Exaggerated liver injury induced by renal ischemia reperfusion in diabetes: Effect of exenatide

Vaghasiya, Jitendra; Sheth, Navin; Bhalodia, Yagnik; Jivani, N. P.

doi:10.4103/1319-3767.65187

Cited by 41 publications

(32 citation statements)

References 29 publications

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“…These results are in accordance with Mahfoudh-Boussaid et al (2012), Vaghasiya et al (2010) and Şener et al (2005) results. Moreover, bilateral renal I/R showed a cardiac oxidative stress injury indicated by a significant increase in the cardiac tissue LPO level, as well as a significant decrease in cardiac antioxidant enzymes, GR, SOD and CAT, levels compared to the control groups.…”

Section: Discussionsupporting

confidence: 92%

“…Moreover, bilateral renal I/R showed a cardiac oxidative stress injury indicated by a significant increase in the cardiac tissue LPO level, as well as a significant decrease in cardiac antioxidant enzymes, GR, SOD and CAT, levels compared to the control groups. These results are in line with Vaghasiya et al (2010). This could be explained by the cardiac lesions following acute renal I/R injury, evidenced by the increase in cardiac tissue LPO and the decrease in cardiac tissue antioxidants.…”

Section: Discussionsupporting

confidence: 88%

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Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Ibrahim¹,

Elbassuoni²,

Ragy³

et al. 2014

gpb

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Abstract. Renal ischemia-reperfusion (I/R) is the major cause of acute renal failure. Renal I/R have distant effects on other organs, especially the heart. The purpose of this study was to investigate cardiac lesion following bilateral renal ischemia (50 minutes) and reperfusion (48 hours) in adult rats, to test sex differences in the development of cardiac lesions after acute renal I/R and to investigate the effect of estrogen on this type of cardiac lesions. 70 adult albino rats were divided into 7 groups: control male, I/R male, control female, I/R female, female with bilateral ovariectomy, I/R female with bilateral ovariectomy and I/R female with bilateral ovariectomy treated with estrogen. Renal and cardiac functions in both sexes were deteriorated following acute renal I/R injury proved by the increase in serum urea, creatinine, lactate dehydrogenase and creatine kinase levels. These cardiac lesions are mainly due to the oxidative stress response in the form of the increase in cardiac tissue lipid peroxide, and the decrease in cardiac tissue glutathione reductase, superoxide dismutase and catalase levels. In conclusion, female rats are more protected from the renal and cardiac lesions following acute renal I/R injury than male, since estrogen significantly decreases these lesions mainly by inhibiting the oxidative stress response.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 88%

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Ibrahim¹,

Elbassuoni²,

Ragy³

et al. 2014

gpb

View full text Add to dashboard Cite

show abstract

“…Data are meanGS.E.M., nZ10, * or # P!0.05, **P!0.01 and *** or Vaghasiya et al (2010). In exenatide-treated diabetic rats, there were significant decreases in serum levels of alanine and aspartic aminotransferases, cholesterol, triglyceride, uric acids, blood urea nitrogen and creatinine compared with untreated diabetic rats.…”

Section: Figurementioning

confidence: 97%

“…The effect of exenatide on pancreatic b-cell differentiation after PDX1 stimulation may occur via protein kinase B and cAMP-dependent mechanisms (Drucker 2003a, Holz 2004). Moreover, exenatide may initiate its action on pancreatic b-cells via the stimulation of PI3K/PKB, a cell protecting system, and/or through the suppression of the caspase-3 apoptotic pathway (Vaghasiya et al 2010).…”

Section: Effect Of Exenatide On Gene Expression Of Selected Moleculesmentioning

confidence: 99%

Mechanism of the beneficial and protective effects of exenatide in diabetic rats

Lotfy

Singh

Rashed

et al. 2013

Journal of Endocrinology

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Glucagon-like peptide 1 (GLP1) agonists are promising therapeutic agents in the treatment of diabetes mellitus. This study examines the mechanism of the protective effects of exenatide in experimental diabetes, employing four groups of ten rats each, in which two groups were streptozotocin-induced diabetic and two were control groups. One control and one diabetic group were treated with exenatide (1 mg/kg body weight (BW)) for 10 weeks. Blood plasma was taken for biochemical analyses while pancreatic tissue was taken for immunofluorescence and immunoelectron microscopy studies and real-time PCR to examine the expression of genes. The results show that exenatide improved BW gain and reduced blood glucose in diabetic rats compared with controls. Similarly, exenatide enhanced insulin release from the pancreatic fragments and improved liver and kidney functions and lipid profile in diabetic rats compared with controls. Exenatide not only induced significant increases in serum insulin level but also elevated the number of insulin-, GLP1-and exenatide-positive cells compared with untreated controls. Exenatide also elevated the number of catalase-and glutathione reductase-positive cells in diabetic rat pancreas compared with controls. Exenatide caused significant elevation in the expressions of pancreatic duodenal homeobox-1, heat shock protein-70, glutathione peroxidase, insulin receptor and GLP1 receptor genes in the pancreas of both control and diabetic rats compared with untreated animals. The results have demonstrated that exenatide can exert its beneficial and protective effects by elevating the levels of endogenous antioxidants and genes responsible for the survival, regeneration and proliferation of pancreatic b-cell.

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“…Exendin-4 is an United States Food and Drug Administration (FDA) approved glucagon-like peptide-1 that increases insulin-dependent glycogen synthesis and the liver’s glucose uptake [3]. In one study, exendin-4 demonstrated a reduction in ROS generation and an enhancement effect on antioxidant enzyme activity, such as SOD, GPX, and CAT in rats [4]. Exendin-4 has been used for glucose stimulated insulin secretion, gastric emptying, and appetite suppression in type 2 diabetic patients.…”

Section: Introductionmentioning

confidence: 99%

Exendin-4 protects mice from D-galactose-induced hepatic and pancreatic dysfunction

Ahangarpour

Oroojan

Badavi

2017

Pathobiology of Aging & Age-related Diseases

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Investigations into pharmaceutical intervention of pancreatic and hepatic dysfunction associated with metabolic disturbances have received relatively little attention. The aim of this study was to investigate the protective effects of exendin-4 in mice receiving D-galactose, a reducing sugar that triggers ROS production and inflammatory mediators affecting the pancreas and liver. Exendin-4 is an United States Food and Drug Administration (FDA) approved glucagon-like peptide that increases insulin dependent glycogen synthesis and glucose uptake. Male NMRI mice (20–25 g), 3 months of age, were randomly divided into 6 groups of 12 mice each: control, exendin-4 (1 nmol/kg), exendin-4 (10 nmol/kg), D-galactose, D-galactose + exendin-4 (1 nmol/kg) and D-galactose + exendin-4 (10 nmol/kg). D-galactose (500 mg/kg) was given daily by oral gavage for 6 weeks. During the last 10 days, exendin-4 (1 and 10 nmol/kg) was injected intraperitoneally daily. Glucose, insulin, insulin resistance, lipid profiles, and hepatic enzyme levels significantly increased in the D-galactose group (p < 0.05), along with a significant decrease in superoxide dismutase activity and pancreatic islet insulin secretion (p < 0.05). Exendin-4 decreased D-galactose-induced increases in serum glucose and insulin, insulin resistance, lipid profiles, and hepatic enzymes, and improved pancreatic islet insulin secretion and antioxidant defense status. The results show that exendin-4 can prevent complications in mice with compromised pancreatic and hepatic function. Long term administration of D-galactose in mice may be a useful model to study insulin resistance, metabolic syndrome, and aging.

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Exaggerated liver injury induced by renal ischemia reperfusion in diabetes: Effect of exenatide

Cited by 41 publications

References 29 publications

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Mechanism of the beneficial and protective effects of exenatide in diabetic rats

Exendin-4 protects mice from D-galactose-induced hepatic and pancreatic dysfunction

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Exaggerated liver injury induced by renal ischemia reperfusion in diabetes: Effect of exenatide

Cited by 41 publications

References 29 publications

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Mechanism of the beneficial and protective effects of exenatide in diabetic rats

Exendin-4 protects mice from D-galactose-induced hepatic and pancreatic dysfunction

Contact Info

Product

Resources

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Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats

Gender difference in the development of cardiac lesions following acute ischemic-reperfusion renal injury in albino rats