l-glutamine supplementation exerts cardio-renal protection in estrogen-progestin oral contraceptive-treated female rats

Olaniyi, Kehinde S.; Sabinari, Isaiah Woru; Olatunji, Lawrence Aderemi

doi:10.1016/j.etap.2019.103305

Cited by 7 publications

(6 citation statements)

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“…This suggests the involvement of postpartum COC treatment in the alteration of nitric oxide and glutathione-dependent antioxidant pathway. This finding is in consonance with a recent report that showed that COC treatment reduced G6PD activity and glutathione content in female rats [ 44 ]. However, the current findings further show that MR or GR blockade restores renal nitric oxide and glutathione-dependent antioxidant pathway that was altered by postpartum COC treatment.…”

Section: Discussionsupporting

confidence: 93%

“…It can damage all the cells of the kidney via diverse means such as increased ROS production, NADPH oxidase activation, elevated lipid peroxidation, tissue inflammation, and mitochondrial damage [ 42 – 43 ]. A recent report has shown that administration of COC caused lipid influx into the kidneys [ 44 ]. However, in the current study, postpartum COC treatment led to increase renal TG/HDL-C ratio and FFA, suggesting that postpartum COC treatment induced lipid nephrotoxicity.…”

Section: Discussionmentioning

confidence: 99%

“…Previous study has linked impaired Na + -K + -ATPase activity to renal tubular injury that was induced by elevated uric acid [ 66 ]. Also, in earlier studies, estrogen-progestin oral contraceptive treatment has been documented to reduce Na + -K + -ATPase activity in the heart and kidney [ 44 , 67 ]. Similarly, in the current study, postpartum COC treatment led to impaired renal Na + -K + -ATPase activity that was restored by either MR or GR blockade.…”

Section: Discussionmentioning

confidence: 99%

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Suppression of Adenosine Deaminase and Xanthine Oxidase Activities by Mineralocorticoid and Glucocorticoid Receptor Blockades Restores Renal Antioxidative Barrier in Oral Contraceptive-Treated Dam

Badmus

Areola

Benjamin

et al. 2021

J Renin Angiotensin Aldosterone Syst

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Objective. We tested the hypothesis that postpartum combined oral contraceptive (COC) treatment would induce oxidative stress via the adenosine deaminase-xanthine oxidase pathway in the kidney. We also sought to determine whether mineralocorticoid receptor (MR) or glucocorticoid receptor (GR ) blockade would suppress the activities of ADA and xanthine oxidase caused by postpartum COC treatment in the kidney. Methods. Twenty-four Wistar dams were randomly assigned to 4 groups ( n = 6 / group ). Dams received vehicle (po), COC (1.0 μg ethinylestradiol and 5.0 μg levonorgestrel; po), COC with GR blockade (mifepristone; 80.0 mg/kg; po), and COC with MR blockade (spironolactone; 0.25 mg/kg; po) daily between 3rd and 11th week postpartum. Results. Data showed that postpartum COC caused increased plasma creatinine and urea, increased renal triglyceride/high-density lipoprotein ratio, free fatty acid accumulation, alanine aminotransferase, gamma-glutamyltransferase, uric acid, and activities of renal XO and ADA. On the other hand, postpartum COC resulted in decreased plasma albumin, renal glutathione, and Na+-K+-ATPase activity with no effect on lactate production. However, MR or GR blockade ameliorated the alterations induced by postpartum COC treatment. The present results demonstrate that MR or GR blockade ameliorates postpartum COC-induced increased activities of ADA and xanthine oxidase and restores glutathione-dependent antioxidative defense. Conclusion. These findings implicate the involvements of GR and MR in renal dysfunctions caused by COC in dams via disrupted glutathione antioxidative barrier.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Suppression of Adenosine Deaminase and Xanthine Oxidase Activities by Mineralocorticoid and Glucocorticoid Receptor Blockades Restores Renal Antioxidative Barrier in Oral Contraceptive-Treated Dam

Badmus

Areola

Benjamin

et al. 2021

J Renin Angiotensin Aldosterone Syst

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“…Interestingly, supplementation with GLN normalized uric acid concentration with corresponding improvement in placental efficiency and fetal outcome. Similarly, earlier studies including study from our non-pregnant laboratory animals have demonstrated the beneficial effects of GLN in disorders such as prediabetes, type 2 diabetes, cardiac hypertrophy, liver disease among others, and attributed its impacts to anti-inflammatory and anti-oxidant properties [30,31,32,62]. However, to the best of our knowledge, this is the first study to report the ameliorative effect of GLN on placental lipid-associated defects and adverse fetal outcome by suppression of ADA, XO with consequent decrease in uric acid during maternal fructose consumption.…”

Section: Discussionmentioning

confidence: 63%

Oral L-glutamine rescues fructose-induced poor fetal outcome by preventing placental triglyceride and uric acid accumulation in Wistar rats

Olaniyi

Sabinari

Olatunji

2020

Heliyon

Self Cite

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Background: Metabolic adaptation of pregnant mothers is crucial for placental development and fetal growth/ survival. However, evidence exists that indiscriminate consumption of fructose-enriched drink (FED) during pregnancy disrupts maternal-fetal metabolic tolerance with attendant adverse fetal outcomes. Glutamine supplementation (GLN) has been shown to exert a modulatory effect in metabolic disorders. Nevertheless, the effects of GLN on FED-induced poor fetal outcome, and in particular the impacts on placental uric acid/lipid accumulation are unknown. The present study was conducted to test the hypothesis that oral GLN improves fetal outcome by attenuating placental lipid accumulation and uric acid synthesis in pregnant rats exposed to FED. Materials and methods: Pregnant Wistar rats (160-180 g) were randomly allotted to control, GLN, FED and FED þ GLN groups (6 rats/group). The groups received vehicle by oral gavage, glutamine (1 g/kg) by oral gavage, fructose (10%; w/v) and fructose þ glutamine, respectively, through gestation. Results: Data showed that FED during pregnancy caused placental inefficiency, reduced fetal growth, and caused insulin resistance with correspondent increase in fasting blood glucose and plasma insulin. FED also resulted in an increased placental triglyceride, total cholesterol and de novo uric acid synthesis by activating adenosine deaminase and xanthine oxidase activities. Moreover, FED during pregnancy led to increased lipid peroxidation, lactate production with correspondent decreased adenosine and glucose-6-phosphate dehydrogenase-dependent antioxidant defense. These alterations were abrogated by GLN supplementation. Conclusion: These findings implicate that high FED intake during pregnancy causes poor fetal outcome via defective placental uric acid/triglyceride-dependent mechanism. The findings also suggest that oral GLN improves fetal outcome by ameliorating placental defects through suppression of uric acid/triglyceride accumulation.

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“…5,6 Notably, increasing evidence has shed more light on the involvement of glutamine (Gln) in renal metabolism. 7,8 As the most abundant and versatile amino acid in the human body, Gln participates in energy generation, metabolism homeostasis, cell proliferation, and apoptosis. 9,10 Interestingly, several studies have reported that podocytes rely on Gln for maintaining cellular structure and function, and Gln supplementation could reduce Jijia Hu and Zongwei Zhang are co-first authors.…”

mentioning

confidence: 99%

LRH‐1 activation alleviates diabetes‐induced podocyte injury by promoting GLS2‐mediated glutaminolysis

Zhang

et al. 2023

Cell Proliferation

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Alteration of metabolic phenotype in podocytes directly contributes to the development of albuminuria and renal injury in conditions of diabetic kidney disease (DKD). This study aimed to identify and evaluate liver receptor homologue‐1 (LRH‐1) as a possible therapeutic target that alleviates glutamine (Gln) metabolism disorders and mitigates podocyte injury in DKD. Metabolomic and transcriptomic analyses were performed to characterize amino acid metabolism changes in the glomeruli of diabetic mice. Next, Western blotting, immunohistochemistry assays, and immunofluorescence staining were used to detect the expression of different genes in vitro and in vivo. Furthermore, Gln and glutamate (Glu) content as well as ATP generation were examined. A decrease in LRH‐1 and glutaminase 2 (GLS2) expression was detected in diabetic podocytes. Conversely, the administration of LRH‐1 agonist (DLPC) upregulated the expression of GLS2 and promoted glutaminolysis, with an improvement in mitochondrial dysfunction and less apoptosis in podocytes compared to those in vehicle‐treated db/db mice. Our study indicates the essential role of LRH‐1 in governing the Gln metabolism of podocytes, targeting LRH‐1 could restore podocytes from diabetes‐induced disturbed glutaminolysis in mitochondria.

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l-glutamine supplementation exerts cardio-renal protection in estrogen-progestin oral contraceptive-treated female rats

Cited by 7 publications

References 58 publications

Suppression of Adenosine Deaminase and Xanthine Oxidase Activities by Mineralocorticoid and Glucocorticoid Receptor Blockades Restores Renal Antioxidative Barrier in Oral Contraceptive-Treated Dam

Suppression of Adenosine Deaminase and Xanthine Oxidase Activities by Mineralocorticoid and Glucocorticoid Receptor Blockades Restores Renal Antioxidative Barrier in Oral Contraceptive-Treated Dam

Oral L-glutamine rescues fructose-induced poor fetal outcome by preventing placental triglyceride and uric acid accumulation in Wistar rats

LRH‐1 activation alleviates diabetes‐induced podocyte injury by promoting GLS2‐mediated glutaminolysis

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