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"Non alcoholic fatty liver disease and eNOS dysfunction in humans".

Abstract NAFLD is associated to Insulin Resistance (IR). IR is responsible for Endothelial Dysfunction (ED) through the impairment of eNOS function. Although eNOS derangement has been demonstrated in experimental models, no studies have directly shown that eNOS dysfunction is associated with NAFLD in humans. The aim of this study is to investigate eNOS function in NAFLD patients.
PMID
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Authors

Mayor MeshTerms

Vasodilation

Keywords

Endothelial dysfunction

Insulin resistance

Metabolic syndrome

Non-alcoholic fatty liver disease

Journal Title bmc gastroenterology
Publication Year Start




PMID- 28264657
OWN - NLM
STAT- MEDLINE
DA  - 20170307
DCOM- 20170310
LR  - 20170312
IS  - 1471-230X (Electronic)
IS  - 1471-230X (Linking)
VI  - 17
IP  - 1
DP  - 2017 Mar 07
TI  - "Non alcoholic fatty liver disease and eNOS dysfunction in humans".
PG  - 35
LID - 10.1186/s12876-017-0592-y [doi]
AB  - BACKGROUND: NAFLD is associated to Insulin Resistance (IR). IR is responsible for
      Endothelial Dysfunction (ED) through the impairment of eNOS function. Although
      eNOS derangement has been demonstrated in experimental models, no studies have
      directly shown that eNOS dysfunction is associated with NAFLD in humans. The aim 
      of this study is to investigate eNOS function in NAFLD patients. METHODS:
      Fifty-four NAFLD patients were consecutively enrolled. All patients underwent
      clinical and laboratory evaluation and liver biopsy. Patients were divided into
      two groups by the presence of NAFL or NASH. We measured vascular reactivity
      induced by patients' platelets on isolated mice aorta rings. Immunoblot assays
      for platelet-derived phosphorylated-eNOS (p-eNOS) and immunohistochemistry for
      hepatic p-eNOS have been performed to evaluate eNOS function in platelets and
      liver specimens. Flow-mediated-dilation (FMD) was also performed. Data were
      compared with healthy controls. RESULTS: Twenty-one (38, 8%) patients had NAFL
      and 33 (61, 7%) NASH. No differences were found between groups and controls
      except for HOMA and insulin (p < 0.0001). Vascular reactivity demonstrated a
      reduced function induced from NAFLD platelets as compared with controls (p <
      0.001), associated with an impaired p-eNOS in both platelets and liver (p <
      0.001). NAFL showed a higher impairment of eNOS phosphorylation in comparison to 
      NASH (p < 0.01). In contrast with what observed in vitro, the vascular response
      by FMD was worse in NASH as compared with NAFL. CONCLUSIONS: Our data showed, for
      the first time in humans, that NAFLD patients show a marked eNOS dysfunction,
      which may contribute to a higher CV risk. eNOS dysfunction observed in platelets 
      and liver tissue didn't match with FMD.
FAU - Persico, Marcello
AU  - Persico M
AUID- ORCID: http://orcid.org/0000-0002-1399-6498
AD  - Internal Medicine and Hepatology Unit, PO G. Da Procida-AOU- San Giovanni e Ruggi
      D'Aragona, University of Salerno, Via Salvatore Calenda 162, CAP: 84126, Salerno,
      Italy. [email protected]
FAU - Masarone, Mario
AU  - Masarone M
AD  - Internal Medicine and Hepatology Unit, PO G. Da Procida-AOU- San Giovanni e Ruggi
      D'Aragona, University of Salerno, Via Salvatore Calenda 162, CAP: 84126, Salerno,
      Italy.
FAU - Damato, Antonio
AU  - Damato A
AD  - Vascular Physiopathology Unit IRCCS, INM Neuromed, Pozzilli, IS, Italy.
FAU - Ambrosio, Mariateresa
AU  - Ambrosio M
AD  - Vascular Physiopathology Unit IRCCS, INM Neuromed, Pozzilli, IS, Italy.
FAU - Federico, Alessandro
AU  - Federico A
AD  - Hepato-Gastroenterology Division, University of Campania "L. Vanvitelli", Naples,
      Italy.
FAU - Rosato, Valerio
AU  - Rosato V
AD  - Internal Medicine and Hepatology Department, University of Campania "L.
      Vanvitelli", Naples, Italy.
FAU - Bucci, Tommaso
AU  - Bucci T
AD  - Internal Medicine and Hepatology Unit, PO G. Da Procida-AOU- San Giovanni e Ruggi
      D'Aragona, University of Salerno, Via Salvatore Calenda 162, CAP: 84126, Salerno,
      Italy.
FAU - Carrizzo, Albino
AU  - Carrizzo A
AD  - Vascular Physiopathology Unit IRCCS, INM Neuromed, Pozzilli, IS, Italy.
FAU - Vecchione, Carmine
AU  - Vecchione C
AD  - Department of Medicine and Surgery, University of Salerno, Salerno, Italy.
LA  - eng
PT  - Journal Article
DEP - 20170307
PL  - England
TA  - BMC Gastroenterol
JT  - BMC gastroenterology
JID - 100968547
RN  - EC 1.14.13.39 (NOS3 protein, human)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
SB  - IM
MH  - Adult
MH  - Animals
MH  - Aorta/metabolism
MH  - Biopsy
MH  - Blood Platelets/metabolism
MH  - Case-Control Studies
MH  - Fatty Liver/pathology/physiopathology
MH  - Female
MH  - Humans
MH  - Insulin Resistance
MH  - Liver/*blood supply/pathology
MH  - Male
MH  - Mice
MH  - Middle Aged
MH  - Nitric Oxide Synthase Type III/*metabolism
MH  - Non-alcoholic Fatty Liver Disease/*enzymology/pathology/*physiopathology
MH  - Phosphorylation
MH  - Prospective Studies
MH  - *Vasodilation
PMC - PMC5340006
OTO - NOTNLM
OT  - Endothelial dysfunction
OT  - Insulin resistance
OT  - Metabolic syndrome
OT  - Non-alcoholic fatty liver disease
EDAT- 2017/03/08 06:00
MHDA- 2017/03/11 06:00
CRDT- 2017/03/08 06:00
PHST- 2016/10/09 [received]
PHST- 2017/03/01 [accepted]
AID - 10.1186/s12876-017-0592-y [doi]
AID - 10.1186/s12876-017-0592-y [pii]
PST - epublish
SO  - BMC Gastroenterol. 2017 Mar 7;17(1):35. doi: 10.1186/s12876-017-0592-y.

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