in NAFLD patients, but also the components of Mets increase the risk of NAFLD, such as existing etiology: obesity, Type 2 diabetes, hypertension, and dyslipidemia and emerging elements: sleep apnea, colorectal cancer, osteoporosis, psoriasis, endocrinopathies, and polycystic ovary syndrome (Nasr, Ignatova, Kechagias, & Ekstedt, 2018;Stefan, Kantartzis, & Haring, 2008).…”

Section: Discussionmentioning

confidence: 99%

Association between ADIPOQ G276T and C11377G polymorphisms and the risk of non‐alcoholic fatty liver disease: An updated meta‐analysis

Liu

Shang

et al. 2019

Molec Gen & Gen Med

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Background Nonalcoholic fatty liver disease (NAFLD) is a significant contributor to global hepatic disorders. ADIPOQ gene single‐nucleotide polymorphisms have been associated with NAFLD susceptibility, but with inconsistent results across the studies. This study aimed to investigate the association between ADIPOQ polymorphisms (+276G>T, rs1501299 and −11377C>G, rs266729) and the risk of NAFLD. Methods PubMed, Embase, Wanfang, Web of Science, and China National Knowledge Infrastructure databases were used to identify the relevant published literature. Statistical analyses were calculated with STATA 11.0 software and RevMan 5.2. Summary odds ratios (OR) and 95% confidence intervals (CIs) were generated to assess the strength of the associations. Results Eleven relevant articles with a total of 3,644 participants (1,847 cases/1,797 controls) were included. Our meta‐analysis results revealed that ADIPOQ gene +276G>T polymorphism was not associated with NAFLD under various genetic models (allele model: OR = 0.99, 95% CI [0.69, 1.41]; dominant model: OR = 1.06, 95% CI [0.71, 1.58]; recessive model: OR = 0.83, 95% CI [0.42, 1.65]; homozygous model: OR = 0.86, 95% CI [0.38, 1.95]; heterozygous model: OR = 1.10, 95% CI [0.80, 1.53]; respectively). Moreover, no statistical significant association was found between +276G>T and NAFLD risk in the subgroups. ADIPOQ gene −11377C>G polymorphism significantly increased the risk of NAFLD (allele model: OR = 1.49, 95% CI [1.28, 1.75]; dominant model: OR = 1.64, 95% CI [1.35, 1.99]; recessive model: OR = 1.77, 95% CI [1.16, 2.70]; homozygous model: OR = 2.13, 95% CI [1.38, 3.28]; heterozygous model: OR = 1.58, 95% CI [1.29, 1.93]; respectively). Conclusion ADIPOQ gene −11377C>G may be a risk factor for NAFLD, while there was no association between ADIPOQ gene +276G>T polymorphism and the risk of NAFLD. Further studies are needed to detect the relationship between these ADIPOQ polymorphisms and NAFLD.

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Section: Discussionmentioning

confidence: 99%

Association between ADIPOQ G276T and C11377G polymorphisms and the risk of non‐alcoholic fatty liver disease: An updated meta‐analysis

Liu

Shang

et al. 2019

Molec Gen & Gen Med

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“…[62, 63,65] metastatic breast cancer. [55] Additionally, using an LOXL2antibody in 4T1 mouse breast cancer cells decreased the expression level of -SMA, implying that fibroblast activation of these cells was reduced following treatment.…”

Section: Primary Sclerosing Cholangitismentioning

confidence: 99%

Lysyl Oxidase Like‐2 (LOXL2): An Emerging Oncology Target

Chopra

Sangarappillai

Romero‐Canelón

et al. 2020

Advanced Therapeutics

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Lysyl oxidase‐like 2 (LOXL2) is an emerging drug target against metastatic disease owing to its role in the upregulation of key processes including epithelial‐mesenchymal transition (EMT) and invasion. Recent activity in the field of small molecule LOXL2 inhibitor development by pharmaceutical and academic laboratories has renewed interest in targeting LOXL2. Herein, 1) the viability of LOXL2 as a drug target for the treatment of metastatic disease through an investigation of its biological actions is determined; 2) the pitfalls of an antibody approach are considered; and 3) the small molecule approaches emerging in the scientific and patent literature are reviewed. This review identifies that LOXL2 is localized and active intracellularly and extracellularly in invasive cancer cells. LOXL2 has been implicated in a number of established signaling pathways involved in tumor progression, further highlighting its appeal as a target in metastatic disease. Previously, limited chemical inhibitors have been developed; however, their selectivity profile for the LOX family has proven controversial. Antibodies, such as simtuzumab, have been developed selectively against LOXL2. Simtuzumab, in particular, progresses into phase II trials but it was ultimately terminated. The small molecule inhibitors of LOXL2 are summarized, some of which are now in the early stages of clinical trials.

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“…A clear understanding of NAFLD, and other manifestations of metabolic syndrome (MetS), is required to develop effective therapies and improve existing ones [3]. Prevention and treatment of NAFLD are expensive and lengthy processes; further efforts are needed to help people to avoid unhealthy diets, maintain healthy lifestyles, and implement existing therapies using antioxidants, oral hypoglycemics, and fat-lowering agents [4].…”

Section: Introductionmentioning

confidence: 99%

Probiotic mixture improves fatty liver disease by virtue of its action on lipid profiles, leptin, and inflammatory biomarkers

Al‐Muzafar

Amin

2017

BMC Complement Altern Med

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BackgroundA high fat diet has an essential role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). This condition is characterized by hepatic fat accumulation (steatosis) and is associated with obesity, diabetes, and fibrosis or cirrhosis of the liver. Probiotics may be useful in the treatment of steatosis. This study examined the effects of an ingested probiotic formulation on the lipid profiles, liver functions, leptin levels, and inflammatory marker levels of rats with NAFLD that had been induced via high fat and sucrose diet (HFSD).MethodsYoung male albino rats were randomly divided into three groups: a control group that was fed a standard diet; a second group that was fed a HFSD; and a third group that was given both a HFSD and ingestible probiotic mixtures. The groups were fed these diets for 16 weeks, and were then examined.ResultsHFSD-only rats showed hypertriglyceridemia, hypercholesterolemia, and elevated low density lipoprotein (LDL) levels, and their serum alanine transaminase (ALT) and bilirubin levels were significantly higher than those of the control group. Compared to rats on the standard diet, HFSD-only rats showed higher levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6), increased serum leptin levels, and increased resistin hormone levels in the adipose tissues. In the third group, the inclusion of the probiotic mixture seemed to ameliorate the effects of the HFSD diet. The NAFD + probiotics group showed improved lipid profiles, better leptin and resistin levels, and better TNF-α and IL-6 levels than the NAFD-only group. They also showed no signs of NAFLD.ConclusionsThe probiotic mixture showed promise as a treatment for NAFLD pathogenesis, and may improve HFSD-induced steatosis through its effects on leptin, resistin, inflammatory biomarkers, and hepatic function markers. We also established that gut microbiota-mediated regulation of lipid profiles was dependent on dietary lipids and carbohydrates.

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Non-alcoholic fatty liver disease in 2016

Abstract: Improved understanding of the pathophysiology of NAFLD should help us identify which patients progress to significant liver disease and to develop therapies to target this population.

Cited by 68 publications

References 85 publications

Association between ADIPOQ G276T and C11377G polymorphisms and the risk of non‐alcoholic fatty liver disease: An updated meta‐analysis

Association between ADIPOQ G276T and C11377G polymorphisms and the risk of non‐alcoholic fatty liver disease: An updated meta‐analysis

Lysyl Oxidase Like‐2 (LOXL2): An Emerging Oncology Target

Probiotic mixture improves fatty liver disease by virtue of its action on lipid profiles, leptin, and inflammatory biomarkers

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