PMID- 31672448
OWN - NLM
STAT- MEDLINE
DCOM- 20200219
LR  - 20200219
IS  - 1532-8600 (Electronic)
IS  - 0026-0495 (Linking)
VI  - 101
DP  - 2019 Dec
TI  - Effects of newer antidiabetic drugs on nonalcoholic fatty liver and 
      steatohepatitis: Think out of the box!
PG  - 154001
LID - S0026-0495(19)30216-1 [pii]
LID - 10.1016/j.metabol.2019.154001 [doi]
AB  - Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease 
      in Western societies and a major cause of hepatic disease worldwide. Its more 
      severe type, namely nonalcoholic steatohepatitis (NASH), may result in the 
      development of cirrhosis and hepatocellular carcinoma. NAFLD, and especially 
      NASH, are also associated with increased cardiovascular morbidity and mortality. 
      Type 2 diabetes mellitus (T2DM) predisposes to NAFLD development and progression 
      via insulin resistance and hyperglycemia. It has also been reported that the 
      majority of T2DM patients have NAFLD/NASH, thus potentially further increasing 
      their cardiometabolic risk. Current guidelines recommend to screen for NAFLD in 
      all T2DM patients and vice-versa. Lifestyle remains the first-line therapeutic 
      option for NAFLD/NASH. Among antidiabetic drugs, pioglitazone was shown to 
      improve histological features of NASH. More recently, there is an increasing 
      interest regarding the effects of newer anti-diabetic drugs, such as dipeptidyl 
      peptidase 4 inhibitors (DPP-4i), sodium glucose cotransporter 2 inhibitors 
      (SGLT2i), and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) on 
      NAFLD/NASH. The present narrative review considers the up-to-date data on the 
      impact of DPP-4i, SGLT2i, and GLP-1 RAs on biochemical and/or histological 
      markers of NAFLD/NASH. The potential clinical implications of these findings in 
      daily practice are also discussed. Taking into consideration the global 
      increasing prevalence of NAFLD/NASH, therapeutic options that can prevent or 
      treat this disease will exert considerable benefits on human health.
CI  - Copyright (c) 2019 Elsevier Inc. All rights reserved.
FAU - Ranjbar, Golnaz
AU  - Ranjbar G
AD  - Department of Nutrition, Faculty of Medicine, Mashhad University of Medical 
      Sciences, Mashhad, Iran.
FAU - Mikhailidis, Dimitri P
AU  - Mikhailidis DP
AD  - Department of Clinical Biochemistry, Royal Free Hospital Campus, University 
      College London Medical School, University College London (UCL), London, United 
      Kingdom.
FAU - Sahebkar, Amirhossein
AU  - Sahebkar A
AD  - Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad 
      University of Medical Sciences, Mashhad, Iran; Neurogenic Inflammation Research 
      Center, Mashhad University of Medical Sciences, Mashhad, Iran; School of 
      Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic 
      address: sahebkara@mums.ac.ir.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20191028
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 0 (Dipeptidyl-Peptidase IV Inhibitors)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Sodium-Glucose Transporter 2 Inhibitors)
RN  - 89750-14-1 (Glucagon-Like Peptide 1)
RN  - X4OV71U42S (Pioglitazone)
SB  - IM
MH  - Diabetes Mellitus, Type 2/complications
MH  - Dipeptidyl-Peptidase IV Inhibitors/therapeutic use
MH  - Fatty Liver/*drug therapy
MH  - Glucagon-Like Peptide 1/therapeutic use
MH  - Humans
MH  - Hypoglycemic Agents/*pharmacology/therapeutic use
MH  - Non-alcoholic Fatty Liver Disease/complications/*drug therapy
MH  - Pioglitazone/therapeutic use
MH  - Sodium-Glucose Transporter 2 Inhibitors/therapeutic use
OTO - NOTNLM
OT  - Dipeptidyl peptidase 4 inhibitors
OT  - Glucagon-like peptide-1 receptor agonists
OT  - Nonalcoholic fatty liver disease
OT  - Nonalcoholic steatohepatitis
OT  - Sodium glucose cotransporter 2 inhibitors
OT  - Type 2 diabetes mellitus
EDAT- 2019/11/02 06:00
MHDA- 2020/02/20 06:00
CRDT- 2019/11/02 06:00
PHST- 2019/07/29 00:00 [received]
PHST- 2019/10/02 00:00 [revised]
PHST- 2019/10/15 00:00 [accepted]
PHST- 2019/11/02 06:00 [pubmed]
PHST- 2020/02/20 06:00 [medline]
PHST- 2019/11/02 06:00 [entrez]
AID - S0026-0495(19)30216-1 [pii]
AID - 10.1016/j.metabol.2019.154001 [doi]
PST - ppublish
SO  - Metabolism. 2019 Dec;101:154001. doi: 10.1016/j.metabol.2019.154001. Epub 2019 
      Oct 28.