ijms-logo

Journal Browser

Journal Browser

Recent Advances in Diabetic Liver Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 2775

Special Issue Editor

1. Department of Hepatology and Pancreatology, Aichi Medical University of Medicine, Nagakute, Aichi, Japan
2. Japan Strategic Medical Administration Research Center (J-SMARC), Nagoya, Aichi, Japan
Interests: nonalcoholic steatohepatitis; oxidative stress; hepatic fibrosis; diabetes mellitus; liver cirrhosis; hepatocellular carcinoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of the Special Issue “Diabetic Liver Disease”. The first edition presented 10 high-quality papers.

Nonalcoholic fatty liver disease (NAFLD), the most prevalent chronic liver disease, is associated with type 2 diabetes (T2D). Nonalcoholic steatohepatitis (NASH), a severe form of NAFLD, can progress to cirrhosis, hepatocellular carcinoma (HCC), and hepatic failure. Liver-related mortality is the third leading cause in T2D patients. NASH can be called “diabetic liver disease” (DLD). Accumulating evidence shows that PNPLA3 SNP is associated with fibrosis progression or HCC development. This Special Issue will include papers investigating the pathological mechanisms of T2DM and liver diseases such as NASH, as well as diagnostics using new biomarkers. Furthermore, experimental in vitro and in vivo studies and clinical studies examining potential new approaches to attenuate DLD are welcome. This Special Issue welcomes original research and review papers.

Suggested Topics:

  1. Mechanisms of insulin resistance and hepatic steatosis/fibrosis;
  2. The role of SNPs with disease severity in DLD;
  3. The role of microbiota in DLD;
  4. Endocrine system in DLD;
  5. Antifibrotic agents in DLD;
  6. How can we stop HCC development?
  7. Mechanisms of cardiac/renal disease and DLD;
  8. Mechanisms of extrahepatic neoplasms development in DLD;
  9. Novel antidiabetic drugs in DLD;

Noninvasive tests (NITs) of hepatic fibrosis in DLD.

Dr. Yoshio Sumida
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Nonalcoholic fatty liver disease
  • Hepatocellular carcinoma
  • Nonalcoholic steatohepatitis
  • Type 2 diabetes
  • Hepatic fibrosis
  • Liver cirrhosis
  • PNPLA3

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

14 pages, 2136 KiB  
Article
Role of ANGPTL8 in NAFLD Improvement after Bariatric Surgery in Experimental and Human Obesity
by Carolina M. Perdomo, Javier Gómez-Ambrosi, Sara Becerril, Víctor Valentí, Rafael Moncada, Eva M. Fernández-Sáez, Leire Méndez-Giménez, Silvia Ezquerro, Victoria Catalán, Camilo Silva, Javier Escalada, Gema Frühbeck and Amaia Rodríguez
Int. J. Mol. Sci. 2021, 22(23), 12945; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222312945 - 30 Nov 2021
Cited by 7 | Viewed by 2159
Abstract
Angiopoietin-like protein 8 (ANGPTL8) is an hepatokine altered in several metabolic conditions, such as obesity, type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease (NAFLD). We sought to explore whether ANGPTL8 is involved in NAFLD amelioration after bariatric surgery in experimental models and [...] Read more.
Angiopoietin-like protein 8 (ANGPTL8) is an hepatokine altered in several metabolic conditions, such as obesity, type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease (NAFLD). We sought to explore whether ANGPTL8 is involved in NAFLD amelioration after bariatric surgery in experimental models and patients with severe obesity. Plasma ANGPTL8 was measured in 170 individuals before and 6 months after bariatric surgery. Hepatic ANGPTL8 expression was evaluated in liver biopsies of patients with severe obesity undergoing bariatric surgery with available liver pathology analysis (n = 75), as well as in male Wistar rats with diet-induced obesity subjected to sham operation, sleeve gastrectomy or Roux-en-Y gastric bypass (RYGB) (n = 65). The effect of ANGPTL8 on lipogenesis was assessed in human HepG2 hepatocytes under palmitate-induced lipotoxic conditions. Plasma concentrations and hepatic expression of ANGPTL8 were increased in patients with obesity-associated NAFLD in relation to the degree of hepatic steatosis. Sleeve gastrectomy and RYGB improved hepatosteatosis and reduced the hepatic ANGPTL8 expression in the preclinical model of NAFLD. Interestingly, ANGPTL8 inhibited steatosis and expression of lipogenic factors (PPARG2, SREBF1, MOGAT2 and DGAT1) in palmitate-treated human hepatocytes. Together, ANGPTL8 is involved in the resolution of NAFLD after bariatric surgery partially by the inhibition of lipogenesis in steatotic hepatocytes. Full article
(This article belongs to the Special Issue Recent Advances in Diabetic Liver Disease)
Show Figures

Figure 1

Back to TopTop