Naringin protects against HIV-1 protease inhibitors-induced pancreatic β-cell dysfunction and apoptosis

Nzuza, Sanelisiwe; Ndwandwe, Duduzile; Owira, Peter M. O.

doi:10.1016/j.mce.2016.07.041

Cited by 19 publications

(13 citation statements)

References 49 publications

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“…It is established that naringin reduces the β-cell oxidative stress and increases the insulin secretion in a dosedependent manner in protease inhibitor-treated RIN5F cell lines [Nzuza et al, 2016]. Similarly, in the present study, administration of naringin increased fasting serum insulin levels in diabetic animals.…”

Section: Discussionsupporting

confidence: 81%

“…Being a common constituent of dietary products, humans are exposed to naringin in some form or the other. Previous in vitro and in vivo studies show naringin has antidiabetic activity, and almost all studies attribute that effect to its antioxidant property and its ability to counter oxidative stress [Meier et al, 2008;Pari and Suman, 2010;Liu et al, 2016;Nzuza et al, 2016;Ahmed et al, 2017;Lim et al, 2018]. Most of the studies show that naringin has a beneficial effect on diabetes through extrapancreatic mechanisms like reduced glucose absorption [Reshmi et al, 2017;Taslimi et al, 2017], regulation of hepatic enzyme dysfunction [Punithavathi et al, 2008;Sharma et al, 2011;Pu et al, 2012;Ahmed et al, 2017;Pari and Chandramohan, 2017] and improvement in peripheral resistance [Priscilla et al, 2015;Ahmed et al, 2017].…”

Section: Introductionmentioning

confidence: 99%

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Naringin (4′,5,7-Trihydroxyflavanone 7-Rhamnoglucoside) Attenuates β-Cell Dysfunction in Diabetic Rats through Upregulation of PDX-1

Subramanian

Balaji

Sekaran

et al. 2018

Cells Tissues Organs

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Background: Pancreatic duodenal homeobox-1 (PDX-1) is a key transcription factor which regulates Insulin gene expression and insulin secretion in adult β-cells and helps to maintain β-cells mass. Naringin, a flavanone, owing to its antioxidant property, is reported to have antidiabetic effects. Objectives: The present study tries to evaluate the role of naringin on the β-cell-specific transcription factor PDX-1 in diabetic rats. Methods: Diabetes was induced in male rats using streptozotocin and treated with naringin (100 mg/kg) orally for 4 and 8 weeks. Serum insulin level, Pdx-1 and Insulin gene expression, and PDX-1 protein expression were assessed in the rat pancreas. Histopathological and ultrastructural changes in the islet and β-cells were observed. Results: Naringin prevented leukocytic infiltration in the pancreas of diabetic rats and recouped the β-cells with adequate secretory granules. Naringin-treated diabetic rats showed significantly increased mRNA expression of Pdx-1 and Insulin genes, increased expression of transcription factor PDX-1, and higher serum insulin levels than the diabetic control animals. These changes were more pronounced in the 8-week naringin-treated diabetic animals. Conclusions: Naringin was found to be an effective antidiabetic agent which increased Insulin gene expression and insulin secretion by upregulating the PDX-1 gene and protein expression.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Naringin (4′,5,7-Trihydroxyflavanone 7-Rhamnoglucoside) Attenuates β-Cell Dysfunction in Diabetic Rats through Upregulation of PDX-1

Subramanian

Balaji

Sekaran

et al. 2018

Cells Tissues Organs

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“…Exposures to ritonavir, lopinavir, atazanavir, or tipranavir resulted in increased apoptosis and reduced insulin-secretory capacity in insulinoma cells and human pancreatic islet cells [75]. PIs impaired beta-cell function by increasing oxidative stress and apoptosis [76]. Diabetes can result from the association of PIinduced insulin resistance and impaired secretion.…”

Section: Pathophysiologymentioning

confidence: 99%

Metabolic complications affecting adipose tissue, lipid and glucose metabolism associated with HIV antiretroviral treatment

Lagathu

Béréziat

Gorwood

et al. 2019

Expert Opinion on Drug Safety

124

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Introduction: Efficient antiretroviral-treatment(ART) generally allows control of HIV infection. However, persons-living-with-HIV(PLWH), when ageing, present a high prevalence of metabolic diseases. Area covered: Altered adiposity, dyslipidemias, insulin resistance, diabetes and their consequences are prevalent in PLWH and could be partly related to ART. Expert opinion: At first, personal and lifestyle factors are involved in the onset of these complications. The persistence of HIV in tissue reservoirs could synergize with some ART and enhance metabolic disorders. Altered fat repartition, diagnosed as lipodystrophy, has been related to first-generation nucleoside-reverse-transcriptase-inhibitors(NRTIs) (stavudine zidovudine) and some protease inhibitors(PIs). Recently, use of some integraseinhibitors(INSTI) resulted in weight/fat gain, which represents a worrisome unresolved situation.Lipid parameters were affected by some first-generation NRTIs, non-NRTIs(efavirenz) but also PIs boosted by ritonavir, with increased total and LDL-cholesterol and triglycerides.Insulin resistance is common in aging PLWH, often associated with abdominal obesity.Diabetes incidence, high with first-generation-ART (zidovudine, stavudine, didanosine, indinavir) has declined with contemporary ART close to that of the general population.Metabolic syndrome, a dysmetabolic situation with central obesity and insulin resistance, and liver steatosis are common in PLWH and could indirectly result from ART-associated fat gain and insulin resistance. All these dysmetabolic situations increase the atherogenic cardiovascular risk.Before 2000, PLWH received first-generation ART, as nucleoside analogue reverse transcriptase inhibitors (thymidine NRTIs, stavudine, zidovudine, didanosine) and protease inhibitors (PI, indinavir, ritonavir, nelfinavir) responsible for marked adverse events on lipid and glucose metabolism and on adipose tissue. These ART were replaced by newer molecules presenting a markedly lower metabolic toxicity.However, some PLWH, previously treated with first-generation NRTIs, present long-lasting fat alterations with metabolic consequences [1]. Some contemporary ART as integrase inhibitors (INSTI), considered as metabolic-friendly, were recently associated with weight/fat gain. Therefore, there are remaining and evolving concerns regarding the effect of ART on metabolism and adipose tissue in PLWH.As a consequence of the metabolic effects of some ART, increased prevalence of cardiovascular diseases (CVD), particularly atherosclerotic CVD[2] and diabetes, has been reported, but differ according to the calendar years and the geographic area. It is important to consider the metabolic profile of each patients to adapt ART. If required, classical lipid and glucose-lowering medications are prescribed.

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“…This antioxidant potential may contribute to their favorable effects on pancreatic islet survival. Indeed, naringin protected pancreatic β‐cells against human immunodeficiency virus‐1 protease inhibitor‐induced oxidative damage and apoptosis in vitro . In addition, oral administration of naringenin ameliorated hyperglycemia, oxidative stress, and inflammatory responses in diabetic animal models .…”

Section: Introductionmentioning

confidence: 96%

Naringin Protects Pancreatic β‐Cells Against Oxidative Stress‐Induced Apoptosis by Inhibiting Both Intrinsic and Extrinsic Pathways in Insulin‐Deficient Diabetic Mice

Lim

Kim

Pan

et al. 2018

Molecular Nutrition Food Res

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Naringin protects against HIV-1 protease inhibitors-induced pancreatic β-cell dysfunction and apoptosis

Cited by 19 publications

References 49 publications

Naringin (4′,5,7-Trihydroxyflavanone 7-Rhamnoglucoside) Attenuates β-Cell Dysfunction in Diabetic Rats through Upregulation of PDX-1

Naringin (4′,5,7-Trihydroxyflavanone 7-Rhamnoglucoside) Attenuates β-Cell Dysfunction in Diabetic Rats through Upregulation of PDX-1

Metabolic complications affecting adipose tissue, lipid and glucose metabolism associated with HIV antiretroviral treatment

Naringin Protects Pancreatic β‐Cells Against Oxidative Stress‐Induced Apoptosis by Inhibiting Both Intrinsic and Extrinsic Pathways in Insulin‐Deficient Diabetic Mice

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