Role of APN and TNF-α in type 2 diabetes mellitus complicated by nonalcoholic fatty liver disease

Lin, Xu; Zhang, Z.; Chen, J.M.; Xu, Ying; Ye, H.R.; Chen, Ju; Fang, Yun; Yao, Jin; Zhu, Di; Yuan, Ling

doi:10.4238/2015.april.10.1

Cited by 24 publications

(16 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TNF-α could also be involved in the second hit process of NAFLD as TNF-α may intensify the dysfunction of mitochondria and induce the release of cytochrome C from mitochondria, which would increase ROS production and formation of lipid peroxidation and eventually caused liver injury44. All these suggested that TNF-α was an important cytokine in the progression of NAFLD from NAFL to NASH45.…”

Section: Discussionmentioning

confidence: 95%

Probiotics may delay the progression of nonalcoholic fatty liver disease by restoring the gut microbiota structure and improving intestinal endotoxemia

Xue

Gao

et al. 2017

Sci Rep

243

165

View full text Add to dashboard Cite

Gut-derived bacterial lipopolysaccharide (LPS) and subsequent hepatic toll-like receptor 4 (TLR4) activation have been recognized to be involved in the onset of diet-induced nonalcoholic fatty liver disease (NAFLD), but little is known about the variation of LPS and TLR4 during the progression of NAFLD. Probiotics were able to inhibit proliferation of harmful bacteria and improve gastrointestinal barrier function. However, it’s unclear whether LPS/TLR4 is involved in the protection effect of probiotics on NAFLD. In this study, we described characteristic of gut microbiota structure in the progression of NAFLD, and we also analyzed the relationship between gut microbiota and LPS/TLR4 in this process. Furthermore, we applied probiotics intervention to investigate the effect of probiotics on gut flora structure, intestinal integrity, serum LPS, liver TLR4 and liver pathology. Our results showed that serum LPS and liver TLR4 were highly increased during progression of NAFLD, with gut flora diversity and gut mircobiological colonization resistance (B/E) declining. Furthermore, probiotics could improve gut microbiota structure and liver pathology. Probiotics could also downregulate serum LPS and liver TLR4. Our results suggested that both gut flora alteration and endotoxemia may be involved in the progression of NAFLD. Probiotics may delay the progression of NAFLD via LPS/TLR4 signaling.

show abstract

Section: Discussionmentioning

confidence: 95%

Probiotics may delay the progression of nonalcoholic fatty liver disease by restoring the gut microbiota structure and improving intestinal endotoxemia

Xue

Gao

et al. 2017

Sci Rep

243

165

View full text Add to dashboard Cite

show abstract

“…APN is an insulin-sensitive adipocytokine that plays critical roles in adipose tissue inflammation [40]. APN can inhibit NAFLD by reducing fat content and promoting fatty acid oxidation; it also inhibits liver inflammation by attenuating TNF-α levels [41]. A low serum APN indicates an advanced fibrosis condition in patients with NAFLD [42].…”

Section: Discussionmentioning

confidence: 99%

Efficacy of liraglutide in treating type 2 diabetes mellitus complicated with non-alcoholic fatty liver disease

Tian

Zhang

et al. 2018

Bioscience Reports

View full text Add to dashboard Cite

Type 2 diabetes mellitus (T2DM) complicated with non-alcoholic fatty liver disease (NAFLD) is difficult to treat. The present study explored the efficacy of (liraglutide) Lira in treating T2DM complicated with NAFLD. A total of 127 patients suffering from T2DM complicated with NAFLD were enrolled in the present study, and randomly assigned to a Lira group (liraglutide injection: 0.6–1.2 mg/day, 12 weeks, n=52) or a Metformin (Met) group (oral metformin: 1000–1500 mg/day, 12 weeks, n=75). During the treatment phase, the values for fasting plasma glucose (FPG), 2 h plasma glucose (2hPG), glycated hemoglobin (HbA1c), aspartate aminotransferase (AST)/alanine aminotransferase (ALT), and adiponectin (APN) decreased in both the Lira and Met groups, and the levels of Δ2hPG, ΔAST/ALT, and ΔAPN in the Lira group were significantly lower than those in the Met group. The values for total cholesterol (TC), triglycerides (TG), low-and high-density lipoproteins (LDL and HDL), ALT, AST, weight, body mass index (BMI), waist to hip ratio (WHR), and C-reactive protein were markedly increased in both groups, and levels of ΔAST, ΔALT, Δweight, ΔBMI, ΔWHR, and ΔCRP (C-reactive protein) in the Lira group were significantly higher than those in the Met group. An analysis of treatment efficacy showed that liraglutide was better than metformin in its ability to significantly decrease the ALT levels in patients with combined T2DM and NAFLD. Furthermore, liraglutide was more effective than metformin at ameliorating the severity of T2DM complicated with NAFLD, and produced its effects by alleviating liver inflammation and improving liver function.

show abstract

“…It is considered that insulin resistance and type 2 diabetes are closely related with inflammation [33][34][35]. Pathological conditions of insulin resistance and type 2 diabetes are characterized by increase of IL-1β, TNFα and CRP levels [36][37][38][39][40][41]. In the study, we evaluated the effect of Lycopene on IL-1β, TNFα and CRP levels in mice fed HFD.…”

Section: Discussionmentioning

confidence: 99%

Lycopene Improves Insulin Sensitivity through Inhibition of STAT3/Srebp-1c-Mediated Lipid Accumulation and Inflammation in Mice fed a High-Fat Diet

Zhao-hui

Jia

et al. 2017

Exp Clin Endocrinol Diabetes

View full text Add to dashboard Cite

In the past few years, metabolic disorders, such as type 2 diabetes and metabolic syndrome, have reached global prevalence. Lycopene is one of the major carotenoids in tomatoes, watermelons, red grapefruits, and guava. In the current study, using high fat diet (HFD)-fed mice, we investigated the effect of Lycopene on insulin resistance. We showed that diet containing Lycopene significantly prevented HFD-induced increase of fasting blood glucose and insulin level, glucose and insulin intolerance, and decrease of hepatic glycogen content. We found that Lycopene notably prevented the increase of IL-1β, TNFα and CRP levels in mice fed HFD. We showed that Lycopene improved the lipid profiles in HFD-fed mice, as evidenced by decrease of systemic and hepatic TC, TG and LDL, and increase of HDL. Lycopene suppressed the increase of the expression of Srebp-1c, FAS and ACC-1 in mice fed HFD. The administration of Lycopene notably prevented the expression and phosphorylation of STAT3 in livers of mice induced by HFD. The treatment of adenovirus carrying STAT3 significantly suppressed the decrease of Srebp-1c expression induced by Lycopene. Furthermore, enhancement of STAT3 signaling by adenovirus markedly blocked the reduction of fasting blood glucose and insulin level. In conclusion, in the current study, we found that Lycopene prevented STAT3 signaling and inhibited Srebp-1c and downstream gene expression, resulting in inhibition of lipid accumulation, inflammation, insulin resistance and metabolic dysfunction. Overall, the data in the study provide better understanding of the beneficial effects of Lycopene against insulin resistance and metabolic disorder.

show abstract

Role of APN and TNF-α in type 2 diabetes mellitus complicated by nonalcoholic fatty liver disease

Cited by 24 publications

References 17 publications

Probiotics may delay the progression of nonalcoholic fatty liver disease by restoring the gut microbiota structure and improving intestinal endotoxemia

Probiotics may delay the progression of nonalcoholic fatty liver disease by restoring the gut microbiota structure and improving intestinal endotoxemia

Efficacy of liraglutide in treating type 2 diabetes mellitus complicated with non-alcoholic fatty liver disease

Lycopene Improves Insulin Sensitivity through Inhibition of STAT3/Srebp-1c-Mediated Lipid Accumulation and Inflammation in Mice fed a High-Fat Diet

Contact Info

Product

Resources

About