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AuthorAgouni, Abdelali
AuthorLee, Duck Y
AuthorEid, Assaad A
AuthorGorin, Yves
AuthorSharma, Kumar
Available date2020-10-26T08:49:53Z
Publication Date2020
Publication NameQatar University Annual Research an Exhibition 2020 (quarfe)
CitationAgouni A., Lee D.Y, Eid A.A., Gorin Y.S., Sharma K., " The protective role of Sestrin2 in high fat diet-induced nephropathy", Qatar University Annual Research Forum and Exhibition (QUARFE 2020), Doha, 2020, https://doi.org/10.29117/quarfe.2020.0134
URIhttps://doi.org/10.29117/quarfe.2020.0134
URIhttp://hdl.handle.net/10576/16717
AbstractIntroduction: Obesity is a major risk factor for type-2 diabetes predisposing patients to diabetic nephropathy (DN), the leading cause of end-stage renal failure. Glomerular injury is a prominent pathological feature of DN. Sestrin2 (Sesn2) is a stress-induced protein, but its role in DN has not been investigated. Therefore, we have determined the impact of Sesn2 deletion in a mouse model of obesity-induced nephropathy. Materials and Methods: We examined the effects of Sesn2-deficiency in a long-term (22 weeks) mouse model of high fat diet (HFD)-induced obesity on glomerular structure. The severity of renal injury and fibrosis in wild type (Sesn2+/+) mice (fed HFD or chow diets) was compared to that in Sesn2-deficient mice (Sesn2-/-) fed HFD or chow diets. Animal work was carried out under an IACUC-approved protocol. Results: Data showed that Sesn2 ablation exacerbated HFD-induced glomerular fibrotic injury as evidenced by mesangial matrix hypertrophy and accumulation of both fibronectin and collagen IV. Western blot analysis revealed that HFD- or chow-fed Sesn2-/- mice exhibited higher protein expression of key lipogenic enzymes, fatty acid translocase CD36 (an indicator of lipid uptake), fatty acid synthase and ATP citrate lyase. Sesn2-deficiency in obese mice resulted in podocyte loss as indicated by reduced expression of synaptopodin. Glomerular lesions like those observed in HFD-fed wild-type mice were detected in Sesn2-/- mice fed a chow diet, indicating that the basal deletion of Sesn2 is deleterious by itself. Conclusions: We provide the first evidence that Sesn2 is renoprotective in obesity-induced nephropathy by diminishing lipid accumulation and blocking excessive lipid uptake and de novo lipid synthesis. Understanding the protective of Sesn2 should yield novel therapeutic interventions to effectively preserve glomerular function in obesity and diabetes
Languageen
PublisherQatar University Press
SubjectObesity
SubjectDiabetic Kidney Disease
SubjectOxidative Stress
SubjectSestrin2
SubjectBiomaker
TitleThe protective role of Sestrin2 in high fat diet-induced nephropathy
TypePoster


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