Role of the brain melanocortins in blood pressure regulation

Carmo, Jussara M. do; Silva, Alexandre A. da; Wang, Zhen; Fang, Taolin; Aberdein, Nicola; Lara, Cecilia E. Perez de; Hall, John E.

doi:10.1016/j.bbadis.2017.03.003

Cited by 30 publications

(23 citation statements)

References 79 publications

(115 reference statements)

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“…Brain melanocortins.-A key CNS pathway that links adipokines and hormones with BP control is the brain POMC-melanocortin 4 receptor (MC4R) system 6,189,190 . In the ARC and brainstem, POMC-expressing neurons project to second-order neurons involved in BP regulation (for example, in the paraventricular nucleus (PVN)), where their axons release amelanocyte-stimulating hormone (aMSH), the endogenous ligand for MC4R 191 (FIG.…”

Section: Potential Mediators Of Sns Activationmentioning

confidence: 99%

Obesity, kidney dysfunction and hypertension: mechanistic links

et al. 2019

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Excessive adiposity raises blood pressure and accounts for 65-75% of primary hypertension, which is a major driver of cardiovascular and kidney diseases. In obesity, abnormal kidney function and associated increases in tubular sodium reabsorption initiate hypertension, which is often mild before the development of target organ injury. Factors that contribute to increased sodium reabsorption in obesity include kidney compression by visceral, perirenal and renal sinus fat; increased renal sympathetic nerve activity (RSNA); increased levels of anti-natriuretic hormones, such as angiotensin II and aldosterone; and adipokines, particularly leptin. The renal and neurohormonal pathways of obesity and hypertension are intertwined. For example, leptin increases RSNA by stimulating the central nervous system proopiomelanocortin-melanocortin 4 receptor pathway, and kidney compression and RSNA contribute to renin-angiotensin-aldosterone system activation. Glucocorticoids and/or oxidative stress may also contribute to mineralocorticoid receptor activation in obesity. Prolonged obesity and progressive renal injury often lead to the development of treatment-resistant hypertension. Patient management therefore often requires multiple antihypertensive drugs and concurrent treatment of dyslipidaemia, insulin resistance, diabetes and inflammation. If more effective strategies for the prevention and control of obesity are not developed, cardiorenal, metabolic and other obesity-associated diseases could overwhelm health-care systems in the future. Obesity and its adverse consequences are major burdens to health-care systems worldwide 1. The Global Burden of Disease study, which includes data from 195 countries, reports that

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Section: Potential Mediators Of Sns Activationmentioning

confidence: 99%

Obesity, kidney dysfunction and hypertension: mechanistic links

et al. 2019

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“…Increased sympathetic activity caused by hyperinsulinemia has been shown to decrease when melanocortin receptors are antagonized. 13,14 Adipose tissue produces pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-6. They can induced insülin resistance and promote endothelial dysfunction.…”

Section: Pathogenesismentioning

confidence: 99%

Obesity and Hypertension

Ersoy

2019

Turkish Journal of Internal Medicine

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Obesity is an important public health problem with increasing frequency, leading to different comorbidities including hypertension and can cause mortality. Possible mechanisms that increase blood pressure in overweight and obese people are renal damage, activation of the renin-angiotensin-aldosterone system, insulin resistance, hyperinsulinemia, sleep apnea syndrome, leptin-melanocortin pathway and genetic predisposition. Most of these mechanisms stimulate the sympathetic nervous system. Medical nutrition therapy, lifestyle interventions, medical and/or surgical antiobesity treatment modalities contribute to the control of blood pressure via weight loss. Besides antihypertensive medications should be chosen carefully in overweight and obese patients and drug groups preventing weight loss should not be preferred if possible.

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“…In addition to controlling feeding behavior, the ARC also regulates energy expenditure. For example, POMC/CART neurons decrease food intake and increase energy expenditure through the activation of MC3R or MC4R via the release of α-MSH [39, 40]. Conversely, AgRP/NPY neurons promote food intake and decrease energy expenditure [41].…”

Section: Discussionmentioning

confidence: 99%

Intraventricular Injection of LKB1 Inhibits the Formation of Diet-Induced Obesity in Rats by Activating the AMPK-POMC Neurons-Sympathetic Nervous System Axis

Liang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Obesity is increasingly becoming a major public health problem worldwide. Peripheral LKB1 inhibits white fat generation, but the effect of central LKB1 on diet-induced obesity (DIO) is unknown. Therefore, we examined whether LKB1 over-expression in the hypothalamus can inhibit the development of obesity. Methods: Adult male Sprague-Dawley rats were anesthetized and placed in a stereotaxic apparatus. LKB1-AAV-EGFP (2.0 × 10⁸ or 2.0 × 10¹⁰ vector genomes) or Control-AAV-EGFP (2.0 × 10⁸ vector genomes) was injected into the third ventricle. After administration, the rats were fed a high-fat diet (HFD) for 9 weeks to induce obesity. Rats fed a chow fat diet were used as normal controls. Results: LKB1 delivery decreased body weight, energy intake, fat mass, and serum lipid levels. LKB1 also improved HFD-induced hepatic fatty degeneration. Interestingly, LKB1 over-expression in the hypothalamus activated the AMPK-POMC neurons-sympathetic nervous system (SNS) axis, which can release epinephrine to promote white fat browning. Conversely, the elevated expression of MC3R/MC4R inhibited food intake. These two factors worked together to inhibit the development of obesity. Conclusions: LKB1 in the hypothalamus may have therapeutic potential for DIO through the activation of the AMPK-POMC neurons-SNS axis.

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Role of the brain melanocortins in blood pressure regulation

Cited by 30 publications

References 79 publications

Obesity, kidney dysfunction and hypertension: mechanistic links

Obesity, kidney dysfunction and hypertension: mechanistic links

Obesity and Hypertension

Intraventricular Injection of LKB1 Inhibits the Formation of Diet-Induced Obesity in Rats by Activating the AMPK-POMC Neurons-Sympathetic Nervous System Axis

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