Ghrelin and Growth

Perchard, Reena; Clayton, Peter E.

doi:10.1159/000475732

Cited by 20 publications

(11 citation statements)

References 67 publications

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“…Ghrelin and GHSR1a are widely present in various organs [ 14 ]. After binding together, ghrelin plays a variety of biological effects [ 22 ]. While multiple studies indicate that ghrelin plays an important role in controlling energy supply [ 23 , 24 ], pathways mediating endothelial cells are less well-described.…”

Section: Discussionmentioning

confidence: 99%

Ghrelin Stimulates Endothelial Cells Angiogenesis through Extracellular Regulated Protein Kinases (ERK) Signaling Pathway

Wang

Huwatibieke

et al. 2018

IJMS

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Adipose tissue is hyper-vascularized. Vessels in adipose tissue not only supply nutrients and oxygen to nourish adipocytes, but also provide cytokines that regulate mass and function of adipose tissue. Understanding the fundamental mechanisms how vessels modulate adipocyte functions would provide new therapeutic options for treatment of metabolic disease and obesity. In recent years, researches about ghrelin are focused on glucose and lipid metabolism, but its effect on vascular function remains uncharacterized. In the present study, ghrelin receptor gene deletion mice (Ghsr−/− mice) were used to study ghrelin-regulated vascular metabolism in white adipose tissue. Ghsr−/− mice demonstrated lower food intake, lower body weight, and resistance to high-fat diet-induced obesity. The number of vessels in white adipose tissue was decreased in Ghsr−/− mice when compared with wild type mice fed with high-fat diet. To further define ghrelin effects in vitro, we used endothelial progenitor cells from wild type and Ghsr−/− mice as well as human umbilical vein endothelial cells in our experiments. We found that ghrelin stimulated endothelial cells angiogenesis and migration through the MEK-ERK signaling pathway. [d-Lys3]-GHRP-6 and PD98059 could reverse the effects of ghrelin on endothelial cells. Our study indicates that ghrelin activates its receptor on endothelial cells to promote angiogenesis and migration via a mechanism involving the extracellular regulated protein kinases (ERK) signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Ghrelin Stimulates Endothelial Cells Angiogenesis through Extracellular Regulated Protein Kinases (ERK) Signaling Pathway

Wang

Huwatibieke

et al. 2018

IJMS

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“…In terms of vascular biology, that hypophysectomy in the male rat markedly impaired arterial remodeling after aortic balloon injury in terms of reduced vascular SMC proliferation and myointima formation, was reported in 1978 [ 53 ], and confirmed [ 54 ], but this research was not pursued further. Moreover, that ghrelin, a GH secretagogue and vasodilator (which antagonizes endothelin-1), inhibited hypoxia- or monocrotaline-induced PA remodeling in male rats is now known [ 55 – 57 ], yet neuroendocrine mechanisms have received little attention in the sex bias observed in vascular disease. Thus far, most research on sex bias in the vascular field has focused on the direct effects of sex hormones on vascular tissues [ 6 , 7 , 9 – 18 ].…”

Section: Discussionmentioning

confidence: 99%

Smooth Muscle-Specific BCL6+/− Knockout Abrogates Sex Bias in Chronic Hypoxia-Induced Pulmonary Arterial Hypertension in Mice

Yang

Sehgal

2018

International Journal of Endocrinology

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The “estrogen paradox” in pulmonary arterial hypertension (PAH) refers to observations that while there is a higher incidence of idiopathic PAH in women, rodent models of PAH show male dominance and estrogens are protective. To explain these differences, we previously proposed the neuroendocrine-STAT5-BCL6 hypothesis anchored in the sex-biased and species-specific patterns of growth hormone (GH) secretion by the pituitary, the targeting of the hypothalamus by estrogens to feminize GH secretion patterns, and the role of the transcription factors STAT5a/b and BCL6 as downstream mediators of this patterned GH-driven sex bias. As a test of this hypothesis, we previously reported that vascular smooth muscle cell- (SMC-) specific deletion of the STAT5a/b locus abrogated the male-dominant sex bias in the chronic hypoxia model of PAH in mice. In the present study, we confirmed reduced BCL6 expression in pulmonary arterial (PA) segments in both male and female SMC:STAT5a/b−/− mice. In order to test the proposed contribution of BCL6 to sex bias in PAH, we developed mice with SMC-specific deletion of BCL6+/− by crossing SM22α-Cre mice with BCL6-floxed mice and investigated sex bias in these mutant mice in the chronic hypoxia model of PAH. We observed that the male-bias observed in wild-type- (wt-) SM22α-Cre-positive mice was abrogated in the SMC:BCL6+/− knockouts—both males and females showed equivalent enhancement of indices of PAH. The new data confirm BCL6 as a contributor to the sex-bias phenotype observed in hypoxic PAH in mice and support the neuroendocrine-STAT5-BCL6 hypothesis of sex bias in this experimental model of vascular disease.

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“…Physiologically, GH secretion is controlled by the hypothalamus through stimulating growth hormone releasing hormones (somatoliberin, GHRH) and inhibitory somatostatin (SRIF) [ 76 ]. Moreover, the enteric hormone ghrelin is also involved in the regulation of GH secretion [ 77 , 78 , 79 ]. This corresponds to physiological stimuli, such as sleep and wakefulness, food intake, physical activity and stress [ 76 ].…”

Section: Endocrine Disorders In the Course Of Sepsismentioning

confidence: 99%

“…Ghrelin, mainly secreted by stomach fundus cells, acts as an appetite stimulant, but has many other effects. It is believed to play an important role in the regulation of metabolism [ 77 ]. The increase in ghrelin concentration in sepsis has been observed in patients and in the experimental model [ 97 , 98 ].…”

Section: Endocrine Disorders In the Course Of Sepsismentioning

confidence: 99%

Sepsis as a Pan-Endocrine Illness—Endocrine Disorders in Septic Patients

Wasyluk

Zwolak

2021

JCM

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Sepsis is defined as “life-threatening organ dysfunction caused by a dysregulated host response to infection”. One of the elements of dysregulated host response is an endocrine system disorder. Changes in its functioning in the course of sepsis affect almost all hormonal axes. In sepsis, a function disturbance of the hypothalamic–pituitary–adrenal axis has been described, in the range of which the most important seems to be hypercortisolemia in the acute phase. Imbalance in the hypothalamic–pituitary–thyroid axis is also described. The most typical manifestation is a triiodothyronine concentration decrease and reverse triiodothyronine concentration increase. In the somatotropic axis, a change in the secretion pattern of growth hormone and peripheral resistance to this hormone has been described. In the hypothalamic–pituitary–gonadal axis, the reduction in testosterone concentration in men and the stress-induced “hypothalamic amenorrhea” in women have been described. Catecholamine and β-adrenergic stimulation disorders have also been reported. Disorders in the endocrine system are part of the “dysregulated host response to infection”. They may also affect other components of this dysregulated response, such as metabolism. Hormonal changes occurring in the course of sepsis require further research, not only in order to explore their potential significance in therapy, but also due to their promising prognostic value.

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Ghrelin and Growth

Cited by 20 publications

References 67 publications

Ghrelin Stimulates Endothelial Cells Angiogenesis through Extracellular Regulated Protein Kinases (ERK) Signaling Pathway

Ghrelin Stimulates Endothelial Cells Angiogenesis through Extracellular Regulated Protein Kinases (ERK) Signaling Pathway

Smooth Muscle-Specific BCL6+/− Knockout Abrogates Sex Bias in Chronic Hypoxia-Induced Pulmonary Arterial Hypertension in Mice

Sepsis as a Pan-Endocrine Illness—Endocrine Disorders in Septic Patients

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