Central leptin replacement enhances chemorespiratory responses in leptin-deficient mice independent of changes in body weight

Bassi, Mirian; Giusti, Humberto; Leite, Cristiane Mota; Anselmo-Franci, Janete Aparecida; Carmo, Jussara M. do; Silva, Alexandre A. da; Hall, John E.; Colombari, Eduardo; Glass, Mogens L.

doi:10.1007/s00424-012-1111-1

Cited by 36 publications

(43 citation statements)

References 31 publications

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“…Pulmonary ventilation ( V E ) was measured using whole-body plethysmography as previously described (Malan 1973, Bassi et al 2012). Briefly, mice were acclimatized to the plethysmography chamber (700 mL) at room temperature (25 °C) for 1 h. The ports for gas exit or entrance in the chamber were closed to produce an internal constant volume.…”

Section: Methodsmentioning

confidence: 99%

“…In addition, previous studies demonstrated that leptin is also involved in the control of breathing (Polotsky et al 2001, 2004, Inyushkin et al 2009, Inyushkina et al 2010, Malli et al 2010, Bassi et al 2012). Transgenic leptin-deficient (ob/ob) mice show attenuated breathing responses to CO 2 , suggesting that leptin deficiency impairs ventilatory function.…”

mentioning

confidence: 96%

“…Transgenic leptin-deficient (ob/ob) mice show attenuated breathing responses to CO 2 , suggesting that leptin deficiency impairs ventilatory function. Moreover, systemic or intracerebroventricular leptin replacement reverses the deficit of ventilation in ob/ob mice by still unknown mechanisms (Tankersley et al 1996, O’Donnell et al 2000, Bassi et al 2012). …”

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confidence: 99%

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Leptin into the ventrolateral medulla facilitates chemorespiratory response in leptin‐deficient (ob/ob) mice

et al. 2014

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Aim Leptin, an adipocyte-derived hormone, is suggested to participate in the central control of breathing. We hypothesized that leptin may facilitate ventilatory responses to chemoreflex activation by acting on respiratory nuclei of the ventrolateral medulla. The baseline ventilation and the ventilatory responses to CO2 were evaluated before and after daily injections of leptin into the retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG) for 3 days in obese leptin-deficient (ob/ob) mice. Methods Male ob/ob mice (40–45 g, n = 7 per group) received daily microinjections of vehicle or leptin (1 μg per 100 nL) for 3 days into the RTN/pFRG. Respiratory responses to CO2 were measured by whole-body plethysmography. Results Unilateral microinjection of leptin into the RTN/pFRG in ob/ob mice increased baseline ventilation (VE) from 1447 ± 96 to 2405 ± 174 mL min−1 kg−1 by increasing tidal volume (VT) from 6.4 ± 0.4 to 9.1 ± 0.8 mL kg−1 (P < 0.05). Leptin also enhanced ventilatory responses to 7% CO2 (Δ = 2172 ± 218 mL min−1 kg−1, vs. control: Δ = 1255 ± 105 mL min−1 kg−1), which was also due to increased VT (Δ = 4.71 ± 0.51 mL kg−1, vs. control: Δ = 2.27 ± 0.20 mL kg−1), without changes in respiratory frequency. Leptin treatment into the RTN/pFRG or into the surrounding areas decreased food intake (83 and 70%, respectively), without significantly changing body weight. Conclusion The present results suggest that leptin acting in the respiratory nuclei of the ventrolateral medulla improves baseline VE and VT and facilitates respiratory responses to hypercapnia in ob/ob mice.

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Section: Methodsmentioning

confidence: 99%

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confidence: 96%

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Leptin into the ventrolateral medulla facilitates chemorespiratory response in leptin‐deficient (ob/ob) mice

et al. 2014

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“…To account for the effect of obesity in causing the respiratory deficit in obese ob/ob mice and to determine the role of weight loss in contributing to improved ventilatory responses to hypercapnia during leptin treatment, they investigated the responses to hypercapnia in lean, pair-weighted, ob/ob mice. The results from these experiments showed that the major cause of the impaired ventilatory response in ob/ob mice is leptin deficiency rather than obesity, and that weight loss in obese ob/ob during leptin treatment does not play a major role in mediating the effects of leptin to improve ventilatory responses to hypercapnia [13].…”

Section: Models Of Obesity and Subfertility; The Bridging Role Of Leptinmentioning

confidence: 93%

“…Whether leptin replacement improves chemorespiratory responses to hypercapnia in ob/ob mice and if these effects were due to changes in body weight or to the direct effects of leptin in the central nervous system was examined by Bassi et al [13]. Animals were allowed to recover for 7 days before intracerebroventricular daily microinjections of leptin and ventilation measurements were performed.…”

Section: Models Of Obesity and Subfertility; The Bridging Role Of Leptinmentioning

confidence: 99%

Obesity and Female Fertility: The Bridging Role of Leptin

Karoutsos¹

2017

J Data Mining Genomics Proteomics

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Leptin secretion is a requirement in order for both of energy balance and reproductive capacity to be preserved. That is because leptin plays an important role in appetite regulation and balance of body weight. Leptin binds to leptin receptor in the cells of the hypothalamus. This stimulates an intracrine signaling pathway that drives downregulation of the receptors expression involved in appetite increase. It is clearly set that leptin impairs production of sex steroid hormones in granulosa cells. In addition, alterations noted in follicular fluid from obese women include increased androgen activity and decreased human chorionic gonadotropin levels by other studies. Likewise, adiponectin levels are inversely correlated with levels of insulin, which by inhibiting the production of hepatic sex hormone binding globulin, because increased levels of androgens. On meeting with the fertility problems that arise among these women, scientists must understand the pathophysiology of adipose signaling on reproductive function.

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Leptin: Master Regulator of Biological Functions that Affects Breathing

Gauda

Conde

Bassi

et al. 2020

Comprehensive Physiology

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Obesity is a global epidemic in developed countries accounting for many of the metabolic and cardiorespiratory morbidities that occur in adults. These morbidities include type 2 diabetes, sleepdisordered breathing (SDB), obstructive sleep apnea, chronic intermittent hypoxia, and hypertension. Leptin, produced by adipocytes, is a master regulator of metabolism and of many other biological functions including central and peripheral circuits that control breathing. By binding to receptors on cells and neurons in the brainstem, hypothalamus, and carotid body, leptin links energy and metabolism to breathing. In this comprehensive article, we review the central and peripheral locations of leptin's actions that affect cardiorespiratory responses during health and disease, with a particular focus on obesity, SDB, and its effects during early development. Obesityinduced hyperleptinemia is associated with centrally mediated hypoventilation with decrease CO 2 sensitivity. On the other hand, hyperleptinemia augments peripheral chemoreflexes to hypoxia and induces sympathoexcitation. Thus, "leptin resistance" in obesity is relative. We delineate the circuits responsible for these divergent effects, including signaling pathways. We review the unique effects of leptin during development on organogenesis, feeding behavior, and cardiorespiratory responses, and how undernutrition and overnutrition during critical periods of development can lead to cardiorespiratory comorbidities in adulthood. We conclude with suggestions for future directions to improve our understanding of leptin dysregulation and associated clinical diseases and possible therapeutic targets. Lastly, we briefly discuss the yin and the yang, specifically the contribution of relative adiponectin deficiency in adults with hyperleptinemia to the development of metabolic and cardiovascular disease.

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Central leptin replacement enhances chemorespiratory responses in leptin-deficient mice independent of changes in body weight

Cited by 36 publications

References 31 publications

Leptin into the ventrolateral medulla facilitates chemorespiratory response in leptin‐deficient (ob/ob) mice

Leptin into the ventrolateral medulla facilitates chemorespiratory response in leptin‐deficient (ob/ob) mice

Obesity and Female Fertility: The Bridging Role of Leptin

Leptin: Master Regulator of Biological Functions that Affects Breathing

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