Expression of ob mRNA and its encoded protein in rodents. Impact of nutrition and obesity.

Frederich, Robert; Löllmann, Bettina; Hamann, Andreas; Napolitano-Rosen, A; Kahn, Barbara B.; Lowell, Bradford B.; Flier, Jeffrey S.

doi:10.1172/jci118206

Cited by 545 publications

(363 citation statements)

References 14 publications

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“…Several studies have demonstrated that the leptin gene expression is positively regulated by insulin both in vivo (Saladin et al, 1995;Kolaczynski et al, 1996c) and in vitro (Kolaczynski et al, 1996c;Leroy et al, 1996). Plasma leptin levels decrease after fasting and increase by refeeding in humans (Kolaczynski et al, 1996a,b;Boden et al, 1996;Dubuc et al, 1998;Geldszus et al, 1996;Wadden et al, 1998) and rodents (Frederich et al, 1995), which parallels the change in plasma insulin levels (Kolaczynski et al, 1996b). Accordingly, it is possible that acutely decreased insulin levels during the early phase of an LCD may contribute to a rapid fall in plasma leptin levels.…”

Section: Clinical Implications Of Leptinmentioning

confidence: 99%

Clinical implications of leptin and its potential humoral regulators in long-term low-calorie diet therapy for obese humans

et al. 2002

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Objective: To address the clinical implications of leptin and to re-examine the relationship between leptin and its potential humoral regulators such as insulin, nonesterified fatty acids (NEFA) and triiodothyronine (T3) in low-calorie diet (LCD) for obese humans. Design: Longitudinal study. Setting: University and foundation hospitals. Subjects: Ten obese men and 10 premenopausal obese women. Interventions: Five men and five women took 800 kcal=day LCD and another five men and five women took 1400 kcal=day balanced deficit diet (BDD) during 4 weeks. Results: Plasma leptin levels in the LCD group decreased more markedly (46.2 AE 14.6 to 13.2 AE 3.6 ng=ml) than that expected for the decrement in percentage fat (39.0 AE 1.7 to 35.9 AE 1.7%) and body mass index (BMI; 35.4 AE 2.4 to 33.1 AE 2.2 kg=m 2 ), while that in the BDD group did not decrease significantly (14.9 AE 3.5 to 13.4 AE 2.8 ng=ml). The ratio of the decrease in leptin levels to that of BMI during the first week was significantly greater than that during the following 3 weeks (39.5 AE 2.7 vs 29.3 AE 2.1%, P ¼ 0.017). The plasma insulin and T3 levels also fell substantially in the first week and continued to decrease during the entire course. Plasma leptin levels measured weekly in each subject were correlated well with insulin (r ¼ 0.586, P ¼ 0.0003) and T3 (r ¼ 0.785, P ¼ 0.0004). Multiple regression analyses after adjustment for the time course and BMI revealed that serum levels of T3 were independently correlated with plasma leptin levels (r ¼ 0.928, P < 0.0001). The plasma NEFA level was markedly elevated during the first 2 weeks and decreased thereafter. Conclusions: A rapid fall in leptin during the first week of LCD, coordinated by insulin, T3 and NEFA, should be beneficial for responding to decreased energy intake. Inversely, in view of the powerful effect of leptin on energy dissipation, the present findings suggest the potential usefulness of leptin in combination with caloric restriction for the treatment of obesity.

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Section: Clinical Implications Of Leptinmentioning

confidence: 99%

Clinical implications of leptin and its potential humoral regulators in long-term low-calorie diet therapy for obese humans

et al. 2002

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“…8,9 Obesity may also be associated with adverse treatment outcome of cancer, including resistance to chemotherapies. 10 Leptin, encoded by the obesity gene, 11 directly contributes to leptin receptor (ObR)-positive cancer cell proliferation, migration, and invasion. 12 Zheng et al concluded that leptin was a mammary tumor-initiating factor on the basis of its ability to stimulate cancer stem cells (CSCs) survival, and ObR was defined as breast CSCs surface marker.…”

Section: Introductionmentioning

confidence: 99%

High expression of leptin receptor leads to temozolomide resistance with exhibiting stem/progenitor cell features in gliobalastoma

et al. 2013

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“…It is now appreciated, however, that common human obesity is not associated with mutation-induced leptin deficiency but rather with increased concentrations of circulating leptin. [1][2][3] This common or 'leptin-resistant' obesity is determined by an interaction between environmental influences, especially diet and a unique polygenic susceptibility. 4 Recent data suggest, however, that, regardless of its etiology, obesity appears to be a state of chronic low-grade inflammation characterized by an increase in both the serum levels of several inflammatory mediators and the number of secretory macrophages within white adipose tissue.…”

Section: Introductionmentioning

confidence: 99%

Increased expression of hypothalamic leptin receptor and adiponectin accompany resistance to dietary-induced obesity and infertility in female C57BL/6J mice

2006

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Background: Obesity is strongly associated with female infertility, but the mechanisms underlying this relationship are largely unknown. Methods: We investigated the effect of increasing dietary fat percentage upon body mass, hypothalamic neuropeptide gene expression, adipose hormone secretion and fertility in females of the inbred mouse strains C57BL/6J and DBA/2J. To assess the effect of obesity independent of dietary influence, we also compared these parameters in wild-type female C57BL/6J mice to those congenic for the obesogenic mutations ob/ob and A y /a. Results: After 24 weeks, rather than exhibiting an obese, leptin-resistant phenotype like their female DBA/2J counterparts, wildtype female C57BL/6J mice remained lean, fertile and manifested increased hypothalamic LEPR-B expression. Although both mutant genotypes were associated with obesity and subfertility, ob/ob mice demonstrated significantly increased hypothalamic LEPR-B expression, whereas A y /a mice had a significant reduction. Interestingly, wild-type female C57BL/6J mice were noted to manifest significantly higher and lower levels of adiponectin and tissue plasminogen activator inhibitor-1 (tPAI-1), respectively, than weight-matched wild-type female DBA/2J mice. Conclusions: We conclude that (1) resistance to the obese-infertile phenotype in female C57BL/6J mice is associated with increased hypothalamic leptin receptor expression and alterations in adipokine levels consistent with decreased adipose tissue inflammation and (2) that long-standing hyperleptinemic obesity in mice is associated with a downregulation of the hypothalamic leptin receptor.

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Expression of ob mRNA and its encoded protein in rodents. Impact of nutrition and obesity.

Cited by 545 publications

References 14 publications

Clinical implications of leptin and its potential humoral regulators in long-term low-calorie diet therapy for obese humans

Clinical implications of leptin and its potential humoral regulators in long-term low-calorie diet therapy for obese humans

High expression of leptin receptor leads to temozolomide resistance with exhibiting stem/progenitor cell features in gliobalastoma

Increased expression of hypothalamic leptin receptor and adiponectin accompany resistance to dietary-induced obesity and infertility in female C57BL/6J mice

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