PMID- 26823042
OWN - NLM
STAT- MEDLINE
DCOM- 20180117
LR  - 20220317
IS  - 2210-741X (Electronic)
IS  - 2210-7401 (Linking)
VI  - 40
IP  - 4
DP  - 2016 Sep
TI  - Alterations in serum levels of fetuin A and selenoprotein P in chronic hepatitis 
      C patients with concomitant type 2 diabetes: A case-control study.
PG  - 465-70
LID - S2210-7401(15)00294-6 [pii]
LID - 10.1016/j.clinre.2015.12.003 [doi]
AB  - BACKGROUND: Insulin resistance (IR) and type 2 diabetes mellitus (T2DM) are 
      serious extrahepatic manifestations of chronic hepatitis C virus (HCV) infection. 
      However, the mechanism underlying the IR in chronic HCV is obscure. Hepatokines 
      are group of liver-derived protein, which affect the glucose and lipid metabolism 
      in several tissues. Fetuin A (also known as human alpha2-HS-glycoprotein) is one of 
      the hepatokines, which was recognized as a natural inhibitor of the insulin 
      receptor tyrosine kinase in liver and skeletal muscle. Additionally, 
      selenoprotein P has emerged as an important hepatokine, which primarily acts as 
      selenium transporter and has been reported to be implicated in glucose 
      homeostasis in human. OBJECTIVE: The aim of the current case-control study was to 
      investigate the serum levels of both fetuin A and selenoprotein P in chronic 
      hepatitis C patients with or without T2DM and to correlate their levels with 
      other biochemical parameters of insulin resistance. MAIN FINDINGS: Our results 
      showed that, serum fetuin A levels increased significantly in HCV patients 
      compared with controls (P<0.01) and surplus increase was found in HCV with 
      concomitant T2DM (P>0.001). However, selenoprotein P levels significantly 
      elevated only in patients with both HCV and T2DM (P<0.05) compared with the 
      healthy subjects. Both fetuin A and selenoprotein P were positively correlated 
      with fasting blood glucose. Yet, only fetuin A was significantly correlated to 
      the HOMA-IR (r=0.28; P=0.03). CONCLUSIONS: These results indicate crucial roles 
      played by fetuin A and selenoprotein P in the IR caused by HCV and that both 
      hepatokines may be targets for the development of therapies to treat or inhibit 
      insulin resistance associated to HCV. However, further studies on large scale 
      should be conducted to confirm our findings.
CI  - Copyright (c) 2016 Elsevier Masson SAS. All rights reserved.
FAU - Ali, Sahar A
AU  - Ali SA
AD  - Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Helwan 
      University, Ain Helwan, Helwan, 11795 Cairo, Egypt.
FAU - Nassif, Walaa M H
AU  - Nassif WM
AD  - Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Helwan 
      University, Ain Helwan, Helwan, 11795 Cairo, Egypt.
FAU - Abdelaziz, Dalia H A
AU  - Abdelaziz DH
AD  - Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, Helwan 
      University, Ain Helwan, Helwan, 11795 Cairo, Egypt. Electronic address: 
      dalia_abdelaziz@pharm.helwan.edu.eg.
LA  - eng
PT  - Journal Article
DEP - 20160125
PL  - France
TA  - Clin Res Hepatol Gastroenterol
JT  - Clinics and research in hepatology and gastroenterology
JID - 101553659
RN  - 0 (Blood Glucose)
RN  - 0 (Selenoprotein P)
RN  - 0 (alpha-2-HS-Glycoprotein)
RN  - EC 2.6.1.1 (Aspartate Aminotransferases)
RN  - EC 2.6.1.2 (Alanine Transaminase)
SB  - IM
MH  - Adult
MH  - Alanine Transaminase/blood
MH  - Aspartate Aminotransferases/blood
MH  - Blood Glucose/analysis
MH  - Body Mass Index
MH  - Case-Control Studies
MH  - Diabetes Mellitus, Type 2/*blood
MH  - Female
MH  - Hepatitis C, Chronic/*blood
MH  - Humans
MH  - Male
MH  - Selenoprotein P/*blood
MH  - alpha-2-HS-Glycoprotein/*analysis
EDAT- 2016/01/30 06:00
MHDA- 2018/01/18 06:00
CRDT- 2016/01/30 06:00
PHST- 2015/09/07 00:00 [received]
PHST- 2015/11/23 00:00 [revised]
PHST- 2015/12/15 00:00 [accepted]
PHST- 2016/01/30 06:00 [entrez]
PHST- 2016/01/30 06:00 [pubmed]
PHST- 2018/01/18 06:00 [medline]
AID - S2210-7401(15)00294-6 [pii]
AID - 10.1016/j.clinre.2015.12.003 [doi]
PST - ppublish
SO  - Clin Res Hepatol Gastroenterol. 2016 Sep;40(4):465-70. doi: 
      10.1016/j.clinre.2015.12.003. Epub 2016 Jan 25.