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Control of Blood Pressure, Appetite, and Glucose by Leptin in Mice Lacking Leptin Receptors in Proopiomelanocortin Neurons
Open accessAbstract
Although the central nervous system melanocortin system is an important regulator of energy balance, the role of proopiomelanocortin (POMC) neurons in mediating the chronic effects of leptin on appetite, blood pressure, and glucose regulation is unknown. Using Cre/loxP technology we tested whether leptin receptor deletion in POMC neurons (LepR flox/flox /POMC-Cre mice) attenuates the chronic effects of leptin to increase mean arterial pressure (MAP), enhance glucose use and oxygen consumption, and reduce appetite. LepR flox/flox /POMC-Cre, wild-type, LepR flox/flox , and POMC-Cre mice were instrumented for MAP and heart rate measurement by telemetry and venous catheters for infusions. LepR flox/flox /POMC-Cre mice were heavier, hyperglycemic, hyperinsulinemic, and hyperleptinemic compared with wild-type, LepR flox/flox , and POMC-Cre mice. Despite exhibiting features of metabolic syndrome, LepR flox/flox /POMC-Cre mice had normal MAP and heart rate compared with LepR flox/flox but lower MAP and heart rate compared with wild-type mice. After a 5-day control period, leptin was infused (2 μg/kg per minute, IV) for 7 days. In control mice, leptin increased MAP by ≈5 mm Hg despite decreasing food intake by ≈35%. In contrast, leptin infusion in LepR flox/flox /POMC-Cre mice reduced MAP by ≈3 mm Hg and food intake by ≈28%. Leptin significantly decreased insulin and glucose levels in control mice but not in LepR flox/flox /POMC-Cre mice. Leptin increased oxygen consumption in LepR flox/flox /POMC-Cre and wild-type mice. Activation of POMC neurons is necessary for the chronic effects of leptin to raise MAP and reduce insulin and glucose levels, whereas leptin receptors in other areas of the brain other than POMC neurons appear to play a key role in mediating the chronic effects of leptin on appetite and oxygen consumption.
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In the citing paper
“Disruption of leptin receptor signaling in POMC neurons abolished the ability of exogenous leptin administration to increase blood pressure (39;41) which provides additional support to the notion that leptin is a critical hormone in coupling hypertension and obesity (Figure 1).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [39]
In the citing paper
“Selective LepR deletion in POMC neurons of the ARC and brainstem also abolished BP increases in mice during chronic leptin infusions140.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [140]
In the citing paper
“In fact, deletion of LepR only in POMC neurons, a major type of neuron in the ARC, prevents increased BP during chronic hyperleptinemia97.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [97]
In the citing paper
“Leptin receptor (LR) deletion specifically in POMC neurons completely abolished the chronic effects of leptin to raise BP and to reduce plasma glucose and insulin levels but did not markedly attenuate the effects of leptin on food intake [50].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [50]
In the citing paper
“These findings suggest that LR activation in POMC neurons is critical for leptin’s ability to increase BP and improve glucose homeostasis but not for its effect to reduce food intake.”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [50]
In the citing paper
“Leptin requires activation of POMC neurons and MC4R to mediate its effects on renal SNS activity and BP [28, 50, 51].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [50]
In the citing paper
“Leptin receptor (LR) deletion specifically in POMC neurons completely abolished the chronic effects of leptin to raise BP and to reduce plasma glucose and insulin levels but did not markedly attenuate the effects of leptin on food intake [50].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [50]
In the citing paper
“Similarly, mice lacking leptin signaling in POMC neurons or in the arcuate nucleus of the hypothalamus, where most POMC neurons reside, through deletion of the leptin receptor itself (39;40) or components of its signaling pathway such as the signal transducer and activator of transcription-3 (41) are protected against obesity-associated hypertension.”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [39]
In the citing paper
“Disruption of leptin receptor signaling in POMC neurons abolished the ability of exogenous leptin administration to increase blood pressure (39;41) which provides additional support to the notion that leptin is a critical hormone in coupling hypertension and obesity (Figure 1).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [39]
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Dragano, N. R. V., Fernø, J., Diéguez, C., López, M., & Milbank, E. (2020) · Neuroscience · doi:10.1016/j.neuroscience.2020.08.009 · Cited by 18
Animal Models in Obesity and Hypertension
Segal‐Lieberman, G., & Rosenthal, T. (2013) · Current Hypertension Reports · doi:10.1007/s11906-013-0338-3 · Cited by 17
Inhibitor κB Kinase 2 Is a Myosin Light Chain Kinase in Vascular Smooth Muscle
Ying, Z., do Carmo, J. M., Xiang, L., da Silva, A. A., Chen, M., Ryan, M. J., Ostrowski, M. C., Rajagopalan, S., & Hall, J. E. (2013) · Circulation Research · doi:10.1161/circresaha.113.301510 · Cited by 17
Self-citationRole of SOCS3 in POMC neurons in metabolic and cardiovascular regulation
Wang, Z., do Carmo, J. M., da Silva, A. A., Bailey, K. C., Aberdein, N., Moak, S. P., & Hall, J. E. (2019) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00163.2018 · Cited by 19
Self-citationMolecular Mechanisms of Sodium-Sensitive Hypertension in the Metabolic Syndrome
Nizar, J. M., & Bhalla, V. (2017) · Current Hypertension Reports · doi:10.1007/s11906-017-0759-5 · Cited by 17
da Silva, A. A., Hall, J. E., & do Carmo, J. M. (2017) · PLoS ONE · doi:10.1371/journal.pone.0184805 · Cited by 16
Self-citationPeripheral leptin signaling persists in innate immune cells during diet-induced obesity
Souza-Almeida, G., Palhinha, L., Liechocki, S., Pereira, J. A. D. S., Reis, P. A., Dib, P. R. B., Hottz, E. D., Gameiro, J., Vallochi, A. L., de Almeida, C. J., et al. (2020) · Journal of Leukocyte Biology · doi:10.1002/jlb.3ab0820-092rr · Cited by 15
da Silva, A. A., Moak, S. P., Dai, X., Borges, G. C., Omoto, A. C. M., Wang, Z., Li, X., Mouton, A. J., Hall, J. E., & do Carmo, J. M. (2022) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00300.2021 · Cited by 13
Self-citationSuazo, J., Hodgson, M. I., Obregón, A. M., Valladares, M., Gerardo Weisstaub, N., Amador, P., & Santos, J. L. (2013) · Journal of Pediatric Endocrinology and Metabolism · doi:10.1515/jpem-2013-0084 · Cited by 13
Role of autonomic nervous system in chronic CNS-mediated antidiabetic action of leptin
da Silva, A. A., Hall, J. E., Moak, S. P., Browning, J. R., Houghton, H. J., Micheloni, G. C., & do Carmo, J. M. (2016) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00301.2016 · Cited by 13
Self-citationYalamanchili, C., Chittiboyina, A. G., Haider, S., Vásquez, Y., Khan, S. I., do Carmo, J. M., da Silva, A. A., Pinkerton, M., Hall, J. E., Walker, L., et al. (2019) · Heliyon · doi:10.1016/j.heliyon.2019.e02782 · Cited by 13
Self-citationDrug Discovery for Diabetic Nephropathy: Trying the Leap From Mouse to Man
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do Carmo, J. M., da Silva, A. A., Freeman, J. N., Wang, Z., Moak, S. P., Hankins, M. W., Drummond, H. A., & Hall, J. E. (2018) · Hypertension · doi:10.1161/hypertensionaha.118.11127 · Cited by 11
Self-citationHigh leptin level and leptin receptor Lys656Asn variant are risk factors for preeclampsia
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Physiology and Pathophysiology of Hypertension
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Self-citationFrom pathophysiology to novel approaches for obesity-associated hypertension
Kanbay, M., Yayci, E., Genc, C., Çöpür, S., Aktaş, Ö. Y., Sarafidis, P. A., Covic, A. C., Ortíz, A., & Laffin, L. J. (2025) · Clinical Kidney Journal · doi:10.1093/ckj/sfaf218 · Cited by 10
Morais, R. L., Hilzendeger, A. M., Visniauskas, B., Todiraş, M., Alenina, N. V., Mori, M. A., Araújo, R. C., Nakaie, C. R., Chagas, J. R., Carmona, A. K., et al. (2016) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00485.2016 · Cited by 10
do Carmo, J. M., Hall, J. E., Dai, X., Aitken, N. M., Larson, K., Luna-Suarez, E. M., Wang, Z., Omoto, A. C. M., Mouton, A. J., Li, X., et al. (2024) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00294.2023 · Cited by 9
Self-citationMori, F.-K., & Shimosawa, T. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26010420 · Cited by 11
do Carmo, J. M., da Silva, A. A., Moak, S. P., Browning, J. R., Dai, X., & Hall, J. E. (2018) · Life Sciences · doi:10.1016/j.lfs.2018.09.034 · Cited by 9
Self-citationRole of the Melanocortin System in the Central Regulation of Cardiovascular Functions
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Metabolic Signaling to the Central Nervous System: Routes Across the Blood Brain Barrier
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Obesity and Metabolic Syndrome Hypertension
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Self-citationAl‐Daghri, N. M., Dahman, L. S. B., Al-Attas, O. S., Saleem, T. H., Alokail, M. S., Alkharfy, K. M., Draz, H. M., Yakout, S. M., Mohamed, A. O., Harte, A. L., et al. (2012) · PLoS ONE · doi:10.1371/journal.pone.0051255 · Cited by 8
Mice lacking PC1/3 expression in POMC-expressing cells do not develop obesity
Shakya, M., Gahlot, S., White, A. E., Verchere, C. B., Low, M. J., & Lindberg, I. (2021) · Endocrinology · doi:10.1210/endocr/bqab055 · Cited by 7
Metadata
- Authors
- do Carmo, J. M., da Silva, A. A., Cai, Z., Lin, S., Dubinion, J. H., & Hall, J. E.
- Affiliations
- From the Departments of Physiology and Biophysics (J.M.d.C., A.A.d.S., J.H.D., J.E.H.) and Pediatrics (Z.C., S.L.), University of Mississippi Medical Center, Jackson, MS.
- University of Mississippi Medical Center (US)
- Venue
- Hypertension
- Published
- 2011-05
- Volume
- 57
- Issue
- 5
- Pages
- 918-926
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- PMC
- PMC3092393
- OpenAlex
- W1975214074
- Cited by
- 127
- References
- 34
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 6 · 2023: 1 · 2022: 2 · 2021: 9 · 2020: 13 · 2019: 6 · 2018: 10 · 2017: 18 · 2016: 11 · 2015: 8 · 2014: 12 · 2013: 15 · 2012: 10
- FWCI
- 5.49
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01HL051971)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- leptin, leptin receptor, proopiomelanocortin neurons, melanocortin system, blood pressure regulation, appetite, glucose regulation, insulin, oxygen consumption, energy balance, metabolic syndrome, hyperleptinemia, hyperglycemia, heart rate
- MeSH terms
- Analysis of Variance, Animals, Appetite, Blood Glucose, Blood Pressure, Body Weight, Eating, Enzyme-Linked Immunosorbent Assay, Fluorescent Antibody Technique, Immunohistochemistry, Insulin, Male, Motor Activity, Neurons, Oxygen Consumption, Pro-Opiomelanocortin, Telemetry, Mice, Knockout, Leptin, Mice, Receptors, Leptin
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