Association of [
Insulin resistance
Liver fat content
Magnetic resonance imaging
T2DM
Journal
Diabetology & metabolic syndrome
ISSN: 1758-5996
Titre abrégé: Diabetol Metab Syndr
Pays: England
ID NLM: 101488958
Informations de publication
Date de publication:
2020
2020
Historique:
received:
21
02
2020
accepted:
30
05
2020
entrez:
13
6
2020
pubmed:
13
6
2020
medline:
13
6
2020
Statut:
epublish
Résumé
Previous literatures have implied that the liver fat deposition plays a crucial role in the development and progression of insulin resistance. In the present study, we aimed to investigate the association of liver fat content (LFC) with glucose metabolism status in the population of newly diagnosed type 2 diabetes mellitus (nT2DM), prediabetes mellitus (PDM) and normal controls (NC), and assessing if the LFC could as an indicator for the prediction of T2DM. A total of 242 subjects (including 141 nT2DM patients, 48 PDM subjects and 53 NC) were enrolled. The levels of LFC were quantified by using the proton magnetic resonance spectroscopy ([ There were significantly increased LFC levels in nT2DM (14.72% ± 6.37%) than in PDM (9.62% ± 4.41%) and that of NC groups (5.11% ± 3.66%) (all Our study revealed an increased LFC level and prevalence of NAFLD in nT2DM than in PDM and that of NC groups, the increase of LFC was closely associated with insulin resistance and impaired glucose metabolism status, may be regarded as potential indicator contributing to the development and progression of T2DM.
Sections du résumé
BACKGROUND
BACKGROUND
Previous literatures have implied that the liver fat deposition plays a crucial role in the development and progression of insulin resistance. In the present study, we aimed to investigate the association of liver fat content (LFC) with glucose metabolism status in the population of newly diagnosed type 2 diabetes mellitus (nT2DM), prediabetes mellitus (PDM) and normal controls (NC), and assessing if the LFC could as an indicator for the prediction of T2DM.
METHODS
METHODS
A total of 242 subjects (including 141 nT2DM patients, 48 PDM subjects and 53 NC) were enrolled. The levels of LFC were quantified by using the proton magnetic resonance spectroscopy ([
RESULTS
RESULTS
There were significantly increased LFC levels in nT2DM (14.72% ± 6.37%) than in PDM (9.62% ± 4.41%) and that of NC groups (5.11% ± 3.66%) (all
CONCLUSIONS
CONCLUSIONS
Our study revealed an increased LFC level and prevalence of NAFLD in nT2DM than in PDM and that of NC groups, the increase of LFC was closely associated with insulin resistance and impaired glucose metabolism status, may be regarded as potential indicator contributing to the development and progression of T2DM.
Identifiants
pubmed: 32528557
doi: 10.1186/s13098-020-00558-8
pii: 558
pmc: PMC7282165
doi:
Types de publication
Journal Article
Langues
eng
Pagination
51Informations de copyright
© The Author(s) 2020.
Déclaration de conflit d'intérêts
Competing interestsThe authors declare that they have no competing interests.
Références
Am J Physiol Endocrinol Metab. 2005 Feb;288(2):E462-8
pubmed: 15339742
Endocrine. 2017 Jul;57(1):89-97
pubmed: 28508194
Hepatology. 2004 Dec;40(6):1387-95
pubmed: 15565570
Obesity (Silver Spring). 2015 Sep;23(9):1929-37
pubmed: 26239703
Arab J Gastroenterol. 2015 Jun;16(2):54-8
pubmed: 26174761
Top Magn Reson Imaging. 2009 Apr;20(2):89-97
pubmed: 20010063
Diabetes Care. 2018 Jan;41(Suppl 1):S13-S27
pubmed: 29222373
Obesity (Silver Spring). 2011 Sep;19(9):1747-54
pubmed: 21593811
Liver Int. 2009 Jan;29(1):113-9
pubmed: 18384521
Quant Imaging Med Surg. 2013 Aug;3(4):192-5
pubmed: 24040614
Curr Clin Pharmacol. 2008 May;3(2):70-6
pubmed: 18690881
J Hepatol. 2009 Aug;51(2):389-97
pubmed: 19505740
Intern Med. 2012;51(13):1667-75
pubmed: 22790124
Am J Hypertens. 2001 Jan;14(1):51-3
pubmed: 11206679
Clin Liver Dis (Hoboken). 2012 Sep 25;1(4):99-103
pubmed: 31186860
J Clin Transl Hepatol. 2018 Jun 28;6(2):217-221
pubmed: 29951367
Diabetes Care. 2018 Feb;41(2):372-382
pubmed: 29358469
Nat Rev Dis Primers. 2015 Jul 23;1:15019
pubmed: 27189025
Ann Gastroenterol. 2012;25(1):45-51
pubmed: 24713801
Clin Biochem. 2014 Apr;47(6):383-8
pubmed: 24525254
Diabetol Metab Syndr. 2014 Mar 26;6(1):43
pubmed: 24669786
Gastroenterology. 2012 Apr;142(4):711-725.e6
pubmed: 22326434
Gut. 2017 Jun;66(6):1138-1153
pubmed: 28314735
Diabetes Technol Ther. 2011 Feb;13(2):149-55
pubmed: 21284482
Diabetes Care. 1999 Sep;22(9):1462-70
pubmed: 10480510
Trans Am Clin Climatol Assoc. 2008;119:217-23; discussion 223-4
pubmed: 18596860
J Gastroenterol Hepatol. 2016 May;31(5):936-44
pubmed: 26667191
Gastroenterology. 2012 Jun;142(7):1592-609
pubmed: 22656328
Arterioscler Thromb Vasc Biol. 2004 Apr;24(4):644-9
pubmed: 14715643
Nihon Rinsho. 2012 May;70 Suppl 3:459-64
pubmed: 22768565
Aliment Pharmacol Ther. 2013 Mar;37(6):630-9
pubmed: 23383649
Hepatology. 2017 Apr;65(4):1132-1144
pubmed: 27981615
Cell Metab. 2012 May 2;15(5):570-3
pubmed: 22560209
J Endocrinol. 2010 Jan;204(1):1-11
pubmed: 19770178