Early adaptive thermogenesis is a determinant of weight loss after six weeks of caloric restriction in overweight subjects.
Caloric restriction
Energy balance
Energy metabolism
Obesity
Thermogenesis
Weight loss
Journal
Metabolism: clinical and experimental
ISSN: 1532-8600
Titre abrégé: Metabolism
Pays: United States
ID NLM: 0375267
Informations de publication
Date de publication:
09 2020
09 2020
Historique:
received:
03
04
2020
revised:
22
06
2020
accepted:
25
06
2020
pubmed:
1
7
2020
medline:
9
10
2020
entrez:
30
6
2020
Statut:
ppublish
Résumé
Adaptive thermogenesis during prolonged energy deficit refers to the greater than expected reduction in energy expenditure (EE) independent of concomitant loss of metabolically active body mass. As inter-individual variability in the magnitude of adaptive thermogenesis may influence the extent of energy deficit thereby predicting the amount of weight reduction, we investigated whether early adaptive thermogenesis is a determinant of weight loss after 6 weeks of daily 50% caloric restriction in an inpatient setting. The current study reports the results of an exploratory, secondary analysis in overweight but otherwise healthy subjects (n = 11, 7 men, 35 ± 9y, BMI = 40 ± 7 kg/m The magnitude of adaptive thermogenesis in 24hEE after 1 week of caloric restriction was -178 ± 137 kcal/day (mean ± SD), was overall stable during and following caloric restriction, and demonstrated remarkable intra-individual consistency. A relatively greater decrease in 24hEE of 100 kcal/d after 1 week of caloric restriction was associated on average with reduced energy deficit by 8195 kcal over 6 weeks and predicted 2.0 kg less weight loss, of which 0.5 kg was fat mass, after 6 weeks. No correlations were found between hormonal concentrations and weight loss. The extent of weight loss is influenced by the magnitude of adaptive thermogenesis in the early stage of caloric restriction. Although these results need replication in larger study groups with adequate statistical power, targeting adaptive thermogenesis may help to optimize long-term interventions in obesity therapy.
Sections du résumé
BACKGROUND
Adaptive thermogenesis during prolonged energy deficit refers to the greater than expected reduction in energy expenditure (EE) independent of concomitant loss of metabolically active body mass.
OBJECTIVE
As inter-individual variability in the magnitude of adaptive thermogenesis may influence the extent of energy deficit thereby predicting the amount of weight reduction, we investigated whether early adaptive thermogenesis is a determinant of weight loss after 6 weeks of daily 50% caloric restriction in an inpatient setting.
DESIGN AND METHODS
The current study reports the results of an exploratory, secondary analysis in overweight but otherwise healthy subjects (n = 11, 7 men, 35 ± 9y, BMI = 40 ± 7 kg/m
RESULTS
The magnitude of adaptive thermogenesis in 24hEE after 1 week of caloric restriction was -178 ± 137 kcal/day (mean ± SD), was overall stable during and following caloric restriction, and demonstrated remarkable intra-individual consistency. A relatively greater decrease in 24hEE of 100 kcal/d after 1 week of caloric restriction was associated on average with reduced energy deficit by 8195 kcal over 6 weeks and predicted 2.0 kg less weight loss, of which 0.5 kg was fat mass, after 6 weeks. No correlations were found between hormonal concentrations and weight loss.
CONCLUSIONS
The extent of weight loss is influenced by the magnitude of adaptive thermogenesis in the early stage of caloric restriction. Although these results need replication in larger study groups with adequate statistical power, targeting adaptive thermogenesis may help to optimize long-term interventions in obesity therapy.
Identifiants
pubmed: 32599082
pii: S0026-0495(20)30167-0
doi: 10.1016/j.metabol.2020.154303
pmc: PMC7484122
mid: NIHMS1607484
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
154303Subventions
Organisme : Intramural NIH HHS
ID : ZIA DK069029
Pays : United States
Informations de copyright
Published by Elsevier Inc.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare no conflict of interest.
Références
Int J Obes Relat Metab Disord. 1996 May;20(5):393-405
pubmed: 8696417
Am J Clin Nutr. 1970 Sep;23(9):1212-9
pubmed: 5450839
Int J Obes (Lond). 2018 Jun;42(5):974-984
pubmed: 29777235
J Clin Invest. 1986 Dec;78(6):1568-78
pubmed: 3782471
Am J Clin Nutr. 1991 Jun;53(6):1368-71
pubmed: 2035463
Curr Obes Rep. 2016 Dec;5(4):413-423
pubmed: 27739007
J Clin Endocrinol Metab. 2002 May;87(5):2391-4
pubmed: 11994393
Obes Rev. 2011 May;12(5):e348-61
pubmed: 20524998
N Engl J Med. 2017 Jan 19;376(3):254-266
pubmed: 28099824
Obesity (Silver Spring). 2016 Aug;24(8):1610-1
pubmed: 27460710
Diabetes. 2015 Aug;64(8):2859-67
pubmed: 25964395
Ann N Y Acad Sci. 2000 May;904:359-65
pubmed: 10865771
Eur J Clin Nutr. 1995 Jan;49(1):1-10
pubmed: 7713045
J Clin Endocrinol Metab. 2012 Jul;97(7):2489-96
pubmed: 22535969
Obesity (Silver Spring). 2012 Dec;20(12):2384-9
pubmed: 22627912
Am J Physiol Endocrinol Metab. 2010 Mar;298(3):E449-66
pubmed: 19934407
Int J Obes (Lond). 2013 Jun;37(6):759-64
pubmed: 22846776
Int J Obes. 1982;6(1):23-8
pubmed: 7068313
Obes Rev. 2012 Dec;13 Suppl 2:105-21
pubmed: 23107264
Am J Physiol Endocrinol Metab. 2006 Jul;291(1):E23-37
pubmed: 16449298
JAMA. 2012 Jun 27;307(24):2627-34
pubmed: 22735432
Am J Clin Nutr. 2015 Oct;102(4):807-19
pubmed: 26399868
Am J Clin Nutr. 2019 Sep 1;110(3):593-604
pubmed: 31172178
Am J Clin Nutr. 1979 Aug;32(8):1570-4
pubmed: 463798
Int J Obes Relat Metab Disord. 1994 Jan;18(1):35-40
pubmed: 8130813
Br J Nutr. 1999 Nov;82(5):339-56
pubmed: 10673906
Lancet. 2011 Aug 27;378(9793):826-37
pubmed: 21872751
Am J Clin Nutr. 1995 Mar;61(3):486-94
pubmed: 7872211
Obesity (Silver Spring). 2016 Aug;24(8):1620-9
pubmed: 27460711
Int J Obes (Lond). 2010 Oct;34 Suppl 1:S47-55
pubmed: 20935667
Obesity (Silver Spring). 2019 May;27(5):691-699
pubmed: 31012296
Diabetes. 2013 Dec;62(12):4043-51
pubmed: 23974925
J Clin Endocrinol Metab. 2013 Apr;98(4):E703-7
pubmed: 23418317
IEEE Eng Med Biol Mag. 2010 Jan-Feb;29(1):36-41
pubmed: 20176520
Diabetes. 2017 Aug;66(8):2284-2295
pubmed: 28476931
J Biol Chem. 1953 Jul;203(1):359-66
pubmed: 13069519
Obesity (Silver Spring). 2013 Feb;21(2):218-28
pubmed: 23404923
J Appl Physiol (1985). 1991 Mar;70(3):994-7
pubmed: 2033014
Diabetes Care. 2003 Jan;26 Suppl 1:S5-20
pubmed: 12502614
J Biol Chem. 1956 Dec;223(2):969-75
pubmed: 13385244
Int J Obes (Lond). 2013 Oct;37(10):1371-7
pubmed: 23381557
Am J Physiol. 1988 Sep;255(3 Pt 1):E332-7
pubmed: 3421330
Am J Clin Nutr. 2018 Apr 1;107(4):558-565
pubmed: 29635495
Am J Clin Nutr. 1988 Apr;47(4):608-28
pubmed: 3281434
JAMA. 2006 Apr 5;295(13):1539-48
pubmed: 16595757
J Clin Epidemiol. 2001 Apr;54(4):343-9
pubmed: 11297884
Obesity (Silver Spring). 2016 Aug;24(8):1612-9
pubmed: 27136388
Lancet. 1979 Jan;1(8107):77-9
pubmed: 84131