Ghrelin and obestatin levels in hypertensive obese patients

Wang, Weimin; Li, Shumei; Du, Fang; Zhu, Zhicheng; Zhang, Jichang

doi:10.1177/0300060514543040

Cited by 29 publications

(25 citation statements)

References 25 publications

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“…This is in agreement with the results of previously published studies, proving a compensatory decrease in ghrelin when adipose tissue increases [14,24]. However, some previous studies in children found no correlation between ghrelin and obesity-related hypertension, a correlation that was recently shown in adults [15,25]. In addition, our finding of the role of ghrelin in normal weight hypertension has not been found in any previous studies in children.…”

Section: Discussionsupporting

confidence: 93%

The associations between some biological markers, obesity, and cardiovascular risk in Slovenian children and adolescents

2020

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Introduction: The occurrence of cardiovascular diseases and metabolic disorders steadily increases with the body mass index (BMI). Since the latter is not the best and earliest indicator of obesity and cardiovascular risk, the aim of the study was to evaluate some potential biological markers that would allow us to detect children and adolescents at higher risk at an early stage. Methods: A sample of 330 children and adolescents were included in the study and divided into four groups: obese patients with hypertension, normal-weight patients with hypertension, patients with mildly elevated lipids and a control group of healthy children and adolescents. Some clinical parameters (age, body weight, body height, BMI, waist circumference, hip circumference, blood pressure), biochemical parameters (glucose, total cholesterol, triglycerides, HDL, LDL, apolipoprotein A1, homocysteine) and biological markers of obesity (ghrelin, adiponectin, leptin) were evaluated. Results: Ghrelin and adiponectin were found to have a strong negative statistically significant correlation with BMI in all three observed groups (p < 0.001), but not in the control group (p = 0.053 and p = 0.316, respectively). In addition, leptin had a strong positive statistically significant correlation with BMI in all four groups (p < 0.001 for the research groups, p = 0.009 for the controls). In the group of obese patients with hypertension, statistically significant differences in all three markers of obesity were found in comparison to the control group (p < 0.001 for all markers). In the group of patients with mildly elevated lipids, ghrelin and leptin were significantly different (p = 0.002 and p < 0.001, respectively). In the group of normal-weight hypertensive patients, only values of ghrelin were different compared to the control group (p = 0.001). Conclusion: In the research groups, significant differences were found in clinical, biochemical and biological parameters compared to the control group. The observed biological markers of obesity are useful early markers for identifying groups of patients that are at cardiovascular risk.

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Section: Discussionsupporting

confidence: 93%

The associations between some biological markers, obesity, and cardiovascular risk in Slovenian children and adolescents

2020

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“…Similar to the physiological situation, the data have been somewhat inconsistent (likely due to the reasons previously discussed), although it seems that obestatin levels are generally altered in diabetes and obesity. For example, decreased circulating obestatin has been documented in overweight/obese patients and those with impaired glucose control, metabolic syndrome, T2DM and insulin resistance (Anderwald‐Stadler et al ., ; Qi et al ., ; Fontenot et al ., ; Guo et al ., ; Gao et al ., ; Huda et al ., ; Nakahara et al ., ; Zou et al ., ; Beasley et al ., ; Cui et al ., ; Shen et al ., ; Gu et al ., ; Wang et al ., ). Inverse correlations between circulating obestatin and body mass index, insulin, glucose, leptin, homeostatic model assessment of insulin resistance and glycated haemoglobin have also been reported (Lippl et al ., ; Nakahara et al ., ; Gu et al ., ; Shen et al ., ; Wang et al ., ), with reduced numbers of obestatin‐positive cells evident in the gastric mucosa of overweight/obese subjects with abdominal obesity (Gao et al ., ).…”

Section: Metabolic Actions Of Obestatinmentioning

confidence: 97%

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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“…58 Plasma ghrelin levels are negatively correlated with body mass index and body fat percentage, being considered a "reverse adiposity signal". 20 Accordingly, recent studies have demonstrated that obese people have low ghrelin levels, 59 while patients with anorexia have high plasma ghrelin levels 60 compared with healthy normal weight subjects. Moreover, variations in body weight (weight gain or loss) were observed to lead to compensatory responses of ghrelin levels.…”

Section: Ghrelin and Weight Statusmentioning

confidence: 99%

Effects of ghrelin in energy balance and body weight homeostasis

Mihalache¹,

Gherasim²,

Niţă³

et al. 2016

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ghrelin is a gut peptide composed of 28 amino acids mostly secreted in the gastric fundus mucosa. It was isolated and described in 1999 by Kojima et al. and only three years later its specific receptor, ghsR1a, was also identified. ghrelin, the endogenous ligand for the gh secretagogue receptor, is the only peripheral orexigenic hormone that activates the receptors to be found especially in the appetite center (hypothalamus and pituitary gland). ghrelin is present in human plasma in two forms: an inactive form known as deacylated ghrelin, and an active form called acylated ghrelin synthesized under the action of ghrelin O-acyltransferase enzyme (gOAT). The literature even mentions an extremely complex ghrelin/gOAT/ghsR system involved in the regulation of human energy, metabolism and adaptation of energy homeostasis to environmental changes. In humans, there is a preprandial rise and a postprandial fall in plasma ghrelin levels, which strongly suggest that the peptide plays a physiological role in meal initiation and may be employed in determining the amount and quality of ingested food. Besides the stimulation of food intake, ghrelin determines a decrease in energy expenditure and promotes the storage of fatty acids in adipocytes. Thus, in the human body ghrelin induces a positive energy balance, an increased adiposity gain, as well as an increase in caloric storage, seen as an adaptive mechanism to caloric restriction conditions. In the current world context, when we are witnessing an increasing availability of food and a reduction of energy expenditure to a minimum level, these mechanisms have become pathogenic. As a consequence, the hypothesis that ghrelin is involved in the current obesity epidemic has been embraced by many scholars and researchers

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Ghrelin and obestatin levels in hypertensive obese patients

Cited by 29 publications

References 25 publications

The associations between some biological markers, obesity, and cardiovascular risk in Slovenian children and adolescents

The associations between some biological markers, obesity, and cardiovascular risk in Slovenian children and adolescents

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

Effects of ghrelin in energy balance and body weight homeostasis

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