Birth weight, adulthood BMI, and subsequent weight gain in relation to leptin levels in Swedish women

Citation
L. Lissner et al., Birth weight, adulthood BMI, and subsequent weight gain in relation to leptin levels in Swedish women, OBES RES, 7(2), 1999, pp. 150-154
Citations number
16
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
OBESITY RESEARCH
ISSN journal
10717323 → ACNP
Volume
7
Issue
2
Year of publication
1999
Pages
150 - 154
Database
ISI
SICI code
1071-7323(199903)7:2<150:BWABAS>2.0.ZU;2-S
Abstract
Objective: Leptin seems to be involved in the regulation of energy balance, although little is known about the epidemiology of leptin with respect to prediction of weight gain and incidence of obesity-related diseases. The du al aim of this study is to document characteristics of leptin after long-te rm storage, and to describe its relation to body weight, from birth to old age, in an ongoing prospective study. Research Methods and Procedures: A population-based sample of Swedish women was first examined at the ages of 38 to 60 and re-examined 24 years later. This study used 1358 frozen serum samples that had been stored 29 years fo r analysis of leptin concentrations and their relation to body weight histo ry. Results. Leptin values obtained from stored samples showed the same correla tion with relative weight as that seen in a contemporary sample with simila r demographic characteristics. Lower self-reported birth weight was associa ted with higher leptin levels in adulthood (p = 0.01), controlling for age and adult BMI. Prospective analyses revealed that high leptin in 38 to 46-y ear-olds predicted subsequent long-term weight gain (p=0.003), although no significant associations were seen in women initially aged 50 or older. Discussion: It is feasible to use frozen serum for studying leptin in relat ion to obesity and related developments many years later. High leptin level was a risk factor for subsequent weight gain in 38- and 46-year-old women. Retrospective analyses involving birth weight suggest that leptin resistan ce in adulthood might have fetal origins.