Baseline HOMA IR and Circulating FGF21 Levels Predict NAFLD Improvement in Patients Undergoing a Low Carbohydrate Dietary Intervention for Weight Loss: A Prospective Observational Pilot Study.
Adolescent
Adult
Biomarkers
/ blood
Caloric Restriction
Diet, Carbohydrate-Restricted
Diet, Ketogenic
Fatty Acids, Omega-3
/ administration & dosage
Female
Fibroblast Growth Factors
/ administration & dosage
Humans
Insulin Resistance
Male
Middle Aged
Non-alcoholic Fatty Liver Disease
/ diagnosis
Nutritional Physiological Phenomena
/ physiology
Obesity
/ complications
Observational Studies as Topic
Pilot Projects
Predictive Value of Tests
Prospective Studies
Weight Loss
Young Adult
fibroblast growth factor 21
hepatic steatosis
insulin resistance
ketogenic diet
non-alcoholic fatty liver disease
obesity
very low carbohydrate diet
very low energy diet
very low-calorie diet
very low-calorie ketogenic diet
weight loss
Journal
Nutrients
ISSN: 2072-6643
Titre abrégé: Nutrients
Pays: Switzerland
ID NLM: 101521595
Informations de publication
Date de publication:
18 Jul 2020
18 Jul 2020
Historique:
received:
16
06
2020
revised:
07
07
2020
accepted:
15
07
2020
entrez:
26
7
2020
pubmed:
28
7
2020
medline:
16
3
2021
Statut:
epublish
Résumé
Non-alcoholic fatty liver disease (NAFLD) is a major cause of liver disease. Very low-calorie ketogenic diets (VLCKD) represent a feasible treatment as they induce profound weight loss and insulin resistance (IR) improvement. Despite the recognized benefits on NAFLD deriving from pharmacological administration of fibroblast growth factor 21 (FGF21), whose endogenous counterpart is a marker of liver injury, little is known about its physiology in humans. To identify predictors of NAFLD improvement as reflected by the reduction of the non-invasive screening tool hepatic steatosis index (HSI) in obese patients undergoing a weight loss program. Sixty-five obese patients underwent a 90-day dietary program consisting of a VLCKD followed by a hypocaloric low carbohydrate diet (LCD). Anthropometric parameters, body composition, and blood and urine chemistry were assessed. Unlike most parameters improving mainly during the VLCKD, the deepest HSI change was observed after the LCD ( We suggest that patients with IR and NAFLD derive greater benefit from a VLCKD, and we propose a possible role of human FGF21 in mediating NAFLD amelioration following nutritional manipulation.
Sections du résumé
BACKGROUND
BACKGROUND
Non-alcoholic fatty liver disease (NAFLD) is a major cause of liver disease. Very low-calorie ketogenic diets (VLCKD) represent a feasible treatment as they induce profound weight loss and insulin resistance (IR) improvement. Despite the recognized benefits on NAFLD deriving from pharmacological administration of fibroblast growth factor 21 (FGF21), whose endogenous counterpart is a marker of liver injury, little is known about its physiology in humans.
AIM
OBJECTIVE
To identify predictors of NAFLD improvement as reflected by the reduction of the non-invasive screening tool hepatic steatosis index (HSI) in obese patients undergoing a weight loss program.
METHODS
METHODS
Sixty-five obese patients underwent a 90-day dietary program consisting of a VLCKD followed by a hypocaloric low carbohydrate diet (LCD). Anthropometric parameters, body composition, and blood and urine chemistry were assessed.
RESULTS
RESULTS
Unlike most parameters improving mainly during the VLCKD, the deepest HSI change was observed after the LCD (
CONCLUSIONS
CONCLUSIONS
We suggest that patients with IR and NAFLD derive greater benefit from a VLCKD, and we propose a possible role of human FGF21 in mediating NAFLD amelioration following nutritional manipulation.
Identifiants
pubmed: 32708435
pii: nu12072141
doi: 10.3390/nu12072141
pmc: PMC7400878
pii:
doi:
Substances chimiques
Biomarkers
0
Fatty Acids, Omega-3
0
fibroblast growth factor 21
0
Fibroblast Growth Factors
62031-54-3
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Références
Nutrients. 2020 Jan 27;12(2):
pubmed: 32012661
F1000Res. 2018 Mar 7;7:289
pubmed: 29983922
Annu Rev Physiol. 2016;78:223-41
pubmed: 26654352
Nat Med. 2018 Jul;24(7):908-922
pubmed: 29967350
Diabetes. 2010 Nov;59(11):2781-9
pubmed: 20682689
J Clin Endocrinol Metab. 2020 Sep 1;105(9):
pubmed: 32484877
Lipids Health Dis. 2017 Oct 16;16(1):203
pubmed: 29037210
J Postgrad Med. 2017 Oct-Dec;63(4):242-251
pubmed: 29022562
J Gastroenterol. 2018 Mar;53(3):362-376
pubmed: 29247356
Methodist Debakey Cardiovasc J. 2017 Jan-Mar;13(1):20-24
pubmed: 28413578
Obesity (Silver Spring). 2013 Nov;21(11):2221-4
pubmed: 23794256
Am J Hypertens. 2012 Oct;25(10):1131-7
pubmed: 22785405
Front Psychol. 2015 Feb 02;6:27
pubmed: 25698989
Obes Rev. 2020 Jul 10;:
pubmed: 32648647
Diabetes Metab Syndr Obes. 2012;5:395-401
pubmed: 23152692
J Hepatol. 2016 Jun;64(6):1388-402
pubmed: 27062661
Proc Natl Acad Sci U S A. 2020 Mar 31;117(13):7347-7354
pubmed: 32179679
Obesity (Silver Spring). 2019 Jun;27(6):971-981
pubmed: 31067015
Clin Endocrinol (Oxf). 2014 Dec;81(6):862-70
pubmed: 24841294
PLoS One. 2018 Aug 28;13(8):e0202683
pubmed: 30153310
Mol Metab. 2017 Nov;6(11):1395-1406
pubmed: 29107287
N Engl J Med. 2014 Sep 18;371(12):1131-41
pubmed: 25229917
Mol Metab. 2014 Oct 08;4(1):51-7
pubmed: 25685689
Int J Obes (Lond). 2019 Jan;43(1):139-148
pubmed: 29717276
Cell Metab. 2018 Mar 6;27(3):559-571.e5
pubmed: 29456073
World J Gastroenterol. 2010 Oct 14;16(38):4773-83
pubmed: 20939105
Diabetes Care. 2016 May;39(5):808-15
pubmed: 27002059
Ann Hepatol. 2020 Jul - Aug;19(4):359-366
pubmed: 32349939
Drug Discov Ther. 2015 Dec;9(6):380-5
pubmed: 26781921
Curr Cardiol Rep. 2020 Mar 12;22(4):25
pubmed: 32166448
Dis Model Mech. 2009 May-Jun;2(5-6):231-7
pubmed: 19407331
Nutrients. 2018 May 09;10(5):
pubmed: 29747432
Nutrients. 2018 Aug 23;10(9):
pubmed: 30142943
Int J Obes (Lond). 2017 Oct;41(10):1570-1578
pubmed: 28588304
Nutr Metab Cardiovasc Dis. 2010 Sep;20(7):481-90
pubmed: 20659791
Eat Weight Disord. 2020 May 25;:
pubmed: 32451949
Physiol Rev. 2013 Jan;93(1):359-404
pubmed: 23303913
Br Dent J. 2019 Aug;227(3):235-239
pubmed: 31399683
Clin Gastroenterol Hepatol. 2018 Dec;16(12):1974-1982.e7
pubmed: 29104128
J Nutr. 2000 Jul;130(7):1865S-7S
pubmed: 10867064
J Transl Med. 2019 Oct 29;17(1):356
pubmed: 31665015
Int J Food Sci Nutr. 2016 Sep;67(6):696-706
pubmed: 27193396
Int J Environ Res Public Health. 2016 May 28;13(6):
pubmed: 27240395
Gastroenterology. 2019 Apr;156(5):1264-1281.e4
pubmed: 30660725
Obesity (Silver Spring). 2006 Jan;14(1):115-21
pubmed: 16493129
Hepatol Int. 2017 Jan;11(1):70-78
pubmed: 27783208
Cell Metab. 2007 Jun;5(6):426-37
pubmed: 17550778
Endocrine. 2020 Jan;67(1):95-108
pubmed: 31728756
Diabetes Care. 2010 Oct;33(10):2156-63
pubmed: 20664019
Obes Rev. 2020 Aug;21(8):e13024
pubmed: 32207237
Dig Liver Dis. 2010 Jul;42(7):503-8
pubmed: 19766548
J Clin Invest. 2015 Nov 03;125(12):4601-11
pubmed: 26529252
Endocrine. 2015 Apr;48(3):863-70
pubmed: 25063307
J Endocrinol Invest. 2019 Nov;42(11):1365-1386
pubmed: 31111407
Nat Rev Endocrinol. 2017 Sep;13(9):509-520
pubmed: 28621339
Atherosclerosis. 2020 Apr;299:38-44
pubmed: 32220662
J Am Diet Assoc. 1995 Jul;95(7):791-7
pubmed: 7797810