Relevant bibliographies by topics / Ghrelin levels

Academic literature on the topic 'Ghrelin levels'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Ghrelin levels"

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Takahashi, T., K. Sato, S. Kato, T. Yonezawa, Y. Kobayashi, Y. Ohtani, S. Ohwada, et al. "Increased plasma ghrelin suppresses insulin release in wethers fed with a high-protein diet." Journal of Endocrinology 221, no. 3 (March 17, 2014): 371–80. http://dx.doi.org/10.1530/joe-13-0501.

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Ghrelin is a multifunctional peptide that promotes an increase of food intake and stimulates GH secretion. Ghrelin secretion is regulated by nutritional status and nutrients. Although a high-protein (HP) diet increases plasma ghrelin secretion in mammals, the mechanisms and the roles of the elevated ghrelin concentrations due to a HP diet have not been fully established. To clarify the roles of elevated acylated ghrelin upon intake of a HP diet, we investigated the regulation of ghrelin concentrations in plasma and tissues in wethers fed with either the HP diet or the control (CNT) diet for 14 days, and examined the action of the elevated plasma ghrelin by using a ghrelin-receptor antagonist. The HP diet gradually increased the plasma acylated-ghrelin concentrations, but the CNT diet did not. Although the GH concentrations did not vary significantly across the groups, an injection of ghrelin-receptor antagonist enhanced insulin levels in circulation in the HP diet group. In the fundus region of the stomach, the ghrelin levels did not differ between the HP and CNT diet groups, whereas ghrelinO-acyltransferase mRNA levels were higher in the group fed with HP diet than those of the CNT diet group were. These results indicate that the HP diet elevated the plasma ghrelin levels by increasing its synthesis; this elevation strongly suppresses the appearance of insulin in the circulation of wethers, but it is not involved in GH secretion. Overall, our findings indicate a role of endogenous ghrelin action in secretion of insulin, which acts as a regulator after the consumption of a HP diet.
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Wu, Rongqian, Mian Zhou, Padmalaya Das, Weifeng Dong, Youxin Ji, Derek Yang, Michael Miksa, Fangming Zhang, Thanjavur S. Ravikumar, and Ping Wang. "Ghrelin inhibits sympathetic nervous activity in sepsis." American Journal of Physiology-Endocrinology and Metabolism 293, no. 6 (December 2007): E1697—E1702. http://dx.doi.org/10.1152/ajpendo.00098.2007.

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Our previous studies have shown that norepinephrine (NE) upregulates proinflammatory cytokines by activating α2-adrenoceptor. Therefore, modulation of the sympathetic nervous system represents a novel treatment for sepsis. We have also shown that a novel stomach-derived peptide, ghrelin, is downregulated in sepsis and that its intravenous administration decreases proinflammatory cytokines and mitigates organ injury. However, it remains unknown whether ghrelin inhibits sympathetic activity through central ghrelin receptors [i.e., growth hormone secretagogue receptor 1a (GHSR-la)] in sepsis. To study this, sepsis was induced in male rats by cecal ligation and puncture (CLP). Ghrelin was administered through intravenous or intracerebroventricular injection 30 min before CLP. Our results showed that intravenous administration of ghrelin significantly reduced the elevated NE and TNF-α levels at 2 h after CLP. NE administration partially blocked the inhibitory effect of ghrelin on TNF-α in sepsis. GHSR-la inhibition by the administration of a GHSR-la antagonist, [d-Arg1,d-Phe5, d-Trp7,9,Leu11]substance P, significantly increased both NE and TNF-α levels even in normal animals. Markedly elevated circulating levels of NE 2 h after CLP were also significantly decreased by intracerebroventricular administration of ghrelin. Ghrelin's inhibitory effect on NE release was completely blocked by intracerebroventricular injection of the GHSR-1a antagonist or a neuropeptide Y (NPY)/Y1 receptor antagonist. However, ghrelin's downregulatory effect on TNF-α release was only partially diminished by these agents. Thus ghrelin has sympathoinhibitory properties that are mediated by central ghrelin receptors involving a NPY/Y1 receptor-dependent pathway. Ghrelin's inhibitory effect on TNF-α production in sepsis is partially because of its modulation of the overstimulated sympathetic nerve activation.
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Delporte, Christine. "Recent Advances in Potential Clinical Application of Ghrelin in Obesity." Journal of Obesity 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/535624.

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Ghrelin is the natural ligand of the growth hormone secretagogue receptor (GHS-R1a). Ghrelin is a 28 amino acid peptide possessing a unique acylation on the serine in position 3 catalyzed by ghrelinO-acyltransferase (GOAT). Ghrelin stimulates growth hormone secretion, but also appetite, food intake, weight gain, and gastric emptying. Ghrelin is involved in weight regulation, obesity, type 2 diabetes, and metabolic syndrome. Furthermore, a better understanding of ghrelin biology led to the identification of molecular targets modulating ghrelin levels and/or its biological effects: GOAT, ghrelin, and GHS-R1a. Furthermore, a recent discovery, showing the involvement of bitter taste receptor T2R in ghrelin secretion and/or synthesis and food intake, suggested that T2R could represent an additional interesting molecular target. Several classes of ghrelin-related pharmacological tools for the treatment of obesity have been or could be developed to modulate the identified molecular targets.
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Chuang, Jen-Chieh, and Jeffrey M. Zigman. "Ghrelin's Roles in Stress, Mood, and Anxiety Regulation." International Journal of Peptides 2010 (February 14, 2010): 1–5. http://dx.doi.org/10.1155/2010/460549.

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Several studies suggest that the peptide hormone ghrelin mediates some of the usual behavioral responses to acute and chronic stress. Circulating ghrelin levels have been found to rise following stress. It has been proposed that this elevated ghrelin helps animals cope with stress by generating antidepressant-like behavioral adaptations, although another study suggests that decreasing CNS ghrelin expression has antidepressant-like effects. Ghrelin also seems to have effects on anxiety, although these have been shown to be alternatively anxiogenic or anxiolytic. The current review discusses our current understanding of ghrelin's roles in stress, mood, and anxiety.
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Kellokoski, Eija, Seppo M. Pöykkö, Anna H. Karjalainen, Olavi Ukkola, Jorma Heikkinen, Y. Antero Kesäniemi, and Sohvi Hörkkö. "Estrogen Replacement Therapy Increases Plasma Ghrelin Levels." Journal of Clinical Endocrinology & Metabolism 90, no. 5 (May 1, 2005): 2954–63. http://dx.doi.org/10.1210/jc.2004-2016.

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Ghrelin is a novel peptide hormone that has GH releasing activity and also other endocrine and metabolic functions. The purpose of this study was to investigate the effects of estrogen replacement therapy on plasma active ghrelin levels in 64 hysterectomized postmenopausal women receiving peroral estrogen (PE) or transdermal estrogen therapy for 6 months. Active ghrelin was measured using commercial RIA. Estrogen therapy increased plasma active ghrelin from 479 ± 118 to 521 ± 123 pg/ml (P = 0.002) among all the study subjects. PE therapy increased plasma ghrelin levels from 465 ± 99 to 536 ± 104 pg/ml (P = 0.001). Transdermal estrogen therapy did not increase plasma ghrelin levels significantly (from 491 ± 132 to 509 ± 138 pg/ml; P = 0.332). The relative changes in plasma ghrelin levels were associated with the relative changes in serum estradiol concentrations (r = 0.299; P = 0.017). During the estrogen therapy, negative associations were found between plasma active ghrelin levels and several plasma lipids (total cholesterol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, total triglycerides, and very low-density lipoprotein triglycerides). As a conclusion, estrogen replacement therapy increased active plasma ghrelin levels, particularly PE therapy. Additional studies are needed to determine the possible underlying mechanisms.
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Frazao, Renata, Heather M. Dungan Lemko, Regina P. da Silva, Dhirender V. Ratra, Charlotte E. Lee, Kevin W. Williams, Jeffrey M. Zigman, and Carol F. Elias. "Estradiol modulates Kiss1 neuronal response to ghrelin." American Journal of Physiology-Endocrinology and Metabolism 306, no. 6 (March 15, 2014): E606—E614. http://dx.doi.org/10.1152/ajpendo.00211.2013.

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Ghrelin is a metabolic signal regulating energy homeostasis. Circulating ghrelin levels rise during starvation and fall after a meal, and therefore, ghrelin may function as a signal of negative energy balance. Ghrelin may also act as a modulator of reproductive physiology, as acute ghrelin administration suppresses gonadotropin secretion and inhibits the neuroendocrine reproductive axis. Interestingly, ghrelin's effect in female metabolism varies according to the estrogen milieu predicting an interaction between ghrelin and estrogens, likely at the hypothalamic level. Here, we show that ghrelin receptor (GHSR) and estrogen receptor-α (ERα) are coexpressed in several hypothalamic sites. Higher levels of circulating estradiol increased the expression of GHSR mRNA and the co-xpression of GHSR mRNA and ERα selectively in the arcuate nucleus (ARC). Subsets of preoptic and ARC Kiss1 neurons coexpressed GHSR. Increased colocalization was observed in ARC Kiss1 neurons of ovariectomized estradiol-treated (OVX + E2; 80%) compared with ovariectomized oil-treated (OVX; 25%) mice. Acute actions of ghrelin on ARC Kiss1 neurons were also modulated by estradiol; 75 and 22% of Kiss1 neurons of OVX + E2 and OVX mice, respectively, depolarized in response to ghrelin. Our findings indicate that ghrelin and estradiol may interact in several hypothalamic sites. In the ARC, high levels of E2 increase GHSR mRNA expression, modifying the colocalization rate with ERα and Kiss1 and the proportion of Kiss1 neurons acutely responding to ghrelin. Our findings indicate that E2 alters the responsiveness of kisspeptin neurons to metabolic signals, potentially acting as a critical player in the metabolic control of the reproductive physiology.
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Tsubone, Tetsuo, Takayuki Masaki, Isao Katsuragi, Katsuhiro Tanaka, Tetsuya Kakuma, and Hironobu Yoshimatsu. "Leptin downregulates ghrelin levels in streptozotocin-induced diabetic mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 6 (December 2005): R1703—R1706. http://dx.doi.org/10.1152/ajpregu.00773.2004.

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Ghrelin, an orexigenic peptide produced in the stomach, is increased in streptozotocin (STZ)-induced diabetic (DM) mice. This study clarifies the regulation of ghrelin levels by leptin in STZ-DM mice. STZ-DM mice had higher plasma ghrelin concentrations and greater ghrelin mRNA expression than control mice. Changes in ghrelin levels were dose dependently attenuated by the subcutaneous injection of leptin (0–27 nmol·kg−1·day−1 over 7 days). Leptin treatment also partially reversed the hyperphagia and hyperglycemia observed in STZ-DM mice, but not the hypoinsulinemia, and there was a decrease in plasma ghrelin concentrations and ghrelin mRNA levels compared with STZ-LEP pair-fed mice. These results indicate that leptin treatment partially reverses elevated plasma ghrelin levels in STZ-DM mice independent of food intake and insulin, and suggest that hypoleptinemia in STZ-DM mice upregulates ghrelin.
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Erensoy, Ahmet, Suleyman Aydin, Neslihan Kelestimur, Sevda Kirbag, and Salih Kuk. "The Change of Ghrelin Levels in Intestinal Parasitic Infections." Journal of Medical Biochemistry 29, no. 1 (January 1, 2010): 34–38. http://dx.doi.org/10.2478/v10011-010-0004-0.

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The Change of Ghrelin Levels in Intestinal Parasitic InfectionsThe aim of this work was to examine the relationship between active (acylated ghrelin) and inactive (desacylated ghrelin) ghrelin in the serum and other serum parameters in intestinal parasitic infections and healthy controls. Conventional microscopic methods (saline and iodine solutions, trichrome stain) were used to identify intestinal parasites in stool samples of 29 subjects attending Firat University Hospital. Serum parameters were assessed in a single measurement of serum from 29 parasite subjects, and in 18 healthy controls. Serum acylated ghrelin and desacylated ghrelin levels were measured using a commercial radioimmunoassay (RIA) kit. Paraoxonase and arylesterase were measured by using a spectrophotometer at 405 nm and 270 nm, respectively. Serum concentrations of acylated ghrelin and desacylated ghrelin were more markedly decreased in helminth bearing patients than the control group. Glucose, cholesterol and triglyceride levels were higher in intestinal parasitic infections than in controls. Furthermore, there were no correlations between ghrelin levels and BMI. These results indicate that low ghrelin and PON1/AE level may be important for appetite monitoring in intestinal parasitic infections.
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Holliday, Nicholas D., Birgitte Holst, Elena A. Rodionova, Thue W. Schwartz, and Helen M. Cox. "Importance of Constitutive Activity and Arrestin-Independent Mechanisms for Intracellular Trafficking of the Ghrelin Receptor." Molecular Endocrinology 21, no. 12 (December 1, 2007): 3100–3112. http://dx.doi.org/10.1210/me.2007-0254.

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Abstract The ghrelin receptor (GhrelinR) and its related orphan GPR39 each display constitutive signaling, but only GhrelinRs undergo basal internalization. Here we investigate these differences by considering the roles of the C tail receptor domains for constitutive internalization and activity. Furthermore the interaction between phosphorylated receptors and β-arrestin adaptor proteins has been examined. Replacement of the FLAG-tagged GhrelinR C tail with the equivalent GPR39 domain (GhR-39 chimera) preserved Gq signaling. However in contrast to the GhrelinR, GhR-39 receptors exhibited no basal and substantially decreased agonist-induced internalization in transiently transfected HEK293 cells. Internalized GhrelinR and GhR-39 were predominantly localized to recycling compartments, identified with transferrin and the monomeric G proteins Rab5 and Rab11. Both the inverse agonist [d-Arg1, d-Phe5, d-Trp7,9, Leu11] substance P and a naturally occurring mutant GhrelinR (A204E) with eliminated constitutive activity inhibited basal GhrelinR internalization. Surprisingly, we found that noninternalizing GPR39 was highly phosphorylated and that basal and agonist-induced phosphorylation of the GhR-39 chimera was elevated compared with GhrelinRs. Moreover, basal GhrelinR endocytosis occurred without significant phosphorylation, and it was not prevented by cotransfection of a dominant-negative β-arrestin1(319–418) fragment or by expression in β-arrestin1/2 double-knockout mouse embryonic fibroblasts. In contrast, agonist-stimulated GhrelinRs recruited the clathrin adaptor green fluorescent protein-tagged β-arrestin2 to endosomes, coincident with increased receptor phosphorylation. Thus, GhrelinR internalization to recycling compartments depends on C-terminal motifs and constitutive activity, but the high levels of GPR39 phosphorylation, and of the GhR-39 chimera, are not sufficient to drive endocytosis. In addition, basal GhrelinR internalization occurs independently of β-arrestins.
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Lin, Tsung-Chieh, Yuan-Ming Yeh, Wen-Lang Fan, Yu-Chan Chang, Wei-Ming Lin, Tse-Yen Yang, and Michael Hsiao. "Ghrelin Upregulates Oncogenic Aurora A to Promote Renal Cell Carcinoma Invasion." Cancers 11, no. 3 (March 4, 2019): 303. http://dx.doi.org/10.3390/cancers11030303.

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Ghrelin is a peptide hormone, originally identified from the stomach, that functions as an endogenous ligand of the growth hormone secretagogue receptor (GHSR) and promotes growth hormone (GH) release and food intake. Increasing reports point out ghrelin’s role in cancer progression. We previously characterized ghrelin’s prognostic significance in the clear cell subtype of renal cell carcinoma (ccRCC), and its pro-metastatic ability via Snail-dependent cell migration. However, ghrelin’s activity in promoting cell invasion remains obscure. In this study, an Ingenuity Pathway Analysis (IPA)-based investigation of differentially expressed genes in Cancer Cell Line Encyclopedia (CCLE) dataset indicated the potential association of Aurora A with ghrelin in ccRCC metastasis. In addition, a significant correlation between ghrelin and Aurora A expression level in 15 ccRCC cell line was confirmed by variant probes. ccRCC patients with high ghrelin and Aurora A status were clinically associated with poor outcome. We further observed that ghrelin upregulated Aurora A at the protein and RNA levels and that ghrelin-induced ccRCC in vitro invasion and in vivo metastasis occurred in an Aurora A-dependent manner. Furthermore, MMP1, 2, 9 and 10 expressions are associated with poor outcome. In particular, MMP10 is significantly upregulated and required for the ghrelin-Aurora A axis to promote ccRCC invasion. The results of this study indicated a novel signaling mechanism in ccRCC metastasis.
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Dissertations / Theses on the topic "Ghrelin levels"

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Ramírez, Flores Sara. "Hypothalamic Ceramide Levels regulated by CPT1C mediate the Orexigenic effect of Ghrelin." Doctoral thesis, Universitat Internacional de Catalunya, 2014. http://hdl.handle.net/10803/276184.

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Recent data suggest that ghrelin exerts its orexigenic action through regulation of hypothalamic AMP-activated protein kinase pathway, leading to a decline in malonyl-CoA levels and desinhibition of carnitine palmitoyltransferase 1A (CPT1A), which increases mitochondrial fatty acid oxidation and ultimately enhances the expression of the orexigenic neuropeptides agouti-related protein (AgRP) and neuropeptide Y (NPY). However, it is unclear whether the brain-specific isoform CPT1C, which is located in the endoplasmic reticulum of neurons, may play a role in this action. Here, we demonstrate that the orexigenic action of ghrelin is totally blunted in CPT1C knockout (KO) mice, despite having the canonical ghrelin signaling pathway activated. We also demonstrate that ghrelin elicits a marked upregulation of hypothalamic C18:0 ceramide levels mediated by CPT1C. Notably, central inhibition of ceramide synthesis with myriocin negated the orexigenic action of ghrelin and normalized the levels of AgRP and NPY, as well as their key transcription factors phosphorylated cAMP-response element-binding protein and forkhead box O1. Furthermore, central treatment with ceramide induced food intake and orexigenic neuropeptides expression in CPT1C KO mice. Third, we demonstrate that ceramides act increasing the BSX expression, the transcription factor that works coordinately with pCREB and FoxO1 to increase orexigenic neuropeptides. Finally we link CPT1C and longevity as we have seen that CPT1CKO mice have reduced lifespan. Overall, these data indicate that, in addition to formerly reported mechanisms, ghrelin also induces food intake through regulation of hypothalamic CPT1C and ceramide metabolism
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James, Rachel J. A. "Relationships between cord blood leptin and ghrelin levels, milk intake and weight gain in human infants." Thesis, Durham University, 2003. http://etheses.dur.ac.uk/4065/.

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Leptin and ghrelin are hormones involved in the regulation of appetite and adiposity. Leptin suppresses appetite and induces weight loss; ghrelin stimulates appetite and promotes weight gain. The study reported in this thesis was designed to examine the relationship of cord blood leptin and ghrelin with milk intake over the first week of life, and with infant growth up to twelve weeks of age. One hundred term formula fed newborns were recruited at birth. Leptin and ghrelin were measured in cord blood by radioimmunoassay. Milk intake was measured by weighing of bottles of formula milk before and after feeding. Measurements of weight, length and head circumference were taken at birth, seven days and at twelve weeks of age. A number of control variables were also measured. Birthweight was a significant predictor of mean milk intake, which rose significantly from days 1 to 7, with no difference between males and females. Weight gain or loss in the early neonatal period was a direct and significant consequence of milk intake consumed over that period. There was no relationship between cord blood leptin or ghrelin (controlling for birthweight) on the infants' milk intake over the first 24 hours of life or on their mean milk intake over the first week of life. Weight gain was significantly correlated with birthweight, with higher birthweight associated with lower weight gain. There was no relationship between cord leptin and weight gain to three months of age after adjusting for birthweight; but lower cord ghrelin levels were significantly associated with slower weight gain.
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Jewett, Benjamin E. "Inverse Changes in Ghrelin and A2A Receptor Gene Expression Levels in the Hippocampus of Heart Failure Canines Following Spinal Cord Stimulation." Digital Commons @ East Tennessee State University, 2015. https://dc.etsu.edu/honors/262.

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Myocardial infarction (MI), often referred to as a heart attack, is a serious health issue in the United States. There is a well-documented link between MI and major depressive disorder (MDD), with a high incidence of MDD occurring after an MI. Overlapping pathologies have been observed within the hippocampus of the brain in animal models of MI and depression. These observations suggest that pathobiological cross-talk between the heart and brain could have a role in the etiology of MDD that occurs after an MI. Spinal cord stimulation (SCS) has previously been shown to have both cardioprotective and neuroprotective effects post-MI, and hence may protect individuals from developing depression post-MI. In this study, we examined the potential biochemical mechanisms that might underlie the neuroprotective actions of SCS following MI. Brain tissues were obtained from three groups of canines: sham-operated animals, animals subjected to experimental myocardial infarction/mitral regurgitation (MI/MR), and animals subjected to MI/MR that were simultaneously administered SCS. The whole hippocampus and hippocampal dentate gyrus were dissected from frozen brains. Quantitative endpoint-PCR and RT-qPCR techniques were employed to measure select biochemical mediators of neuroprotection, i.e. adenosine A2A receptor, ghrelin, and ghrelin receptor expression in hippocampal samples. SCS induced a significant decrease in A2A receptor expression and a dramatic increase in ghrelin expression in MI/MR canines as compared to the MI/MR group without SCS. These findings suggest that adenosine receptors and ghrelin may play a biochemical role in SCS-induced neuroprotection of the hippocampus. Understanding the neuroprotective actions of SCS has the potential to aid the development of new treatments or preventative measures for depression following a heart attack.
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Voruganti, Venkata Saroja Freeland-Graves Jeanne H. "Obesity-associated phenotypes and circulating levels of ghrelin, cholecystokinin, low-density lipoprotein and zinc genetic and observational studies /." 2005. http://repositories.lib.utexas.edu/bitstream/handle/2152/1750/vorugantiv45585.pdf.

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Hsieh, Yao-Peng, and 謝堯棚. "The role of serum hepcidin and ghrelin levels in cardiac function among patients with chronic kidney disease." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/58626947831466634365.

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碩士
中國醫藥大學
臨床醫學研究所碩士班
98
Background: Hepcidin, a recently discovered 25-amino acid peptide, is mainly synthesized, processed and secreted by hepatocytes. It is the key regulator in iron homeostasis. Renal clearance may be an important way for its excretion, but the influence of estimated glomerular filtration rate (eGFR) on serum level of hepcidin-25 is inconsistent among different reports. Cardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD). Iron plays a key role in cardiac diseases, such as iron-overload cardiomyopathy, myocardial ischemia-reperfusion injury, and atherosclerosis. Cardiac expression of hepcidin was demonstrated on mRNA and protein level in vivo in a rat model. Ghrelin is a 28-amino-acid pepetide mainly secreted by gastric fundus and it can stimulate secretion of growth hormone, increase food intake and produce weight gain. In animal models, ghrelin decreased blood pressure, increased stroke volume and inhibited apoptosis of myocardiocyte and endothelium, thus protecting heart. Thus, we aim to investigate the relationship of serum hepcidin and ghrelin level to renal function and left ventricular function in patients with CKD. Methods: We enrolled a cohort of 146 CKD patients, ranging from CKD stage 1 to CKD stage 5, not requiring dialysis. After an overnight fasting for at least 8 hours, a one-time blood sample was collected for measurement biochemical data. Plasma bioactive hepcidin-25 and total ghrelin ( acylated and des-acylated forms) were measured in duplicate by competitive ELISA. Echocardiography was performed by a qualified cardiologist. Results: There was a significant difference in serum hepcidin levels between each CKD stage patients by Kruskal Wallis test ( p = 0.039). In addition, serum hepcidin levels in each CKD stage patients were lower significantly, compared with those in higher CKD stage patients by Jonckheere Terpstra test ( p=0.002). The Pearson correlation analysis demonstrated that serum hepcidin level was significantly and positively correlated with serum BUN, creatinine, phosphate, HDL cholesterol and LDL cholesterol, but negatively correlated with eGFR, serum hemoglobin, albumin and fasting blood sugar. There was no correlation between serum hepcidin and IL-6 or CRP( r = 0.183, p = 0.425; r = 0.19, p = 0.514, respectively ). In multivariate analysis, hepcidin was positively associated with ferritin and inversely correlated with eGFR. Hepcidin was also closely with left ventricle mass index (LVMI).( r = -0.014, p = 0.006). Serum ghrelin levels were not correlated with eGFR or CKD stages but positively with LVMI (r = 0.652，P= 0.003). Conclusion: The serum hepcidin level was closely associated with renal function in CKD patients. Hepcidin was also correlated inversely with LVMI and ghrelin was positively correlated with LVMI. Ghrelin and hepcidin may be crucial for cardiovascular morbidity and mortality in CKD patients.
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Voruganti, Venkata Saroja. "Obesity-associated phenotypes and circulating levels of ghrelin, cholecystokinin, low-density lipoprotein and zinc: genetic and observational studies." Thesis, 2005. http://hdl.handle.net/2152/1750.

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Books on the topic "Ghrelin levels"

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Wójcik-Gładysz, Anna. Ghrelin – hormone with many faces. Central regulation and therapy. The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, 2020. http://dx.doi.org/10.22358/mono_awg_2020.

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Discovered in 1999, ghrelin, is one of the peptides co-creating the hypothalamicgastrointestinal axis, otherwise known as the brain-gut axis. Ghrelin participates in many physiological processes and spectrum of its activity is still being discovered. This 28 amino acid peptide ‒ a product of the ghrl gene, was found in all vertebrates and is synthesized and secreted mainly from enteroendocrine X/A cells located in the gastric mucosa of the stomach. Expression of the ghrelin receptor has been found in many nuclei of the hypothalamus involved in appetite regulation. Therefore it’s presumed that ghrelin is one of the crucial hormones deciphering the energy status required for the maintenance of organism homeostasis. Ghrelin acts as a signal of starvation or energy insufficiency and its level in plasma is reduced after the meal. Neuropeptide Y (NPY) and agouti-related peptide (AgRP; NPY/AgRP) neurons located in the arcuate nucleus (ARC) area are the main target of ghrelin in the hypothalamus. This subpopulation of neurons is indispensable for inducing orexigenic action of ghrelin. Moreover ghrelin acting as a neurohormone, mainly in the hypothalamus area, plays an important role in the regulation of growth and reproduction processes. Indeed, ghrelin action on reproductive processes has been observed in the systemic effects exerted at both hypothalamus-pituitary and gonadal levels. Similarly the GH-releasing ghrelin action was observed both on the hypothalamus level and directly on the somatotrophic cells in the pituitary and this dose-related GH releasing activity was found in in vitro as well as in in vivo experiments. In recent years, numerous studies revealed that ghrelin potentially takes part in the treatment of diseases associated with serious disturbances in the organism energy balance and/or functioning of the gastrointestinal tract. It was underlined that ghrelin may be a hormone with a broad spectrum of therapeutic effect on obesity and anorexia nervosa, as well as may also have protective effect on neurodegenerative diseases, inflammatory disorders or functional changes in the body caused by cancers. In overall, ghrelin treatment has been tested in over 100 preclinical studies with healthy volunteers as well as patients with various types of cancer, eating disorders such as anorexia nervosa and bulimia nervosa. It was observed that ghrelin has an excellent clinical safety profile and emerging side effects occurred only in 3–10% of patients and did not constitute a sufficient premise to discontinue the therapy. In general, it can be concluded that ghrelin may be sufficiently used as a prescription drug.
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Jürimäe, Jaak. Hormones and training. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0033.

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Physical exercise regulates energy balance and is important to growth and maturation. These processes are regulated by the endocrine system. Endocrine mechanisms in the response to sport training include growth hormone-insulin-like growth factor-1 (GH-IGF-1), hypothalamic-pituitary-gonadal and hypothalamic-pituitary-adrenal axes, and peripheral markers of energy homeostasis. Physical performance is associated with anabolic adaptations of the GH-IGF-1 system in child athletes alongside spontaneous growth, while heavy training does not affect basal testosterone levels. In female adolescent athletes, the major factor altering reproductive hormone secretion is energy deficiency, rather than exercise stress or increase in exercise energy expenditure. Ghrelin is another indicator of energy imbalance across the menstrual cycle. Pubertal onset decreases ghrelin, and leptin levels are reduced and may remain unchanged between prepuberty and maturation in athletes. To better understand the influence of high training load on hormonal markers responsible for overall growth and energy homeostasis, growing athletes should be monitored often.
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Book chapters on the topic "Ghrelin levels"

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Malik, Sajid, and Sujith Wijerathne. "Laparoscopic Sleeve Gastrectomy." In Mastering Endo-Laparoscopic and Thoracoscopic Surgery, 285–90. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-3755-2_41.

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AbstractBariatric surgery (BS) has proved its role in treating obesity and related comorbidities. The number of Laparoscopic Sleeve Gastrectomies (LSGs) performed globally has increased markedly and has become “trendy” among bariatric surgeons in the last few years [1]. LSG has attained its position as the primary procedure of choice in bariatric surgery for morbid obesity. In this procedure, 80% of the stomach, mainly the body and fundus are removed longitudinally, leaving behind a sleeve of the stomach along the lesser curve [2, 3]. The procedure can be performed by minimally invasive approaches as well as single incision access or even robotic surgery with comparable results [4, 5]. The weight loss is achieved by restricting the food entering the stomach. Another factor in the effectiveness of weight loss in sleeve gastrectomy is the decrease in blood levels of ghrelin, “the hormone that stimulates hunger,” and a majority of cells responsible for producing this hormone is found in the fundus which is removed during this procedure. This procedure can be performed as the first stage in more complex bariatric cases including cases of super-obesity before procedures like Roux-en-Y gastric bypass or the duodenal switch can be performed [6]. The objective is to achieve an initial weight loss that would help to perform more extensive mixed restrictive or malabsorptive procedures safely and effectively [7–9].
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Biyikli, Halil Huseyin, Serhat Isik, Gonul Erden, Ufuk Ozuguz, Fatma Dogru, Ayse Arduc, Dilek Berker, and Serdar Guler. "Assessment of the Relation between Serum Ghrelin Levels of Patients with Hashimoto Thyroiditis and Obesity." In CLINICAL - Obesity: Causes & Consequences, P3–413—P3–413. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part3.p35.p3-413.

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Yeoh, Ester Chai Kheng, Chee Fang Sum, Su Chi Lim, Kian Chong Lim, Li Jiuen Ong, and Ling Choo Lim. "The Effect of Treatment of Hyperthyroidism on Body Composition and Its Correlation with Ghrelin Levels." In BASIC/TRANSLATIONAL/CLINICAL - Thyroid Gland Development & Function, P3–590—P3–590. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part4.p8.p3-590.

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Valsamakis, Georgios, Dimitrios Papatheodorou, Alexandra Margeli, Sudhesh Kumar, Ioannis Papassotiriou, and George Mastorakos. "Maternal Fasting Plasma Active Ghrelin Levels at Second Trimester of Pregnancy Predict Neonatal Waist Circumference at Birth." In CLINICAL - Diabetes: Observations, Interventions & Trials, P3–481—P3–481. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part4.p4.p3-481.

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Keni, Jyotsna, and Anna Pawlikowska –. Haddal. "Growth Regulation." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0014.

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While multiple hormones influence somatic growth, the main regulator of postnatal growth is growth hormone. Growth hormone (GH) is secreted in a pulsatile manner from the anterior pituitary primarily as a 22-kilodalton molecule (although other forms may be found). The development of the pituitary gland as well as GH gene expression is regulated by the multiple pituitary transcription factors listed in Table11-1. The Pit-1 and Prop-1 genes encode proteins that are often mutated or deleted in cases of congenital hypopituitarism. Under normal waking conditions, GH levels are often low or undetectable, but several times during the day, and particularly at night during stage 3 of sleep, surges of GH secretion occur. The pulsatile pattern characteristic of GH secretion largely reflects the interaction of multiple regulators, including two hypothalamic regulatory peptides: GH-releasing hormone (GHRH), which stimulates GH secretion, and somatostatin (somatotropin release–inhibiting factor [SRIF]), which inhibits GH secretion. Multiple neurotransmitters and neuropeptides are involved in regulation of release of these hypothalamic factors, including, but not limited to, serotonin, histamine, norepinephrine, dopamine, acetylcholine, γ -aminobutyric acid (GABA), thyroid-releasing hormone, vasoactive intestinal peptide, gastrin, neurotensin, substance P, calcitonin, neuropeptide Y, vasopressin, corticotropinreleasing hormone, and galanin. Many factors influence GH secretion; notably, glucose that inhibits, and certain amino acids and Ghrelin that stimulate GH secretion. GH secretion is also impacted by a variety of nonpeptide hormones, including androgens, estrogens, thyroxine, and glucocorticoids. The precise mechanisms by which these hormones regulate GH secretion are complex, potentially involving actions at both the hypothalamic and pituitary levels. Exogenous physiological and pharmacological factors are known to stimulate GH secretion. Some of these agents, including clonidine, L-dopa, and exercise, are used in GH stimulation tests. In plasma, the majority of GH is bound with high specificity and affinity, but with relatively low capacity to a carrier protein termed GH binding protein (GHBP). The GHBP is a cleavage product of the extracellular domain of the GH receptor.
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Conference papers on the topic "Ghrelin levels"

1

Kizilirmak, Deniz, and Bülent Bozkurt. "Relation of ghrelin, obestatin levels and ghrelin/obestatin ratio with asthma." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa1095.

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Kizilirmak, Deniz, and Bülent Bozkurt. "Relation of ghrelin, obestatin levels and ghrelin/obestatin ratio with sleep quality." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2331.

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Bucur-Grosu, L&acaron;cr&acaron;mioara, Andreea Avasiloaiei, Cristina Dimitriu, Mihaela Moscalu, and Maria Stamatin. "OC-81 Umbilical cord ghrelin levels in newborns with intrauterine growth restriction." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.81.

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Yamamoto, Yoshifumi, Masanori Yoshikawa, Kouichi Tomoda, Motoo Yamauchi, Atsuhiko Fukuoka, Shinji Tamaki, Noriko Koyama, and Hiroshi Kimura. "Circulating Ghrelin And Adipocytokine Levels In Patients With Chronic Obstructive Pulmonary Disease." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5940.

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Ayada, Ceylan, Ümran Toru, Osman Genç, Server Sahin, Özlem Arik, and Ismet Bulut. "Increased total serum levels of ghrelin and nesfatin in chronic obstructive pulmonary disease." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3011.

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Gharraf, Heba, Mostafa Shahin, and Abeer Alhadidy. "Study of Leptin and Ghrelin Serum Levels in Patients with Obstructive Sleep Apnea." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2125.

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Sánchez-de-la-Torre, Manuel, Javier Pierola, Antonia Barceló, Mónica de la Peña, Silvia Gómez, Francisco Capote, Juan F. Masa, et al. "Ghrelin, Leptin And Adiponectin Plasma Levels In Sleep Apnea Patients With And Without Excessive Daytime Sleepiness." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2542.

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Lwin, Wai Phyo, Aye Min Soe, Phyo Wai Kyaw, and Tin Moe Wai. "IDDF2019-ABS-0156 Decreased serum acylated ghrelin level with the extent of olga and olgim stages in dyspeptic patients." In International Digestive Disease Forum (IDDF) 2019, Hong Kong, 8–9 June 2019. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-iddfabstracts.171.

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