Ghrelin alleviates biliary obstruction-induced chronic hepatic injury in rats

İşeri, Sevgin Özlem; Şener, Göksel; Sağlam, Beyhan; Ercan, Feríha; Gedik, Nursal; Yeğen, Berrak Ç.

doi:10.1016/j.regpep.2007.08.014

Cited by 66 publications

(40 citation statements)

References 41 publications

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“…A ghrelin analog, GHRP-2, has a protective effect on the liver in rats, which seems to be mediated by insulin-like growth factor 1 (IGF1), tumour necrosis factor a (TNFa), and nitric oxide (25). Ghrelin alleviates biliary obstruction-induced chronic hepatic injury in rats (26). Ghrelin treatment ameliorates pancreaticobiliary inflammation and remote organ injury in rats (27).…”

Section: Introductionmentioning

confidence: 99%

Altered fasting and postprandial plasma ghrelin levels in patients with liver failure are normalized after liver transplantation

Diz-Lois

García-Buela²,

Suárez³

et al. 2010

European Journal of Endocrinology

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Context: Anorexia is a problem of paramount importance in patients with advanced liver failure. Ghrelin has important actions on feeding and weight homeostasis. Experimental data exist, which suggest that ghrelin could protect hepatic tissue. Both fasting and post-oral glucose tolerance test (OGTT) ghrelin concentrations are controversial in liver cirrhosis and are unknown after liver transplantation. Objective: Our aim was to study fasting ghrelin concentrations and their response to an OGTT in liver failure patients before and after liver transplantation. Design and methods: We included 21 patients with severe liver failure studied before (pretransplantation, PreT) and 6 months after liver transplantation (posttransplantation, PostT), and 10 age-and body mass index-matched healthy or overweight subjects as the control group (Cont). After an overnight fast, 75 g of oral glucose were administered; glucose, insulin, and ghrelin were obtained at baseline and at times 30, 60, 90, and 120 min.

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Section: Introductionmentioning

confidence: 99%

Altered fasting and postprandial plasma ghrelin levels in patients with liver failure are normalized after liver transplantation

Diz-Lois

García-Buela²,

Suárez³

et al. 2010

European Journal of Endocrinology

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“…25 In addition, patients with risk factors for severe acute pancreatitis were shown to have higher ghrelin concentrations than the low risk group, and ghrelin concentrations significantly increased after recovery from acute pancreatitis, 26,27 indicating that ghrelin has the potential to protect against the inflammatory responses in acute pancreatitis. Protecting effects against oxidative damage have been also noted in the kidney, 28 the hepatobiliary system, 29,30 and the stomach. 31 Protection of gastric mucosa was reported to involve sensory nerves and endogenous nitric oxide release after acute gastric mucosal damage induced by ethanol.…”

Section: Discussionmentioning

confidence: 98%

Augmenting Effect of DA-9601 on Ghrelin in an Acute Gastric Injury Model

Baek

Lee²,

Jun³

et al. 2011

Gut Liver

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Background/Aims: Acute gastric injury by alcohol or indomethacin has been reported to be prevented by DA-9601, an extract of the herb Artemisia asiatica. Ghrelin, an endogenously produced gastrointestinal peptide hormone, has also been demonstrated to play a role in gastric mucosal defense. The aim of this study was to investigate the effects of DA-9601 on ghrelin in an acute gastric injury model induced by alcohol or indomethacin. Methods: A total of 140 SpragueDawley rats were divided into two groups, a placebo group and a DA-9601-pretreated group. Thirty minutes later, half of the rats in each group received ethanol injury and the other half received indomethacin injury. Levels of serum ghrelin and gastric mucosal ghrelin mRNA were measured by ELISA and RT-PCR, respectively. Results: Immediately after ethanol administration, ghrelin increased in both groups pretreated with DA-9601 and placebo. However, the increase occurred more rapidly and was higher in the DA-9601-pretreated rats than in the controls that did not receive DA-9601-pretreatment. Similarly, from 30 minutes to 2 hours after indomethacin administration, the DA-9601-pretreated rats showed a significant increase in serum and gastric mucosal ghrelin concentrations, whereas placebo-pretreated rats showed only a mild increase. Conclusions: DA-9601 potentiates the endogenous production and secretion of ghrelin in acute gastric injury models induced by ethanol or indomethacin. (Gut Liver 2011;5:52-56) Key Words: DA-9601; Ghrelin; Acute gastric injury INTRODUCTIONThe gastric mucosa defends its structural integrity against many noxious substances such as alcohol and nonsteroidal anti-inflammatory drugs (NSAIDs) via pre-epithelial, epithelial and sub-epithelial factors that include the mucus barrier, bicarbonate secretion, epithelial tight junctions, prostaglandin (PG) synthesis, cell restitution, and mucosal blood flow.1 Alcohol ingestion may lead to gastric mucosal lesions by penetrating the gastric mucosa and causing mucosal inflammation, erosions and ulcer formation. 2-4 Alcohol-induced gastric injury is mediated by free radicals, which is supported by the fact that ethanol administration depletes cells of major antioxidants such as superoxide dismutase, catalase, and glutathione peroxidase. Gastric injury induced by NSAIDs such as indomethacin is mediated by nonselective inhibition of the cyclooxygenase pathways, which results in decreased PG synthesis. DA-9601, an extract of Artemisia asiatica, has been reported to have anti-inflammatory, antioxidative and cytoprotective effects and therefore to play a protective role in experimentallyinduced gastrointestinal damage and hepatic and pancreatic lesions. [5][6][7][8][9] However, the underlying mechanisms of its gastric mucosal protective effects have not been fully elucidated. Another gastro-protective agent, ghrelin, which is made endogenously, has been recently found as one of the gut hormones. It affects the secretory and motor functions of gut as well as energy homeostasis by controlling appetite...

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“…UCP-2 mRNA expression was downregulated in INS-1 beta cell by ghrelin in the presence of 26.4 mM glucose [151]. Other studies showed that ghrelin decreased oxidative injury in the stomach [152], brain [153], blood vessels [154], and liver [155]. [160,161].…”

Section: Ghrelin and Hexarelin Promote Mitochondrial Activity And Biomentioning

confidence: 99%

Implications of ghrelin and hexarelin in diabetes and diabetes-associated heart diseases

et al. 2015

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Ghrelin and its synthetic analog hexarelin are specific ligands of growth hormone secretagogue (GHS) receptor. GHS have strong growth hormone-releasing effect and other neuroendocrine activities such as stimulatory effects on prolactin and adrenocorticotropic hormone secretion. Recently, several studies have reported other beneficial functions of GHS that are independent of GH. Ghrelin and hexarelin, for examples, have been shown to exert GH-independent cardiovascular activity. Hexarelin has been reported to regulate peroxisome proliferator-activated receptor gamma (PPAR-γ) in macrophages and adipocytes. PPAR-γ is an important regulator of adipogenesis, lipid metabolism, and insulin sensitization. Ghrelin also shows protective effects on beta cells against lipotoxicity through activation of phosphatidylinositol-3 kinase/protein kinase B, c-Jun N-terminal kinase ( JNK) inhibition, and nuclear exclusion of forkhead box protein O1. Acylated ghrelin (AG) and unacylated ghrelin (UAG) administration reduces glucose levels and increases insulinproducing beta cell number, and insulin secretion in pancreatectomized rats and in newborn rats treated with streptozotocin, suggesting a possible role of GHS in pancreatic regeneration. Therefore, the discovery of GHS has opened many new perspectives in endocrine, metabolic, and cardiovascular research areas, suggesting the possible therapeutic application in diabetes and diabetic complications especially diabetic cardiomyopathy. Here, we review the physiological roles of ghrelin and hexarelin in the protection and regeneration of beta cells and their roles in the regulation of insulin release, glucose, and fat metabolism and present their potential therapeutic effects in the treatment of diabetes and diabetic-associated heart diseases. Disciplines Medicine and Health Sciences Publication DetailsMosa, R., Zhang, Z., Shao, R., Deng, C., Chen, J. & Chen, C. (2015). Implications of ghrelin and hexarelin in diabetes and diabetes-associated heart diseases. Endocrine, 49 (2) AbstractGhrelin and its synthetic analog hexarelin are specific ligands of growth hormone secretagogue (GHS) receptor. GHS have strong growth hormone-releasing effect and other neuroendocrine activities such as stimulatory effects on prolactin and adrenocorticotropic hormone secretion. Recently, several studies have reported other beneficial functions of GHS that are independent of GH. Ghrelin and hexarelin, for examples, have been shown to exert GH-independent cardiovascular activity. Hexarelin has been reported to regulate peroxisome proliferator-activated receptor gamma (PPAR-γ) in macrophages and adipocytes. PPAR-γ is an important regulator of adipogenesis, lipid metabolism, and insulin sensitization. Ghrelin also shows protective effects on beta cells against lipotoxicity through activation of phosphatidylinositol-3 kinase/protein kinase B, c-Jun N-terminal kinase (JNK) inhibition, and nuclear exclusion of forkhead box protein O1. Acylated ghrelin (AG) and unacylated ghrelin (UAG) administration redu...

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Ghrelin alleviates biliary obstruction-induced chronic hepatic injury in rats

Cited by 66 publications

References 41 publications

Altered fasting and postprandial plasma ghrelin levels in patients with liver failure are normalized after liver transplantation

Altered fasting and postprandial plasma ghrelin levels in patients with liver failure are normalized after liver transplantation

Augmenting Effect of DA-9601 on Ghrelin in an Acute Gastric Injury Model

Implications of ghrelin and hexarelin in diabetes and diabetes-associated heart diseases

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