Serum leptin in relation to resting energy expenditure and fuel metabolism in obese subjects.
Int J Obes Relat Metab Disord
; 21(4): 309-13, 1997 Apr.
Article
em En
| MEDLINE
| ID: mdl-9130029
OBJECTIVE: Leptin is the product of ob gene shown to regulate body fat in mice. It is produced by human adipose tissue as well, but its physiological functions in man are not known. We explored if there is a relationship in obese humans with serum leptin and energy and fuel metabolism. DESIGN: Cross-sectional study including 45 obese (10 men, 35 women; age and body mass index: 42 +/- 7 y and 35.1 +/- 3.6 kg/m2, respectively). MEASUREMENTS: Food intake by a four-day-food record, blood samples for serum leptin concentrations and resting energy expenditure by indirect calorimetry. RESULTS: Leptin concentrations showed an inverse association (adjusted for fat mass, age and sex) with resting energy expenditure, respiratory quotient and carbohydrate oxidation rate (r = -0.324, P < 0.05; r = -0.420, P < 0.01; r = 0.478, P = < 0.01, respectively), and interestingly, also with dietary fat intake (unadjusted r = -0.30, P < 0.05). Especially, leptin concentrations were elevated in those with low resting energy expenditure and respiratory quotient (below the median). CONCLUSION: Serum leptin concentrations in obese subjects showed an inverse association with resting energy expenditure, respiratory quotient and carbohydrate oxidation rate. The physiological significance of these associations is unclear at the moment but could indicate that obese subjects show resistance to the actions of leptin also outside the brain in terms of regulating metabolic rate and fuel metabolism.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Consumo de Oxigênio
/
Proteínas
/
Metabolismo Energético
/
Obesidade
Tipo de estudo:
Etiology_studies
/
Health_economic_evaluation
/
Incidence_studies
/
Observational_studies
/
Prevalence_studies
/
Risk_factors_studies
Limite:
Adult
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Female
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Humans
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Male
/
Middle aged
Idioma:
En
Revista:
Int J Obes Relat Metab Disord
Ano de publicação:
1997
Tipo de documento:
Article
País de afiliação:
Finlândia
País de publicação:
Reino Unido