Plasma levels of active and total ghrelin in renal failure: A relationship with GH/IGF-I axis

Jarkovská, Z; Hodková, Magdaléna; Sazamová, M.; Rosická, M; Dusilová-Sulková, Sylvie; Jakóbisiak, Marek; Justová, V; Lacinová, Z; Haluzı́k, Martin; Haas, T; Kršek, Michal

doi:10.1016/j.ghir.2005.07.004

Cited by 31 publications

(30 citation statements)

References 25 publications

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“…Increased levels of TG with decreasing GFR have been reported by others (15)(16)(17)(18)(19)21,26) as well as variable removal by dialysis (16,18,21). Some studies reported a decrease in both AG and DG (16,18) by hemodialysis that would not be expected for AG, which is highly bound to large plasma molecules such as lipoprotein (27,28).…”

Section: Discussionmentioning

confidence: 76%

“…Some studies reported a decrease in both AG and DG (16,18) by hemodialysis that would not be expected for AG, which is highly bound to large plasma molecules such as lipoprotein (27,28). Other studies report no change in plasma ghrelin levels with hemodialysis (21).…”

Section: Discussionmentioning

confidence: 99%

“…It is a 28 amino acid peptide that acts at the GH secretagogue receptor (GHSR) to stimulate appetite, carbohydrate utilization, and GH release. Conflicting reports of the levels of total ghrelin (TG) and acyl ghrelin (AG) in patients with renal dysfunction have been difficult to interpret and reconcile (15)(16)(17)(18)(19)(20)(21). Most reports have used single antibody ghrelin assays that recognize an epitope found only on AG or alternatively, an epitope common to both AG and des-acyl ghrelin (DG).…”

Section: Introductionmentioning

confidence: 99%

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Association of Plasma Des-acyl Ghrelin Levels with CKD

Gupta

Kuppusamy²,

Patrie

et al. 2013

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives There are no effective therapies for malnutrition in CKD/ESRD patients. This study hypothesized that ghrelin, an endogenous orexigenic hormone, would correlate with renal function and might suggest therapeutic interventions for CKD/ESRD malnutrition.Design, setting, participants, & measurements Fifty-one CKD and 15 hemodialysis patients were enrolled. Acyl ghrelin (AG) and des-acyl ghrelin (DG) were determined using separate two-site-specific assays. Leptin, insulin, growth hormone, insulin-link growth factor-1, C-reactive protein, TNF-a, and IL-6 were also measured.Results Univariate correlation analyses showed that CKD stage was highly, positively correlated with the levels of preprandial and postprandial DG and positively correlated with TNF-a, IL-6, leptin, and age. Multivariate partial-correlation analyses showed that CKD was independently associated with the proportion of preprandial and postprandial DG, whereas TNF-a, IL-6, leptin, insulin, and age were not independently associated with either. Geometric mean (GM) preprandial and postprandial AG were comparable between CKD stages #2 and .2, whereas GM preprandial DG and postprandial DG were 1.95-fold and 2.17-fold greater, respectively, for CKD stage .2 versus stage #2. DG was the dominant form of ghrelin preprandially and postprandially for both CKD stages #2 and .2. Dialysis had no effect on AG, but reduced DG by 73% to levels even lower (GM 48.7 pg/ml) than those seen postprandially in CKD stage #2 patients (GM 77.0 pg/ml).Conclusions This study shows a strong and independent correlation of DG with CKD stage. Postprandial suppression of ghrelin is impaired with reduced renal function. Hemodialysis selectively removes DG but not AG.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Association of Plasma Des-acyl Ghrelin Levels with CKD

Gupta

Kuppusamy²,

Patrie

et al. 2013

Clinical Journal of the American Society of Nephrology

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“…Thus, the acute alteration in circulating ghrelin is likely to be due to some combination of a decrease in secretion and an increase in breakdown and clearance from the circulation. Because LPS is known to acutely decrease renal function and ghrelin appears to be primarily cleared from the circulation by the kidney, it is likely that the acute decrease in circulating ghrelin in this study was due to a rapid decrease in its secretion from the stomach rather than an increase in renal clearance (GuebreEgziabher et al 2005, Jarkovska et al 2005. Indeed, direct measurements of the half-life of radiolabeled ghrelin indicate that its circulating half-life is unchanged early in inflammation, and actually increases as the duration of the inflammatory stimulus increases (Wu et al 2003).…”

Section: Discussionmentioning

confidence: 94%

Prostacyclin signaling regulates circulating ghrelin during acute inflammation

Madison

Scarlett

Levasseur

et al. 2007

Journal of Endocrinology

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Ghrelin is an octanoylated 28 amino acid peptide predominantly secreted by the stomach, and has potent stimulatory effects on appetite. Several laboratories, including our own, have demonstrated that ghrelin levels fall in states of acute inflammation brought about by injection of bacterial lipopolysaccharide (LPS). We now demonstrate that the decrease in circulating ghrelin is not due to a decrease in ghrelin gene expression, but is instead likely to be due to an acute decrease in ghrelin secretion. Furthermore, we have found that the change in circulating ghrelin during acute inflammation required a prostaglandin second messenger, but did not require the synthesis of nitric oxide. Interestingly, i.v. injection of prostaglandin E 2 failed to decrease circulating ghrelin levels, whereas prostacyclin decreased circulating ghrelin to a similar extent as did LPS. We also provide anatomical evidence for the mechanism of the regulation of ghrelin by inflammation. We demonstrate that the type 1 interleukin-1b (IL-1b) receptor is expressed within the gastric mucosa, but is not expressed by ghrelin cells. The prostacyclin receptor was also expressed in the gastric mucosa, and the majority of ghrelin-producing cells were found to co-express this receptor. Mice with genetic deletion of the type 1 IL-1 receptor do not suppress circulating ghrelin levels with LPS administration. Collectively, these data support a model in which the mechanism of inflammation induced decreases in ghrelin are due to the action of IL-1b on cells within the gastric mucosa that in turn produce prostacyclin as a second messenger. These data provide further support for the potential role of ghrelin as a therapeutic agent in acute and chronic inflammatory diseases.

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“…Há vários anos, a desnutrição calórico-protéica tem sido referida como a principal causa de atraso no crescimento de crianças e adolescentes com DRC. A anorexia está presente na maioria destes casos, sendo atribuída aos efeitos da uremia, do paladar alterado, das náuseas e dos vômitos, do estresse psicológico e de fatores endógenos, como a orexina ghrelina e a anorexina leptina (13)(14)(15)(16)(17)(18). Vários outros fatores podem contribuir para o atraso no crescimento na DRC, incluindo idade de início da doença renal, etiologia da doença renal, presença de anemia, de acidose metabólica e de osteodistrofia renal, além do próprio potencial genético de crescimento (2,10).…”

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Baixa estatura na doença renal crônica: fisiopatologia e tratamento com hormônio de crescimento

Oliveira

Siviero-Miachon

Spinola-Castro

et al. 2008

Arq Bras Endocrinol Metab

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RESUMOo atraso no crescimento é freqüente e grave em crianças com doença renal crônica (drc). vários fatores contribuem para o comprometimento do crescimento nestas crianças, incluindo as alterações no eixo hormônio de crescimento (gH) -insulin-like growth factor 1 (igF-1), desnutrição, acidose, doença renal óssea e uso de corticóides. em crianças com drc, o tratamento do atraso no crescimento é difícil em virtude da presença de doenças associadas que necessitem de adequado tratamento médico. Apesar de as evidên-cias a respeito da segurança e de a eficácia do gH nesta população, este tratamento ainda é pouco utilizado. esta revisão mostra o impacto, as causas e o tratamento do atraso no crescimento em crianças com drc. H istoricamente, o termo insuficiência renal crônica (IRC) tem sido usado para descrever pacientes com ritmo de filtração glomerular (RFG) menor que 75 mL/min/1,73 m 2 de área corporal (1). Mais recentemente, a National Kidney Foundation (NKF) introduziu o termo doença renal crônica (DRC), bem como a classificação do quadro, a fim de propiciar a detecção precoce, retardar a progressão e prevenir complicações relacionadas. Essa classificação descreve cinco estágios da DRC considerando a presença de lesão

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Plasma levels of active and total ghrelin in renal failure: A relationship with GH/IGF-I axis

Cited by 31 publications

References 25 publications

Association of Plasma Des-acyl Ghrelin Levels with CKD

Association of Plasma Des-acyl Ghrelin Levels with CKD

Prostacyclin signaling regulates circulating ghrelin during acute inflammation

Baixa estatura na doença renal crônica: fisiopatologia e tratamento com hormônio de crescimento

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