Obesity and cortisol

Björntorp, Per; Rosmond, Roland

doi:10.1016/s0899-9007(00)00422-6

Cited by 514 publications

(396 citation statements)

References 96 publications

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“…49 Preliminary human studies have shown an inverse association between birth weight and both basal cortisol and adrenal responsivity to ACTH in adults. 50 Animal models show that exposure to a variety of stressors during pregnancy, including malnutrition, also results in the birth of offspring with elevated basal or stress-induced glucocorticoids.…”

Section: Animal Models For Programming Of Obesitymentioning

confidence: 99%

Programming of obesity and cardiovascular disease

2004

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BACKGROUND: There is evidence that malnutrition in early life induces a growth retardation leading, in adult life, to manifest components of the metabolic syndrome. However, the impact on obesity seems less clearly established. OBJECTIVE: To review the effects of foetal and postnatal malnutrition on the programming of obesity in the context of the metabolic syndrome, as well as the link between central obesity and cardiovascular diseases. METHODS: Included in the review were recent papers exploring the mechanisms linking maternal nutrition with impaired foetal growth and later obesity, cardiovascular disease, hypertension and diabetes in humans and animals. RESULTS: The programming of obesity during foetal and early postnatal life depends of the timing of maternal malnutrition as well as the postnatal environment. Obesity arises principally in offspring submitted to malnutrition during early stages of gestation and which presented early catch-up growth. The programming may involve the dysregulation of appetite control or the hormonal environment leading to a context favourable to obesity development (hypersecretion of corticosteroids, hyperinsulinaemia and hyperleptinaemia and anomalies in the IGF axis). Adipose tissue secretes actively several factors implicated in inflammation, blood pressure, coagulation and fibrinolysis. The programmed development of intra-abdominal obesity after early growth restriction may thus favour higher prevalence of hypertension and cardiovascular diseases. CONCLUSIONS: Abdominal obesity appears in malnourished offspring and is aggravated by early catch-up growth. Higher rates of intra-abdominal obesity observed after growth restriction may participate to hypertension and create atherothrombotic conditions leading to the development of cardiovascular diseases.

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Section: Animal Models For Programming Of Obesitymentioning

confidence: 99%

Programming of obesity and cardiovascular disease

2004

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“…9 Obesity seems to be followed by various signs of hypothalamic dysfunctions, similar to those observed in rodents, but usually to a lesser degree. 10 Alterations in cortisol concentrations in obesity are related to central obesity. 11 Rosmond et al 12 found positive correlations with abdominal circumference and sagittal-abdominal diameter, and more importantly, with some metabolic variables, such as triglycerides, insulin, HDL cholesterol (inverse proportion), IGF-1 and with blood pressure, i.e., with parameters indicative of the metabolic syndrome (MS).…”

Section: Introductionmentioning

confidence: 99%

Plaqueta e leptina em adolescentes com obesidade

Foschini¹,

Santos²,

Prado³

et al. 2008

J. Pediatr. (Rio J.)

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Objective: To analyze the influence of obesity status on immune cell count and concentration of the hormones cortisol and leptin, in order to establish a relationship among the variables analyzed. Methods:We recruited 27 obese [body mass index (BMI) ≥ 95th percentile] and 21 non-obese (BMI ≤ 75th percentile) adolescent boys and girls, aged 15-19 years at the post-pubertal stage. BMI was calculated as body weight divided by height squared, and body composition was estimated by plethysmography in the Bod Pod TM system. Blood samples were collected to analyze leukocytes, neutrophils, lymphocytes, monocytes, platelets, cortisol, and leptin.The Kolmogorov-Smirnov test was performed, followed by the independent Student t test in case of normal distribution.Significance values were set at p < 0.05 and expressed as means ± standard deviation. The statistical package SPSS for Windows version 12.0 was used.Results: There was no difference between obese and non-obese adolescents in terms of leukocyte, neutrophil, lymphocyte, monocyte and cortisol serum concentrations. The group of obese adolescents presented higher platelet and leptin concentrations (p < 0.01). The prevalence of hyperleptinemia was 25.92% in the obese adolescents (15.38% in boys and 35.7% in girls). Conclusions:Obese adolescents have higher platelet and leptin concentrations in comparison with non-obese adolescents. It was also found that obese girls presented a higher prevalence of hyperleptinemia than obese boys.

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“…5,6 Glucocorticoids have been proposed to play a role both in programming the fetus to develop the metabolic syndrome 7 and in causing this syndrome in the adult. 8 Moreover, glucocorticoid exposure during late gestation has been linked to b-cell dysfunction and impaired insulin secretion in adult life. 9 High fetal glucocorticoid levels in the small baby syndrome may result from decreased expression of type 2 11b-hydroxysteroid dehydrogenase (11b-HSD2) in the placenta.…”

Section: Introductionmentioning

confidence: 99%

Modulation of susceptibility to weight gain and insulin resistance in low birthweight rats by treatment of their mothers with leptin during pregnancy and lactation

et al. 2003

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OBJECTIVES:To investigate whether administration of leptin to rats during pregnancy and lactation affects placental 11b-hydroxysteroid dehydrogenase (11b-HSD2) activity and the susceptibility of their offspring to weight gain and insulin resistance. DESIGN: Pregnant rats fed on a low-protein diet were administered leptin or saline by subcutaneous minipump from day 14 of gestation and throughout lactation. A further group was fed a normal diet and given saline. After weaning, the offspring of each group were fed on a normal diet until 6 weeks of age and then half of each group was transferred to a high-fat diet until 12 months of age. RESULTS: Plasma leptin levels were raised two-fold on days 16-18 of pregnancy in the leptin-treated dams, but, despite a constant rate of infusion, at parturition they dipped to control levels before rising again. The activity of placental 11b-HSD2 was reduced by the low-protein diet; this reduction was prevented by treating the dams with leptin. The male offspring of the salinetreated dams gained more weight and had higher plasma leptin levels on the high fat than the chow diet, but the offspring of the leptin-treated dams did not. Fasting blood glucose and intraperitoneal glucose tolerance at 6 and 12 months of age was unaffected by the high-fat diet, but only the offspring of the leptin-treated dams achieved this control without raised insulin levels. CONCLUSIONS: The rate of leptin clearance appears to increase at parturition. The administration of leptin to rats during late pregnancy and lactation makes their male offspring less susceptible to high-fat-diet-induced weight gain and insulin resistance.

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Obesity and cortisol

Cited by 514 publications

References 96 publications

Programming of obesity and cardiovascular disease

Programming of obesity and cardiovascular disease

Plaqueta e leptina em adolescentes com obesidade

Modulation of susceptibility to weight gain and insulin resistance in low birthweight rats by treatment of their mothers with leptin during pregnancy and lactation

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