Free and protein bound leptin are distinct and independently controlled factors in energy regulation

Brabant, Georg; Horn, Rüdiger; Mühlen, A. von zur; Mayr, B; Wurster, U.; Heidenreich, Fedor; Schnabel, Dirk; Grüters-Kieslich, Annette; Zimmermann-Belsing, Tina; Feldt‐Rasmussen, Ulla

doi:10.1007/s001250051326

Cited by 74 publications

(83 citation statements)

References 30 publications

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“…This study indicates that both BL and FL are present in the plasma of DS prepubertal children and that FL concentrations increase, relatively to BL, together with adiposity and become prevalent once obese levels are reached, like in obese adults (Sinha et al, 1996;Magni et al, 2000). The significance of FL and BL partitioning is not completely understood: at least in adults, BL correlates with resting energy expenditure, whereas FL reflects adiposity (Brabant et al, 2000). The observation of elevated plasma sOB-R levels concentrations in children (Kratzsch et al, 2002) and the increased BL fraction, here reported, may contribute to the temporary blockade of the reproductive axis in prepubertal children, which may be overcome, once an increase of FL occurs, in association with an increased adiposity and possibly other factors, giving rise to pubertal development.…”

Section: Discussionmentioning

confidence: 90%

Free and bound leptin in prepubertal children with Down's syndrome and different degrees of adiposity

et al. 2004

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Objective: To evaluate plasma total, free (FL) and protein-bound (BL) leptin in children with Down's syndrome (DS) and different degrees of adiposity and its relationship with thyroid stimulating hormone (TSH), free thyroxine (FT 4 ), and free triiodothyronine (FT 3 ). Subjects: A total of 24 prepubertal clinically euthyroid DS children. Methods: Plasma leptin, TSH, FT 4 , and FT 3 concentrations were determined by immunometric/radioimmunologic assays. FL and BL were evaluated by fast protein liquid chromatography. Results: In DS children, leptin circulates in two fractions, corresponding to BL and FL. The amount of BL and FL is negatively and positively correlated to body mass index (BMI), respectively. Plasma leptin concentrations correlate with BMI, but not with TSH, FT 4 , and FT 3 . Conclusions: In prepubertal DS children, leptin circulates as both BL and FL, correlates with adiposity and its concentration appears independent of thyroid function. Sponsorship: MIUR, Università degli Studi di Milano, Banca Popolare di Milano Foundation.

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Section: Discussionmentioning

confidence: 90%

Free and bound leptin in prepubertal children with Down's syndrome and different degrees of adiposity

et al. 2004

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“…13 The leptin concentration of 10 nmol=l employed in this study exceeds the peripheral plasma concentrations of $ 5 nmol=l reported in lean and obese humans. 16 In severe obesity, however, vascular endothelium is likely to be exposed to much higher concentrations resulting from local leptin release. 17,18 Of note, leptin correlates with the severity of hypertensive retinopathy 3 and stimulates proliferation of renal glomerular cells leading to kidney damage, glomerulosclerosis and proteinuria.…”

Section: Discussionmentioning

confidence: 99%

Modulation by leptin of proliferation and apoptosis in vascular endothelial cells

et al. 2002

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AIM: Plasma leptin concentrations not only correlate with body fat mass, but also with the degree of hypertensive retinopathy. The present study was designed to further examine, whether leptin's proliferative, proangiogenic activity relates to a yet uncovered anti-apoptotic effect. RESULTS: Leptin (10 -50 nmol=l) concentration-dependently reduced apoptosis in HUVECs (human umbilical vein endothelial cells), HAVECs (human adult vein endothelial cells) and HMECs (human microvascular endothelial cells) by 20% (P 0.05). These findings were supported by increased expression of the apoptosis inhibitor bcl-2 ( þ 55%, P 0.05) as well as by differential modulation of the respective cell cycle checkpoint genes=proteins p53 ( 7 20%, P 0.01), p21 WAF-1=Cip1 ( 7 23%, P 0.05) and the Retinoblastoma protein ( þ 123%, P 0.01). CONCLUSION: bcl-2 dependent anti-apoptotic action might contribute to leptin's proangiogenic activity and thereby promote the development of vascular proliferative disease in obesity.

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“…Leptin has been demonstrated to stimulate CO 2 ventilatory responses in mice (126,(142)(143)(144). Its action is antagonized by other adipose-related factors, namely the soluble leptin receptor (sOB-R) and C-reactive protein (CRP) (145), which bind circulating leptin and can decrease its central nervous system (CNS) uptake and action (145,146). Levels of sOB-R and CRP are elevated in sleep apnea compared with matched control patients (147,148) and decline with weight loss and the loss of visceral compared with central adiposity.…”

Section: Putative Adipokine Modulators Of Upper Airway Functionmentioning

confidence: 99%

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

Schwartz

Patil²,

Laffan

et al. 2008

Proceedings of the American Thoracic Society

584

395

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Obstructive sleep apnea is a common disorder whose prevalence is linked to an epidemic of obesity in Western society. Sleep apnea is due to recurrent episodes of upper airway obstruction during sleep that are caused by elevations in upper airway collapsibility during sleep. Collapsibility can be increased by underlying anatomic alterations and/or disturbances in upper airway neuromuscular control, both of which play key roles in the pathogenesis of obstructive sleep apnea. Obesity and particularly central adiposity are potent risk factors for sleep apnea. They can increase pharyngeal collapsibility through mechanical effects on pharyngeal soft tissues and lung volume, and through central nervous system-acting signaling proteins (adipokines) that may affect airway neuromuscular control. Specific molecular signaling pathways encode differences in the distribution and metabolic activity of adipose tissue. These differences can produce alterations in the mechanical and neural control of upper airway collapsibility, which determine sleep apnea susceptibility. Although weight loss reduces upper airway collapsibility during sleep, it is not known whether its effects are mediated primarily by improvement in upper airway mechanical properties or neuromuscular control. A variety of behavioral, pharmacologic, and surgical approaches to weight loss may be of benefit to patients with sleep apnea, through distinct effects on the mass and activity of regional adipose stores. Examining responses to specific weight loss strategies will provide critical insight into mechanisms linking obesity and sleep apnea, and will help to elucidate the humoral and molecular predictors of weight loss responses.

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Free and protein bound leptin are distinct and independently controlled factors in energy regulation

Abstract: Our data indicate a distinct role of free and bound leptin in the feedback regulating energy intake and expenditure and could have important implications for our understanding of the physiology and pathophysiology of leptin-dependent signalling.

Cited by 74 publications

References 30 publications

Free and bound leptin in prepubertal children with Down's syndrome and different degrees of adiposity

Free and bound leptin in prepubertal children with Down's syndrome and different degrees of adiposity

Modulation by leptin of proliferation and apoptosis in vascular endothelial cells

Obesity and Obstructive Sleep Apnea: Pathogenic Mechanisms and Therapeutic Approaches

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