Nonalcoholic Fatty Liver Disease (NAFLD), the Metabolic Disorder Par Excellence

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 4481

Special Issue Editor

Special Issue Information

Dear Colleagues,

NAFLD, recently renamed MAFLD, is a common condition that places a heavy burden on public health and exacts a major clinical and financial toll on a worldwide basis. Although it has been the subject of ever-increasing clinical and research interest over the last 40 years, this condition remains enigmatic as to its development and progression in the individual patient. Noninvasive diagnostic protocols are still to be validated, and optimal management options still remain to be identified. On these grounds, Metabolites (ISSN 2218-1989, 2019 IF: 4.097) intends to publish a Special Issue entitled “NAFLD, the Metabolic Disorder Par Excellence” and has approached me to serve as Guest Editor.

Potential topics include but are not limited to the following:

  • Lessons from epidemiology;
  • Sex differences in NAFLD;
  • Lean NAFLD;
  • Modifiers of the natural history of NAFLD;
  • NAFLD in children, adolescents and elderly people;
  • NAFLD as a systemic disorder;
  • Molecular and clinical bases of NAFLD physiopathology;
  • Role of the gut–liver axis in the development and progression of disease;
  • Cardio-nephrometabolic risk in people with NAFLD;
  • The bidirectional association of NAFLD with the metabolic syndrome;
  • NAFLD secondary to endocrine disorders;
  • Personalized medicine as applied to NAFLD;
  • Ethics in NAFLD research;
  • Role of industry-sponsored research in NAFLD;
  • NAFLD and SARS-CoV-2 infection;
  • Updates in diagnosis and management;
  • Impact of genetics and molecular biology on clinical practice;
  • Implications of novel terminology and definitions.

Dr. Amedeo Lonardo
Guest Editor

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Review

11 pages, 689 KiB  
Review
Sodium-Glucose Cotransporter-2 Inhibitors for Treatment of Nonalcoholic Fatty Liver Disease: A Meta-Analysis of Randomized Controlled Trials
Metabolites 2021, 11(1), 22; https://doi.org/10.3390/metabo11010022 - 30 Dec 2020
Cited by 69 | Viewed by 3944
Abstract
Recent randomized controlled trials (RCTs) tested the efficacy of sodium-glucose cotransporter-2 (SGLT-2) inhibitors to specifically treat nonalcoholic fatty liver disease (NAFLD). We systematically searched three electronic databases (up to 31 October 2020) for identifying placebo-controlled or head-to-head RCTs that used SGLT-2 inhibitors for [...] Read more.
Recent randomized controlled trials (RCTs) tested the efficacy of sodium-glucose cotransporter-2 (SGLT-2) inhibitors to specifically treat nonalcoholic fatty liver disease (NAFLD). We systematically searched three electronic databases (up to 31 October 2020) for identifying placebo-controlled or head-to-head RCTs that used SGLT-2 inhibitors for treatment of NAFLD. No published RCTs with paired liver biopsy data were available for the meta-analysis. Primary outcome measures were changes in serum liver enzyme levels and liver fat content on imaging techniques. Overall, we included a total of twelve RCTs testing the efficacy of dapagliflozin (n = six RCTs), empagliflozin (n = three RCTs), ipragliflozin (n = two RCTs) or canagliflozin (n = one RCT) to specifically treat NAFLD for a median period of 24 weeks with aggregate data on 850 middle-aged overweight or obese individuals with NAFLD (90% with type 2 diabetes). Compared to placebo/reference therapy, treatment with SGLT-2 inhibitors significantly decreased serum alanine aminotransferase (weighted mean differences (WMD): −10.0 IU/L, 95%CI −12.2 to −7.79 IU/L; I2 = 10.5%) and gamma-glutamyltransferase levels (WMD: −14.49 IU/L, 95%CI −19.35 to −9.63 IU/L, I2 = 38.7%), as well as the absolute percentage of liver fat content on magnetic resonance-based techniques (WMD: −2.05%, 95%CI −2.61 to −1.48%; I2 = 0%). In conclusion, SGLT-2 inhibitors seem to be a promising treatment option for NAFLD. Full article
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