Ghrelin: Impact on Muscle Energy Metabolism in Sepsis

Yorulmaz, Hatice; Özkök, Elif; Ates, Gulten; Aksu, Abdullah; Balkıs, Nuray; Tamer, Sule

doi:10.1007/s10989-017-9610-8

Cited by 3 publications

(3 citation statements)

References 27 publications

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“…So there may be some degree of balance between the up- and downregulation of ghrelin in septic rats, and the end results downregulate ghrelin; however, appetite cannot regulate ghrelin levels (38), and Ariyasu et al (39) demonstrated that ghrelin secretion even increased in anorexia, which proved the administration of ghrelin did not necessarily lead to the amelioration of appetite. In addition, ghrelin treatment significantly increased adenosine triphosphate values and improved tissue histology in septic rats (40). Therefore, we believe that the sepsis itself lead to the ischemia of stomach greater curvature by downregulating ghrelin as opposed to other reasons.…”

Section: Discussionmentioning

confidence: 99%

Ghrelin regulates sepsis‑induced rat acute gastric injury

Lin

Guo

et al. 2019

Mol Med Report

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Ghrelin, a peptide expressed in the gastric mucosa, has an essential role in sustaining the normal function of the digestive system. Sepsis is one of the primary causes of mortality in intensive care units and can lead to multiple organ dysfunction, especially in the gastrointestinal system. The aim of the present study was to explore the effect of ghrelin on gastric blood flow in a rat model of sepsis, as well as the effect of ghrelin on the expression of the apoptotic markers, B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X (Bax), in gastric tissues. The sepsis model was established using cecal ligation and puncture (CLP). The expression levels of apoptosis-related factors in gastric epithelial cell were determined by immunohistochemistry, reverse transcription quantitative-PCR and western blotting. Collectively, the present results suggested that ghrelin administration attenuated sepsis symptoms induced by CLP. Blood flow in the stomach greater curvature was significantly higher in the CLP-induced sepsis group rats (284.3±95.7 perfusion units) compared with the sham operation group (317.8±5.2 perfusion units; P<0.05), whereas there was no difference between the CLP group treated with ghrelin (377.8±99.0 perfusion units) and the sham rats. Ghrelin administration also reduced the secretion of pro-inflammatory cytokines compared with the CLP-induced sepsis group rats. In addition, CLP significantly reduced the expression of Bcl-2 and enhanced the expression of the pro-apoptotic proteins, Bax and cleaved caspase-3; whereas, ghrelin application reversed the effects of CLP on these apoptosis-associated proteins. In conclusion, the present study revealed that ghrelin has the ability to increase blood flow in the gastrointestinal tract in a sepsis model and can also regulate the expressions of apoptosis-associated factors in gastric tissues. These results suggest that ghrelin could be a novel treatment for sepsis-induced gastric injury.

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Section: Discussionmentioning

confidence: 99%

Ghrelin regulates sepsis‑induced rat acute gastric injury

Lin

Guo

et al. 2019

Mol Med Report

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“…SIMD is a common complication of severe sepsis, with clinical manifestations including myocardial damage and cardiac dysfunction. The mechanism of SIMD is very complicated; excessive release of cytokines [20], excessive activation of complement [21], apoptosis of myocardial cells [22], and an imbalance in energy metabolism are all considered related factors [23]. Through clinical research, Edo Y et al observed a reduction in LVEF and left ventricular dilatation in patients in the early stage of sepsis [24].…”

Section: Discussionmentioning

confidence: 99%

Adenosine Attenuates LPS-Induced Cardiac Dysfunction by Inhibition of Mitochondrial Function via the ER Pathway

Zeng

Zhang

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Sepsis is a life-threatening organ dysfunction syndrome with a high rate of mortality. It is caused by an abnormal immune response to infection, and the occurrence of sepsis-induced cardiomyopathy is the primary cause of death. The present study was designed to examine the effects of adenosine on lipopolysaccharide- (LPS-) induced cardiac anomalies and the underlying mechanisms involved. Adenosine (25, 50, and 100 mg/kg, i.g., 2 times/day) was administered for three days, followed by the induction of sepsis by intraperitoneal injection of LPS (10 mg/kg/2h). The effects of adenosine on inflammatory factors, LVEF, LVFS, and MAPK in septic rats (half male and half female) were observed. Subsequently, the effect of adenosine (10 μM) on the mitochondrial function of H9c2 cells stimulated with LPS (20 μg/mL, 24 h) was observed in the presence and absence of the estrogen receptor-specific antagonist ICI182,780. The results show that medium to high doses of adenosine can significantly promote cardiac function (LVEF and LVFS) and reduce the levels of inflammatory factors (TNF-α, IL-6, PCT, and cTnI) and p-JNK in septic rats, with a significant difference seen between male and female rats. The results of flow cytometry show that adenosine significantly inhibited increases in ROS levels, mitochondrial membrane potential, and the swelling degree of mitochondria in H9c2 cells stimulated with LPS, but this effect could be blocked by ICI182,780, indicating that adenosine attenuated LPS-induced cardiac dysfunction by inhibiting mitochondrial function via the ER pathway.

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“…While LPS caused significant elevation of liver enzymes and nitrites/nitrates, ghrelin receptor agonist administration inhibited these increases. In LPS-treated mice, this agonist also increased Insulin-like growth factor-1 (IGF-1) concentration in the serum and expression in hepatocytes ( 150 ). IGF-1 plays a significant role in preventing liver damage.…”

Section: Role Of Ghrelin In Sepsismentioning

confidence: 99%

Ghrelin as an Anti-Sepsis Peptide: Review

et al. 2021

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Sepsis continues to produce widespread inflammation, illness, and death, prompting intensive research aimed at uncovering causes and therapies. In this article, we focus on ghrelin, an endogenous peptide with promise as a potent anti-inflammatory agent. Ghrelin was discovered, tracked, and isolated from stomach cells based on its ability to stimulate release of growth hormone. It also stimulates appetite and is shown to be anti-inflammatory in a wide range of tissues. The anti-inflammatory effects mediated by ghrelin are a result of both the stimulation of anti-inflammatory processes and an inhibition of pro-inflammatory forces. Anti-inflammatory processes are promoted in a broad range of tissues including the hypothalamus and vagus nerve as well as in a broad range of immune cells. Aged rodents have reduced levels of growth hormone (GH) and diminished immune responses; ghrelin administration boosts GH levels and immune response. The anti-inflammatory functions of ghrelin, well displayed in preclinical animal models of sepsis, are just being charted in patients, with expectations that ghrelin and growth hormone might improve outcomes in patients with sepsis.

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Ghrelin: Impact on Muscle Energy Metabolism in Sepsis

Cited by 3 publications

References 27 publications

Ghrelin regulates sepsis‑induced rat acute gastric injury

Ghrelin regulates sepsis‑induced rat acute gastric injury

Adenosine Attenuates LPS-Induced Cardiac Dysfunction by Inhibition of Mitochondrial Function via the ER Pathway

Ghrelin as an Anti-Sepsis Peptide: Review

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