Leptin and leptin receptor mRNA and protein expression  in the murine fetus and placenta

Hoggard, Nigel; Hunter, Leif; Duncan, J.L.; Williams, Lynda M.; Trayhurn, Paul; Mercer, Julian G.

doi:10.1073/pnas.94.20.11073

Cited by 446 publications

(323 citation statements)

References 24 publications

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“…O receptor Ob-Rb faz parte da família de receptores das citoquinas, ativando o sistema JAK/STAT de transdução do sinal após sua ligação com a leptina (24). A forma longa do receptor foi encontrada nos mais diversos órgãos incluindo pâncreas, rim, medula adrenal, placenta, ovários e tecido adiposo (25)(26)(27). Uma forte presença da expressão do gene do receptor Ob-Rb é vista nos diversos núcleos hipotalâmicos que regulam a ingestão alimentar e o controle do gasto energético (28).…”

Section: Receptor E Mecanismo De Açãounclassified

Leptina: o diálogo entre adipócitos e neurônios

Negrão¹,

Licinio

2000

Arq Bras Endocrinol Metab

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The discovery of leptin led to a renewed interest in the study of enegy homeostasis. It is now recognized that white adipose tissue is the major site of leptin synthesis. After it is secreted into the bloodstream leptin binds itself to specific receptors in the brain, providing the central nervous system with a satiety signal that reflects the amount of energy stored as fat. Acting through receptors that transduce a signal by the JAK/STAT pathway, leptin modifies the expression and activity of hypothalamic peptides that regulate appetite and energy expenditure. In addition, leptin signals nutritional status to other physiological systems and modulates the function of several target glands. More recently, recombinant leptin was successfully given to an obese patient with leptin deficiency due to a mutation in the ob gene. On the other hand, the effects of recombinant leptin in the only study with obese patients and increased levels of circulating leptin were less impressive.Here we review the complexity of leptin actions with a focus on its integrative role as a signal of nutritional status for the organism.

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Section: Receptor E Mecanismo De Açãounclassified

Leptina: o diálogo entre adipócitos e neurônios

Negrão¹,

Licinio

2000

Arq Bras Endocrinol Metab

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“…In fact, the administration of this hormone, while proven to be effective in reducing fat and normalizing metabolic disorders in leptin-deficient mice and humans, has not proven to be effective in most cases of obesity. 4,[8][9][10] Although leptin is mainly produced by the adipose tissue, this hormone is also produced by other tissues, such as stomach, [11][12][13] placenta, 14,15 skeletal muscle 16 and mammary epithelium, 17 and it is naturally present in maternal milk. 18,19 Although leptin produced by the adipose tissue is known to play a main role in the chronic control of energy balance, the role of leptin produced by the stomach has been related with the short-term control of food intake, acting as a satiety signal.…”

Section: Introductionmentioning

confidence: 99%

The intake of physiological doses of leptin during lactation in rats prevents obesity in later life

et al. 2007

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Ciber Fisiopatología obesidad y nutrición (CB06/03) Instituto Salud Carlos III, SpainBackground: There is epidemiological evidence that perinatal nutritional factors may have long-term effects on obesity. Which nutrients or food components are involved in this programming mechanism are unknown. Breast milk contains leptin, a hormone that regulates food intake and energy expenditure, and previous studies in rats have shown that leptin orally administered during lactation exerts anorexigenic effects. Objective: To evaluate whether supplementation with physiological doses of oral leptin during lactation has long-term effects on body weight regulation. Design: A daily oral dose of leptin (equivalent to five times the amount of leptin ingested normally from maternal milk during the suckling period) or the vehicle was given to suckling male rats during lactation. Animals were fed after weaning with a normal fat (NF) or a high-fat (HF) diet. We followed body weight and food intake of animals until the age of 6 months, and measured the size of adipose tissue depots, the thermogenic capacity, the expression of leptin in the stomach and adipose tissues and the expression of two appetite-related peptides (neuropeptide Y (NPY) and proopiomelanocortin (POMC)), leptin receptor (OB-Rb) and suppressor of cytokine signalling 3 (SOCS-3) in the hypothalamus at the age of 6 months. Results: Leptin-treated animals had, in adulthood, lower body weight and fat content and ate fewer calories than their untreated controls. Unlike adipocitary leptin production, adult animals that were leptin-treated during lactation displayed higher gastric leptin production without changes in OB-Rb mRNA levels. In addition, in response to HF diet, leptin-treated animals (contrary to controls) showed lower hypothalamic NPY/POMC mRNA ratio. Hypothalamic OB-Rb mRNA levels decreased in control animals as an effect of HF diet feeding, but remained unchanged in leptin-treated animals; SOCS-3 mRNA levels were lower in leptin-treated animals than in their controls, both under normal or HF diet. Conclusion: The animals that received leptin during lactation become more protected against fat accumulation in adult life and seem to be more sensitive to the short-and long-term regulation of food intake by leptin. Thus, leptin plays an important role in the earlier stages of neonatal life, as a component of breast milk, in the prevention of later obesity.

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“…The other leptin sources include gastric mucosa cells (Bado et al, 1998), mammary epithelial cells (Smith-Kirwin et al, 1998), myocytes (Wang et al, 1998), and the placenta (Senaris et al, 1997). Leptin expression has also been reported in the testes, ovary, and hair follicles (Hoggard et al, 1997). Subsequent studies documented that in addition to its primary function as a regulator of food intake, leptin can affect fetal development, sex maturation, lactation, hematopoiesis, and immune responses (Wauters et al, 2000;Bonnet et al, 2002;Brann et al, 2002;Neville et al, 2002;Goumenou et al, 2003).…”

Section: Leptin and Its Activitiesmentioning

confidence: 99%

Leptin and cancer

Garofalo

Surmacz

2005

Journal Cellular Physiology

539

486

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The prevalence of obesity has markedly increased over the past two decades, especially in the industrialized countries. While the impact of excess body weight on the development of cardiac disease and diabetes has been well documented, the link between obesity and carcinogenesis is just being recognized. This review will focus on the link between leptin, a cytokine that is elevated in obese individuals, and cancer development. First, we briefly discuss the biological functions of leptin and its signaling pathways. Then, we summarize the effects of leptin on different cancer types in experimental cellular and animal models. Next, we analyze epidemiological data on the relationship between obesity and the presence of cancer or cancer risk in patients. Finally, leptin as a target for cancer treatment and prevention will be discussed.

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Leptin and leptin receptor mRNA and protein expression in the murine fetus and placenta

Cited by 446 publications

References 24 publications

Leptina: o diálogo entre adipócitos e neurônios

Leptina: o diálogo entre adipócitos e neurônios

The intake of physiological doses of leptin during lactation in rats prevents obesity in later life

Leptin and cancer

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