A low visceral fat proportion, independent of total body fat mass, protects obese adolescent girls against fatty liver and glucose dysregulation: a longitudinal study.
Journal
International journal of obesity (2005)
ISSN: 1476-5497
Titre abrégé: Int J Obes (Lond)
Pays: England
ID NLM: 101256108
Informations de publication
Date de publication:
04 2019
04 2019
Historique:
received:
03
02
2018
accepted:
29
08
2018
revised:
13
08
2018
pubmed:
20
10
2018
medline:
12
3
2020
entrez:
20
10
2018
Statut:
ppublish
Résumé
The relative proportion of visceral fat (VAT) to subcutaneous fat (SAT) has been described as a major determinant of insulin resistance (IR). Our study sought to evaluate the effect of body fat distribution on glucose metabolism and intrahepatic fat content over time in a multiethnic cohort of obese adolescents. We examined markers of glucose metabolism by oral glucose tolerance test, and body fat distribution by abdominal MRI at baseline and after 19.2 ± 11.4 months in a cohort of 151 obese adolescents (88 girls, 63 boys; mean age 13.3 ± 3.4 years; mean BMI z-score 2.15 ± 0.70). Hepatic fat content was assessed by fast-gradient MRI in a subset of 93 subjects. We used the median value of VAT/(VAT + SAT) ratio within each gender at baseline to stratify our sample into high and low ratio groups (median value 0.0972 in girls and 0.118 in boys). Female subjects tended to remain in their VAT/(VAT + SAT) category over time (change over follow-up P = 0.14 among girls, and P = 0.04 among boys). Baseline VAT/(VAT + SAT) strongly predicted the hepatic fat content, fasting insulin, 2-h glucose, and whole-body insulin sensitivity index at follow-up among girls, but not in boys. The VAT/(VAT + SAT) ratio is a major determinant of impaired glucose metabolism and hepatic fat accumulation over time, and its effects are more pronounced in girls than in boys.
Sections du résumé
BACKGROUND
The relative proportion of visceral fat (VAT) to subcutaneous fat (SAT) has been described as a major determinant of insulin resistance (IR). Our study sought to evaluate the effect of body fat distribution on glucose metabolism and intrahepatic fat content over time in a multiethnic cohort of obese adolescents.
SUBJECTS/METHODS
We examined markers of glucose metabolism by oral glucose tolerance test, and body fat distribution by abdominal MRI at baseline and after 19.2 ± 11.4 months in a cohort of 151 obese adolescents (88 girls, 63 boys; mean age 13.3 ± 3.4 years; mean BMI z-score 2.15 ± 0.70). Hepatic fat content was assessed by fast-gradient MRI in a subset of 93 subjects. We used the median value of VAT/(VAT + SAT) ratio within each gender at baseline to stratify our sample into high and low ratio groups (median value 0.0972 in girls and 0.118 in boys).
RESULTS
Female subjects tended to remain in their VAT/(VAT + SAT) category over time (change over follow-up P = 0.14 among girls, and P = 0.04 among boys). Baseline VAT/(VAT + SAT) strongly predicted the hepatic fat content, fasting insulin, 2-h glucose, and whole-body insulin sensitivity index at follow-up among girls, but not in boys.
CONCLUSIONS
The VAT/(VAT + SAT) ratio is a major determinant of impaired glucose metabolism and hepatic fat accumulation over time, and its effects are more pronounced in girls than in boys.
Identifiants
pubmed: 30337653
doi: 10.1038/s41366-018-0227-6
pii: 10.1038/s41366-018-0227-6
pmc: PMC9354568
mid: NIHMS1826584
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
673-682Subventions
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK111038
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK045735
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD028016
Pays : United States
Organisme : NCRR NIH HHS
ID : UL1 RR024139
Pays : United States
Références
Diabetologia. 2005 Oct;48(10):2090-6
pubmed: 16086140
Nat Genet. 2010 Nov;42(11):949-60
pubmed: 20935629
Diabetologia. 2012 Oct;55(10):2622-2630
pubmed: 22898763
N Engl J Med. 2016 Jun 23;374(25):2430-40
pubmed: 27074389
Mol Cell Endocrinol. 2015 Dec 15;418 Pt 3:306-21
pubmed: 26033249
Pediatr Clin North Am. 2011 Oct;58(5):1241-55, xi
pubmed: 21981958
J Clin Endocrinol Metab. 2004 Mar;89(3):1096-101
pubmed: 15001593
Diabetes. 2008 Feb;57(2):367-71
pubmed: 17977954
J Clin Endocrinol Metab. 1998 Jan;83(1):187-94
pubmed: 9435439
Diabetologia. 1985 Jul;28(7):412-9
pubmed: 3899825
Cardiovasc Diabetol. 2009 Aug 05;8:44
pubmed: 19656356
PLoS Genet. 2012;8(5):e1002695
pubmed: 22589738
Nature. 2015 Feb 12;518(7538):187-196
pubmed: 25673412
Clin Obes. 2014 Apr;4(2):101-7
pubmed: 24683420
J Pediatr. 2012 Nov;161(5):875-80
pubmed: 22703953
Lancet. 2003 Sep 20;362(9388):951-7
pubmed: 14511928
J Clin Endocrinol Metab. 2005 Feb;90(2):747-54
pubmed: 15522932
Ann N Y Acad Sci. 2002 Jun;967:363-78
pubmed: 12079864
J Biol Chem. 2003 Aug 8;278(32):30382-93
pubmed: 12756241
Nature. 2006 Dec 14;444(7121):881-7
pubmed: 17167477
Nat Genet. 2017 Jan;49(1):125-130
pubmed: 27918534
Hepatology. 2009 Jun;49(6):1896-903
pubmed: 19434725
Int J Obes Relat Metab Disord. 2002 Feb;26(2):165-75
pubmed: 11850747
J Clin Endocrinol Metab. 2017 May 1;102(5):1520-1528
pubmed: 28324016
J Clin Endocrinol Metab. 2006 Nov;91(11):4287-94
pubmed: 16912127
Obesity (Silver Spring). 2015 Jul;23(7):1345-52
pubmed: 26054752
PLoS Genet. 2009 Jun;5(6):e1000508
pubmed: 19557161
Mol Cell Endocrinol. 2015 Feb 15;402:113-9
pubmed: 25578600
Am J Clin Nutr. 2010 Nov;92(5):1257-64
pubmed: 20861173
Horm Metab Res. 2002 Nov-Dec;34(11-12):731-6
pubmed: 12660891
Magn Reson Med. 2008 Mar;59(3):521-7
pubmed: 18306404
Mol Aspects Med. 2013 Feb;34(1):1-11
pubmed: 23068073
Diabetes. 2010 Sep;59(9):2288-96
pubmed: 20805387
Arch Dis Child. 1976 Mar;51(3):170-9
pubmed: 952550