PROLONGED HIGH-FAT DIET INDUCES KIDNEY DAMAGE BY DECREASED HYDROGEN SULFIDE AND INCREASED OXIDATIVE STRESS IN MICE.

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PROLONGED HIGH-FAT DIET INDUCES KIDNEY DAMAGE BY DECREASED HYDROGEN SULFIDE AND INCREASED OXIDATIVE STRESS IN MICE.

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Co-author 1

Gibong Jang a37333819@gmail.com Kyungpook National University Biomedical Science and BK21 Plus 680 Gukchaebosang-ro, Junggu, Daegu Korea (Republic of) *

Co-author 2

Yong Kwon Han pig891001@hanmail.net Kyungpook National University Anatomy 680 Gukchaebosang-ro, Junggu, Daegu Korea (Republic of) -

Co-author 3

You Ri Park youri0212@naver.com Kyungpook National University Biomedical Science and BK21 Plus 680 Gukchaebosang-ro, Junggu, Daegu Korea (Republic of) -

Co-author 4

Se Young Jang vocjsy@knu.ac.kr Kyungpook National University Hospital Internal Medicine 130 Dongdeok-ro, Jung-gu, Daegu Korea (Republic of) -

Co-author 5

Kwon Moo Park kmpark@knu.ac.kr Kyungpook National University Anatomy 680 Gukchaebosang-ro, Junggu, Daegu Korea (Republic of) -

Co-author 6

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Introduction

Obesity is a major risk factor for the development and progression of chronic kidney disease (CKD). However, its underlying mechanisms remains to be defined. Here, we investigate the role of cystathionine γ-lyase (CSE), which is a key transsulfuration pathway enzyme for the production of cysteine, hydrogen sulfide (H2S), and glutathione (GSH).

Methods

Cse-deficient (Cse⁻/⁻) and wild-type (Cse+/+) mice were fed either a normal-fat diet (NFD) or high-fat diet (HFD) for 16 weeks. Kidney functional and structural changes and oxidative stress were evaluated by creatinine clearance (CrCl), PAS and immunohistological staining, and lipid peroxidation.

Results

HFD feeding led to kidney dysfunction and fibrosis in both Cse+/+ and Cse⁻/⁻ mice, as indicated by reduced CrCl and elevated collagen deposition. These pathological changes in Cse⁻/⁻ mice were significantly greater than those in Cse+/+ mice. Cse deficiency augmented HFD-induced upregulation of TGF-β1, phosphorylated Smad3, plasminogen activator inhibitor-1, and collagen I. Cse deficiency alone decreased renal cysteine, H2S, total GSH levels, and GSSG/(GSH+GSSG); these levels were further decreased by HFD feeding in both genotypes, with more prominent decreases in Cse⁻/⁻ mice. HFD elevated hydrogen peroxide (H2O2) and 4-hydroxynonenal (4-HNE), with greater elevations in Cse⁻/⁻ than in Cse+/+ mice. NaHS treatment in HFD mice markedly decreased H2O2 levels and 4-HNE expression, with the decrease being more evident in Cse+/+ mice than in Cse⁻/⁻ mice.

Conclusion

These findings indicate that Cse gene deletion worsens HFD-induced kidney injury through increased oxidative stress due to decreased GSH and H2S production. Our study suggests that targeting the CSE–cysteine–GSH/H2S system may provide a novel therapeutic strategy for obesity-related kidney diseases.

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