Leptin concentrations do not predict weight gain: The Mexico City Diabetes Study

Haffner, S M; Mykkänen, LA; Gonzalez, CC; Mp, Stern

doi:10.1038/sj.ijo.0800619

Cited by 39 publications

(36 citation statements)

References 18 publications

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“…No differences between weight-gaining subjects and weight-stable subjects in baseline leptin or leptin adjusted for FM were found. This is in accordance with two studies (Haffner et al 1998, Nagy et al 1998) but contrasts with the findings in 36 Pima Indians by Ravussin et al (1997), where relatively low levels of leptin were preceding weight gain. However, the Pima Indians were very obese and the weight gain considerably faster compared with the subjects in the present study (>3·0 kg/year).…”

Section: Weight-stable (N=33) Weight-gain (N=56)supporting

confidence: 89%

Hormone replacement therapy affects body composition and leptin differently in obese and non-obese postmenopausal women

Kristensen

Pedersen²,

Vestergaard³

et al. 1999

Journal of Endocrinology

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Leptin and oestrogen are both involved in the regulation of adipose tissue deposition and feeding behaviour. We investigated whether 5 years of hormone replacement therapy (HRT) affected serum leptin and body composition differently in 89 postmenopausal women treated with HRT compared with 178 controls. At baseline, leptin was significantly correlated with oestradiol (r=0·13, P<0·05) and in multiple backward regression analysis including oestradiol and any estimate of body fat, oestradiol remained a significant determinant of leptin levels. In the control group, all estimates of body fat determined by dual energy X-ray absorptiometry (DEXA) or anthropometry were increased (3·6-16·9%) and leptin increased 31·3% (16·03 1·02 to 20·84 1·2 ng/ml (...), P<0·001). In the HRT group all estimates of body composition also increased during the 5-year observation but to a lesser extent than observed in the control group (1·0-8·5%). Leptin was raised by 19·7% (17·81 1·32 to 20·57 1·65 ng/ml, P<0·001). However, the DEXA scans revealed that the control group gained 2·4-fold more fat during the 5-year observation (1·9 0·3 vs 0·8 0·4 kg, P<0·05), and especially the trunk fat increased (1·4 0·2 vs 0·7 0·3 kg, P<0·05). This was reflected in the increase in leptin levels, which were increased by 7·4% in the control group compared with the HRT group (4·81 0·60 vs 2·76 0·87 ng/ml, P<0·05). Adjusting for the difference in adipose tissue revealed that HRT had no independent effect on leptin levels. Comparisons between obese (body mass index>25 kg/m 2 ) and non-obese (<25 kg/m 2 ) subjects by stratifying for HRT treatment using multiple linear regression revealed that the change in fat mass was significantly less among treated subjects (P=0·038) and especially in the non-obese subjects (P=0·001). The change in trunk fat was similarly correlated with treatment status (P=0·029) and with the degree of obesity (P=0·006). In conclusion, 5 years of HRT treatment significantly reduced fat mass accumulation, especially in the trunk region. This effect of HRT was more pronounced in non-obese as compared with obese subjects. The HRT-induced reduction in fat mass seems not to be mediated by leptin.

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Section: Weight-stable (N=33) Weight-gain (N=56)supporting

confidence: 89%

Hormone replacement therapy affects body composition and leptin differently in obese and non-obese postmenopausal women

Kristensen

Pedersen²,

Vestergaard³

et al. 1999

Journal of Endocrinology

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“…Normal leptin production and action are also critical for the long-term regulation of energy balance in humans subjects, as was convincingly demonstrated by the hyperphagia and obesity in human subjects with mutations in the genes encoding leptin (Montague et al 1997;Strobel et al 1998) or the leptin receptor (Clement et al 1998). Relative deficiency of leptin has been suggested to predict future weight gain in human subjects (Ravussin et al 1996;Matkovic et al 1997) and rodents (Surwit et al 1997;Ahren, 1999); however, such a predictive value has not been observed in all populations examined (Chessler et al 1998;Haffner et al 1998). Ahima et al (1996) reported that leptin administration in mice prevented the decreases in reproductive and thyroid hormones and the activation of the hypothalamic-pituitary-adrenal axis observed in response to fasting.…”

Section: Consequences Of Decreased Leptin Productionmentioning

confidence: 99%

Role of adipose tissue in body-weight regulation: mechanisms regulating leptin production and energy balance

2000

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Adipose tissue performs complex metabolic and endocrine functions. Among the endocrine products produced by adipose tissue are tumour necrosis factor α, interleukin 6, acylationstimulating protein and leptin. The present review will focus primarily on mechanisms regulating leptin production and leptin action, and the implications of this regulation in the control of energy balance. Leptin acts in the central nervous system where it interacts with a number of hypothalamic neuropeptide systems to regulate feeding behaviour and energy expenditure. The presence of extreme obesity in animals and human subjects with mutations of the leptin gene or the leptin receptor demonstrates that normal leptin production and action are critical for maintaining energy balance. Insulin is the major regulator of leptin production by adipose tissue. Insulin infusions increase circulating leptin concentrations in human subjects. Plasma leptin levels are markedly decreased in insulin-deficient diabetic rodents, and the low leptin levels contribute to diabetic hyperphagia. Based on in vitro studies, the effect of insulin to stimulate leptin production appears to involve increased glucose metabolism. Blockade of glucose transport or glycolysis inhibits leptin expression and secretion in isolated adipocytes. Evidence suggests that anaerobic metabolism of glucose to lactate does not stimulate leptin production. Alterations in insulin-mediated glucose metabolism in adipose tissue are likely to mediate the effects of energy restriction to decrease, and refeeding to increase, circulating leptin levels. Changes in glucose metabolism may also explain the observation that high-fat meals lower 24 h circulating leptin levels relative to high-carbohydrate meals in human subjects, suggesting a mechanism that may contribute to the effects that high-fat diets have in promoting increased energy intake, weight gain and obesity. The decreased circulating leptin observed during energy restriction is related to increased sensations of hunger in human subjects. Thus, decreases in leptin during energyrestricted weight-loss regimens may contribute to the strong propensity for weight regain. A better understanding of the precise mechanisms regulating leptin production and leptin action may lead to new approaches for managing obesity.

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“…This absence of correlation seems to be consistent in many ethnic backgrounds. In the Mexico City Diabetes Study, 39 180 non-diabetic men and women were followed over a 3-year period with no relationship found between leptin levels and weight gain. In Mauritius, Hodge et al 40 has shown no association between leptinemia and weight gain in 2888 individuals over a 5-year follow-up period.…”

Section: Entero-insular and Adipose Tissue Factors In Weight Gain M-fmentioning

confidence: 99%

The entero-insular axis and adipose tissue-related factors in the prediction of weight gain in humans

2006

Int J Obes

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Obesity has now reached epidemic proportions. Epidemiological studies in the past decades have shown that adults gain weight and adiposity from the early twenties until their sixties. In the paediatric population, growing numbers of children and adolescents put on unhealthy weight. Many environmental, socio-economical and biological determinants that predispose to weight gain have been identified thus far. The aim of the present review is to summarize the current knowledge on the role of the circulating levels of adipokines and other entero-insular hormones and biological markers of obesity to predict weight gain in humans. The review focuses on relationship between hormonal and biochemical markers (insulin, insulin-like growth factors, gastrointestinal hormones, leptin, adiponectin, resistin, inflammatory proteins and cytokines) and weight gain in prospective studies. The complex relationships displayed by these hormonal factors with future weight gain in humans are critically reviewed and integrative models are proposed. Overall, most of the studies reported to date made adjustments for baseline body mass index but failed to consider dietary intake and physical activity as confounding factors. Outstanding questions are raised and new directions for future prospective studies are proposed in order to improve our understanding of the role of biological determinants of energy balance and development of obesity in humans.

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Leptin concentrations do not predict weight gain: The Mexico City Diabetes Study

Cited by 39 publications

References 18 publications

Hormone replacement therapy affects body composition and leptin differently in obese and non-obese postmenopausal women

Hormone replacement therapy affects body composition and leptin differently in obese and non-obese postmenopausal women

Role of adipose tissue in body-weight regulation: mechanisms regulating leptin production and energy balance

The entero-insular axis and adipose tissue-related factors in the prediction of weight gain in humans

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