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Special Issue "Non-Alcoholic Steatohepatitis (NASH)"

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Endocrinology & Metabolism".

Deadline for manuscript submissions: 30 September 2019

Special Issue Editor

Guest Editor
Prof. Dr. Stefano Fiorucci

Gastroenterology Section, Department of Surgical and Biomedical Sciences, School of Medicine, University of Perugia, Perugia, Italy
Website | E-Mail
Interests: gastroenterology and hepatology

Special Issue Information

Dear Colleagues,

Nonalcoholic fatty liver disease (NAFLD) is a common liver disorder with a high prevalence (20–30%) in Western as well as many Eastern countries, thus representing a rapidly growing health problem worldwide. NAFLD includes a spectrum of disorders ranging from non-alcoholic fatty liver (NAFL), a reversible condition caused by a lipid deposition in the hepatocytes, to non-alcoholic steatohepatitis (NASH), characterized by hepatocytes ballooning and inflammatory cell infiltration. Despite its lower prevalence, ranging from 1.5 to 6.5%, NASH is a progressive liver disease associated with an increased significant risk of developing parenchymal fibrosis, hepatic cirrhosis, and hepatocellular carcinoma. Furthermore, both diseases involve an increased risk for developing cardiovascular complications, including coronary heart disease and stroke. NASH could be considered the hepatic manifestation of metabolic syndrome. The development of NASH is associated with the presence of risk factors, such as weight gain, diabetes, hypertension, menopause, and genetic conditions. Over time, obesity is considered a primary cause of NAFLD and NASH. The accumulation of lipid species, in particular fatty acids, in hepatocytes exerts lipotoxic effects that cause progressive parenchymal cell loss, inflammation, and fibrosis in NASH. However, the pathogenesis of NASH is multifactorial, involving environmental factors, in particular excessive caloric intake associated with a genetic predisposition, but requires second hits, represented by insulin resistance and visceral adipose tissue inflammation, which are thought to be central to the pathogenesis of NASH. To date, there are several available rodent models of NAFLD and NASH, whose relevance to the human NASH is imperfect because they have shown substantial heterogeneity of gene and pathway regulation in comparison to human NASH. However, steatohepatitis induced by long-term administration of a high-fat diet (HFD) and fructose leading to steatosis, inflammation, and fibrosis shows a better correlation to human NAFLD and NASH, confirming the importance of preclinical models. Several agents are currently under development for the treatment of NASH in 2019, but there are no approved drugs to treat this condition. In summary, there is an urgent need to develop novel approaches to treat NASH patients.

Prof. Dr. Stefano Fiorucci
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 papers will be 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. Journal of Clinical Medicine is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). 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

  • Bile acids
  • Liver lipids
  • Cholesterol
  • Steatohepatatis
  • Liver fibrosis
  • Animal models
  • Clinical trials
  • Metabolic syndrome
  • Drug development
  • Nuclear receptors
  • FXR
  • PPARs
  • Cholesterol biosynthesis
  • Diabetes
  • Obesity
  • Vascular complications
  • Liver cirrhosis
  • Hepatocarcinoma
  • Bariatric surgery

Published Papers (1 paper)

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Research

Open AccessArticle
Lysosomal Acid Lipase as a Molecular Target of the Very Low Carbohydrate Ketogenic Diet in Morbidly Obese Patients: The Potential Effects on Liver Steatosis and Cardiovascular Risk Factors
J. Clin. Med. 2019, 8(5), 621; https://doi.org/10.3390/jcm8050621
Received: 19 April 2019 / Revised: 1 May 2019 / Accepted: 3 May 2019 / Published: 7 May 2019
PDF Full-text (1763 KB) | HTML Full-text | XML Full-text
Abstract
A very low carbohydrate ketogenic diet (VLCKD) is an emerging technique to induce a significant, well-tolerated, and rapid loss of body weight in morbidly obese patients. The low activity of lysosomal acid lipase (LAL) could be involved in the pathogenesis of non-alcoholic fatty [...] Read more.
A very low carbohydrate ketogenic diet (VLCKD) is an emerging technique to induce a significant, well-tolerated, and rapid loss of body weight in morbidly obese patients. The low activity of lysosomal acid lipase (LAL) could be involved in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), which is a common feature in morbidly obese patients. Fifty-two obese patients suitable for a bariatric surgery intervention underwent a 25-day-long VLCKD. The biochemical markers of glucose and lipid metabolism, and flow-mediated dilation (FMD) of the brachial artery were measured before and after VLCKD. LAL activity was measured using the dried blood spot technique in 20 obese patients and in a control group of 20 healthy, normal-weight subjects. After VLCKD, we observed a significant reduction in body mass index, fasting glucose, insulinemia, and lipid profile parameters. No significant variation in FMD was observed. The number of patients with severe liver steatosis significantly decreased. LAL activity significantly increased, although the levels were not significantly different as compared to the control group. In conclusion, VLCKD induces the activity of LAL in morbidly obese subjects and reduces the secretion of all circulating lipoproteins. These effects could be attributed to the peculiar composition of the diet, which is particularly poor in carbohydrates and relatively rich in proteins. Full article
(This article belongs to the Special Issue Non-Alcoholic Steatohepatitis (NASH))
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J. Clin. Med. EISSN 2077-0383 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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