Circulating ghrelin and ghrelin to obestatin ratio are low in patients with untreated mild-to-moderate hypertension

Li, Zhaofeng; Guo, Zhian; Yang, Sui-Qin; Zheng, Xiaojiao; Cao, Jiang; Qin, Yong-wen

doi:10.1016/j.regpep.2010.07.168

Cited by 25 publications

(16 citation statements)

References 18 publications

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“…23 The role of obestatin in BP regulation and insulin sensitivity is unclear, but systolic BP has been shown to be an independent predictor of the ghrelin/obestatin ratio. 24 In addition, fasting plasma concentrations of obestatin are reduced in insulin resistance and are positively associated with wholebody insulin sensitivity in nondiabetic humans. 15 In the present study, obese patients had lower fasting plasma obestatin concentrations than controls.…”

Section: Discussionmentioning

confidence: 99%

Ghrelin and obestatin levels in hypertensive obese patients

Wang

et al. 2014

J Int Med Res

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Objectives: To investigate plasma total ghrelin and obestatin levels and the ghrelin/obestatin ratio prospectively, in hypertensive obese patients. Methods: Height, weight, and waist and hip circumferences were measured in hypertensive and normotensive obese patients and matched healthy controls; the body mass index and waist to hip ratio were calculated. Fasting glucose and insulin levels were measured and the homeostasis model assessment of insulin resistance (HOMA-IR) was determined. Fasting ghrelin and obestatin concentrations were measured by radioimmunoassay and the ghrelin/obestatin ratio was calculated.Results: A total of 38 hypertensive obese patients, 40 normotensive obese patients and 38 controls were enrolled. Hypertensive obese patients had lower plasma levels of ghrelin and obestatin than normotensive obese patients or controls. In addition, normotensive obese patients had lower plasma ghrelin and obestatin levels than controls. In hypertensive obese patients, ghrelin and obestatin levels were negatively associated with systolic and diastolic blood pressure, fasting insulin and HOMA-IR. In normotensive obese patients, ghrelin, obestatin and the ghrelin/obestatin ratio were negatively associated with fasting insulin and HOMA-IR. In both patient groups, fasting obestatin and ghrelin concentrations were significantly and positively correlated with each other. Conclusion: Changes in the levels of ghrelin and obestatin may play a role in the pathophysiology of obesity and hypertension.

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Section: Discussionmentioning

confidence: 99%

Ghrelin and obestatin levels in hypertensive obese patients

Wang

et al. 2014

J Int Med Res

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“…46 Untreated hypertensive subjects exhibit decreased circulating ghrelin concentrations. 47 A polymorphism in the ghrelin gene is associated with increased risk of hypertension, although no ghrelin halotypes are associated with BP or body mass index. 48 Thus, it seems plausible that the low ghrelin concentrations observed in common obesity could contribute to obesity-related hypertension.…”

Section: Mechanisms By Which Obesity Increases Snamentioning

confidence: 98%

Sympathetic nervous system in obesity-related hypertension: mechanisms and clinical implications

2011

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Obesity markedly increases the risk of hypertension and cardiovascular disease, which may be related to activation of the sympathetic nervous system (SNS). Sympathetic overactivity directly and indirectly contributes to blood pressure (BP) elevation in obesity, including stimulation of the renin–angiotensin–aldosterone system (RAAS). The adipocyte-derived peptide leptin suppresses appetite, increases thermogenesis, but also raises SNS activity and BP. Obese individuals exhibit hyperleptinemia but are resistant to its appetite-suppressing actions. Interestingly, animal models of obesity exhibit preserved sympathoexcitatory and pressor actions of leptin, despite resistance to its anorexic and metabolic actions, suggesting selective leptin resistance. Disturbance of intracellular signaling at specific hypothalamic neural networks appears to underlie selective leptin resistance. Delineation of these pathways should lead to novel approaches to treatment. In the meantime, treatment of obesity–hypertension has relied on antihypertensive drugs. Although sympathetic blockade is mechanistically attractive in obesity–hypertension, in practice its effects are disappointing because of adverse metabolic effects and inferior outcomes. On the basis of subgroup analyses of obese patients in large randomized clinical trials, drugs such as diuretics and RAAS blockers appear superior in preventing cardiovascular events in obesity–hypertension. An underused alternative approach to obesity–hypertension is induction of weight loss, which reduces circulating leptin and insulin, partially reverses resistance to these hormones, decreases sympathetic activation and improves BP and other risk factors. Though weight loss induced by lifestyle is often modest and transient, carefully selected pharmacological weight loss therapies can produce substantial and sustained antihypertensive effects additive to lifestyle interventions.

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“…However, the nature of this interaction has been differentially reported, similar to the previously discussed findings in regard to metabolic disease, which is frequently associated with hypertension. Fasting plasma obestatin levels were first reported to be negatively correlated with systolic blood pressure in insulin‐resistant patients (Anderwald‐Stadler et al ., ), findings that were later corroborated in patients with mild‐to‐moderate untreated essential hypertension in association with reduced ghrelin and ghrelin/obestatin ratio (Li et al ., ) and in hypertensive versus normotensive obese patients (Wang et al ., ). However, a study conducted in patients with pulmonary arterial hypertension found that circulating obestatin levels tended to increase, whilst the ghrelin/obestatin ratio was decreased compared with controls, and identified as an independent disease predictor (Li et al ., ).…”

Section: Cardiovascular Actions Of Obestatinmentioning

confidence: 99%

Obestatin as a key regulator of metabolism and cardiovascular function with emerging therapeutic potential for diabetes

Cowan

Burch

Green

et al. 2016

British J Pharmacology

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*These two authors contributed equally to this work.Obestatin is a 23-amino acid C-terminally amidated gastrointestinal peptide derived from preproghrelin and which forms an α helix. Although obestatin has a short biological half-life and is rapidly degraded, it is proposed to exert wide-ranging pathophysiological actions. Whilst the precise nature of many of its effects is unclear, accumulating evidence supports positive actions on both metabolism and cardiovascular function. For example, obestatin has been reported to inhibit food and water intake, body weight gain and gastrointestinal motility and also to mediate promotion of cell survival and prevention of apoptosis. Obestatin-induced increases in beta cell mass, enhanced adipogenesis and improved lipid metabolism have been noted along with up-regulation of genes associated with beta cell regeneration, insulin production and adipogenesis. Furthermore, human circulating obestatin levels generally demonstrate an inverse association with obesity and diabetes, whilst the peptide has been shown to confer protective metabolic effects in experimental diabetes, suggesting that it may hold therapeutic potential in this setting. Obestatin also appears to be involved in blood pressure regulation and to exert beneficial effects on endothelial function, with experimental studies indicating that it may also promote cardioprotective actions against, for example, ischaemia-reperfusion injury. This review will present a critical appraisal of the expanding obestatin research area and discuss the emerging therapeutic potential of this peptide for both metabolic and cardiovascular complications of diabetes. AbbreviationsBK Ca , large conductance calcium-activated potassium channel; CART, cocaine-and amphetamine-related transcript; CCK, cholecystokinin; CRF, corticotrophin-releasing factor; GI, gastrointestinal; GLP-1, glucagon-like peptide-1; GLUT-4, glucose transporter type 4; HOMA-IR, homeostatic model assessment of insulin resistance; NPY, neuropeptide Y; PEG, polyethylene glycol; PI3K, phosphoinositide 3-kinase; POMC, proopiomelanocortin; SK6l, ribosomal protein s6 kinase; T1DM, type 1 diabetes mellitus; T2DM, type 2 diabetes mellitus; WAT, white adipose tissue.

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Circulating ghrelin and ghrelin to obestatin ratio are low in patients with untreated mild-to-moderate hypertension

Cited by 25 publications

References 18 publications

Ghrelin and obestatin levels in hypertensive obese patients

Ghrelin and obestatin levels in hypertensive obese patients

Sympathetic nervous system in obesity-related hypertension: mechanisms and clinical implications

Obestatin as a key regulator of metabolism and cardiovascular function with emerging therapeutic potential for diabetes

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