Leptin: a multifunctional hormone

Huang, Lu; Li, Cai

doi:10.1038/sj.cr.7290038

Cited by 193 publications

(145 citation statements)

References 57 publications

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“…Ob/ob mice with mutations in the gene encoding leptin do not produce leptin and become morbidly obese, infertile, hyperphagic, hypothermic, and diabetic due to unopposed appetite (Huang and Li, 2000). In humans, like in animals, leptin is an important regulator of energy balance.…”

Section: Leptin and Its Activitiesmentioning

confidence: 99%

Leptin and cancer

Garofalo

Surmacz

2005

Journal Cellular Physiology

552

497

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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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Section: Leptin and Its Activitiesmentioning

confidence: 99%

Leptin and cancer

Garofalo

Surmacz

2005

Journal Cellular Physiology

552

497

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“…For instance, the adipose tissue produces and releases two hormones, leptin and adiponectin, that exert proinflammatory 46 and anti-inflammatory roles, 47 respectively. Interestingly, serum leptin is known to increase markedly in obesity, 48,49 and is found at higher levels in asthmatics than in nonasthmatics, 50 regardless of the extent of obesity.…”

Section: Potential Mechanisms Of Obesity-asthma Relationshipmentioning

confidence: 99%

Obesity induced bronchopulmonary hyperresponsiveness in Tunisian women

et al. 2010

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Objective: The specific objective of this investigation was to determine whether bronchopulmonary responsiveness (BPR) to methacholine (MCH) was associated with the body mass index (BMI) of Tunisian women. Subjects: In all, 160 healthy nonsmoker women (52 lean, 45 overweight and 63 obese) were recruited and examined in the Clinical Laboratory of Physiology located in the Medical School of Sousse. The average ages ( ± s.e.) of the three categories of lean, overweight and obese subjects were 27.7±1.1, 33.2±1.7 and 37.5±1.3 years, respectively. Their corresponding mean BMIs ( ± s.e.) were 21.9 ± 0.3, 27.7 ± 0.2 and 36.5 ± 0.8 kg m À2 , respectively. Measurements: Before their inclusion into the study, subjects were screened for their lung status by measuring their pulmonary function testing parameters using a whole body plethysmograph. BPR was assessed, using a cumulative concentration response curve technique, by measuring with a spirometer the decrease in forced expiratory volume in 1 s (FEV 1 ) in response to a cumulative dose of MCH. Results: After adjusting for age, significant differences in both FEV 1 and forced vital capacity (VC) were found between the obese and lean groups (Po0.01), as well as between the obese and overweight groups (Po0.01). In addition, forced expiratory flow between 25 and 75% of VC was significantly different between the obese and lean groups (Po0.001), as well as between the lean and overweight groups (P ¼ 0.015). The mean maximum fall of FEV 1 in response to MCH challenge was significantly higher for the obese group (12.0%) than for the overweight (9.8%) or the lean (6.6%) group (Po0.01). Furthermore, the efficacy of the MCH agonist promoting the maximal response (E max ) and its potency or effective dose producing 50% of the maximal response (ED 50 ) were both associated with BMI (the higher the BMI, the higher the E max and the lower the ED 50 ). Conclusion: Our data clearly show that obesity affects pulmonary function performance in Tunisian women by potentially promoting their bronchial hyperreactivity as suggested by the significant correlation between their BMI and the efficacy of the MCH, as well as its potency.

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“…Leptin, a product of the obese (ob) gene is a neuroendocrine hormone that has attracted attention since its identification in 1995 (Halaas et al 1995, MacDougald et al 1995. It is a multifunctional peptide hormone with wide-ranging biological activities including appetite regulation, bone formation, reproductive function and angiogenesis (Bouloumie et al 1998, Sierra-Honigmann et al 1998, Huang & Li 2000. These biological activities suggest an important role in cancer proliferation, invasion and metastasis (Somasunder et al 2004a,b).…”

Section: Introductionmentioning

confidence: 99%

Leptin promotes the proliferative response and invasiveness in human endometrial cancer cells by activating multiple signal-transduction pathways

Sharma¹,

Saxena²,

Vertino³

et al. 2006

Endocr Relat Cancer

152

144

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An increase in the risk of cancer is one of the consequences of obesity. The predominant cancers associated with obesity have a hormonal basis and include breast, prostate, endometrium, colon and gall-bladder cancers. Leptin, the key player in the regulation of energy balance and body weight control also acts as a growth factor on certain organs in both normal and disease states. Therefore, it is plausible that leptin acts to promote cancer growth by acting as a mitogenic agent. However, a direct role for leptin in endometrial cancer has not been demonstrated. In this study, we analyzed the proliferative role of leptin and the mechanism(s) underlying this action in endometrial cancers which express both short and long isoforms of leptin receptors. Treatment with leptin resulted in increased proliferation of ECC1 and Ishikawa cells. The promotion of endometrial cancer cell proliferation by leptin involves activation of STAT3 and ERK2 signaling pathways. Moreover, leptin-induced phosphorylation of ERK2 and AKT was dependent on JAK/ STAT activation. Therefore blocking its action at the JAK/STAT level could be a rational therapeutic strategy for endometrial carcinoma in obese patients. We also found that leptin potently induces invasion of endometrial cancer cells in a Matrigel invasion assay. Leptinstimulated invasion was effectively blocked by pharmacological inhibitors of JAK/STAT (AG490) and phosphatidylinositol 3-kinase (LY294002). Taken together these data indicate that leptin promotes endometrial cancer growth and invasiveness and implicate the JAK/STAT and AKT pathways as critical mediators of leptin action. Our findings have potential clinical implications for endometrial cancer progression in obese patients.

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Leptin: a multifunctional hormone

Cited by 193 publications

References 57 publications

Leptin and cancer

Leptin and cancer

Obesity induced bronchopulmonary hyperresponsiveness in Tunisian women

Leptin promotes the proliferative response and invasiveness in human endometrial cancer cells by activating multiple signal-transduction pathways

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