Exercise training improves diabetic renal injury by reducing fetuin-A, oxidative stress and inflammation in type 2 diabetic rats
© 2024 The Authors..
Background: Diabetic kidney disease (DKD) stands as a primary contributor to end-stage renal disease, associated with heightened mortality in cardiovascular diseases. This study aimed to explore the impact of an eight-week high-intensity interval training (HIIT) on renal injury in diabetic rats.
Methods: Twenty-eight male Wistar rats were randomly allocated into four groups: healthy control (CTL), diabetic control (DC), exercise (EX), and diabetes-exercise (D + EX). Induction of diabetes in the DC and D + EX groups occurred through a two-month high-fat diet followed by a single dose of 35 mg/kg streptozotocin (STZ). Rats in the EX and D + EX groups underwent 4-10 intervals of HIIT (80-100% Vmax) over 8 weeks. Subsequently, pathological and biochemical parameters were assessed in the serum and kidney tissue of the experimental groups.
Results: In the DC group, diabetes led to elevated kidney damage, glomerulosclerosis, fasting blood glucose (FBG), Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) index, animal weight, kidney dysfunction, albuminuria, and glomerular filtration rate. Additionally, serum and kidney levels of fetuin-A increased, along with kidney levels of KIM-1. Mechanistically, diabetes induction resulted in kidney inflammation by elevating levels of tumor necrosis factor-alpha (TNF-α), transforming growth factor beta (TGF-β), and interleukin 6 (IL-6), while reducing IL-10 levels and increasing the IL-6/IL-10 ratio. Furthermore, diabetes triggered renal oxidative stress, evidenced by increased Malondialdehyde (MDA) levels and decreased levels of glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD). HIIT mitigated the adverse effects of diabetes in the D + EX group compared to the DC group.
Conclusion: Our findings suggest that HIIT ameliorates type 2 diabetes (T2D)-induced kidney damage by mitigating inflammation, lowering serum levels of fetuin-A, and bolstering antioxidant defenses. This study highlights the potential of HIIT as a time-efficient intervention for diabetic nephropathy.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:10 |
|---|---|
| Enthalten in: |
Heliyon - 10(2024), 6 vom: 30. März, Seite e27749 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Saberi, Shadan [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Diabetic kidney disease |
|---|
| Anmerkungen: |
Date Revised 22.03.2024 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
|---|
| doi: |
10.1016/j.heliyon.2024.e27749 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM369996305 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM369996305 | ||
| 003 | DE-627 | ||
| 005 | 20240323001451.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 240322s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.heliyon.2024.e27749 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1341.xml |
| 035 | |a (DE-627)NLM369996305 | ||
| 035 | |a (NLM)38510054 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Saberi, Shadan |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Exercise training improves diabetic renal injury by reducing fetuin-A, oxidative stress and inflammation in type 2 diabetic rats |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Revised 22.03.2024 | ||
| 500 | |a published: Electronic-eCollection | ||
| 500 | |a Citation Status PubMed-not-MEDLINE | ||
| 520 | |a © 2024 The Authors. | ||
| 520 | |a Background: Diabetic kidney disease (DKD) stands as a primary contributor to end-stage renal disease, associated with heightened mortality in cardiovascular diseases. This study aimed to explore the impact of an eight-week high-intensity interval training (HIIT) on renal injury in diabetic rats | ||
| 520 | |a Methods: Twenty-eight male Wistar rats were randomly allocated into four groups: healthy control (CTL), diabetic control (DC), exercise (EX), and diabetes-exercise (D + EX). Induction of diabetes in the DC and D + EX groups occurred through a two-month high-fat diet followed by a single dose of 35 mg/kg streptozotocin (STZ). Rats in the EX and D + EX groups underwent 4-10 intervals of HIIT (80-100% Vmax) over 8 weeks. Subsequently, pathological and biochemical parameters were assessed in the serum and kidney tissue of the experimental groups | ||
| 520 | |a Results: In the DC group, diabetes led to elevated kidney damage, glomerulosclerosis, fasting blood glucose (FBG), Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) index, animal weight, kidney dysfunction, albuminuria, and glomerular filtration rate. Additionally, serum and kidney levels of fetuin-A increased, along with kidney levels of KIM-1. Mechanistically, diabetes induction resulted in kidney inflammation by elevating levels of tumor necrosis factor-alpha (TNF-α), transforming growth factor beta (TGF-β), and interleukin 6 (IL-6), while reducing IL-10 levels and increasing the IL-6/IL-10 ratio. Furthermore, diabetes triggered renal oxidative stress, evidenced by increased Malondialdehyde (MDA) levels and decreased levels of glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD). HIIT mitigated the adverse effects of diabetes in the D + EX group compared to the DC group | ||
| 520 | |a Conclusion: Our findings suggest that HIIT ameliorates type 2 diabetes (T2D)-induced kidney damage by mitigating inflammation, lowering serum levels of fetuin-A, and bolstering antioxidant defenses. This study highlights the potential of HIIT as a time-efficient intervention for diabetic nephropathy | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Diabetic kidney disease | |
| 650 | 4 | |a Fetuin-A | |
| 650 | 4 | |a High-intensity interval training | |
| 650 | 4 | |a Inflammation | |
| 650 | 4 | |a Kim-1 | |
| 650 | 4 | |a Oxidative stress | |
| 700 | 1 | |a Askaripour, Majid |e verfasserin |4 aut | |
| 700 | 1 | |a Khaksari, Mohammad |e verfasserin |4 aut | |
| 700 | 1 | |a Amin Rajizadeh, Mohammad |e verfasserin |4 aut | |
| 700 | 1 | |a Abbas Bejeshk, Mohammad |e verfasserin |4 aut | |
| 700 | 1 | |a Akhbari, Mohammad |e verfasserin |4 aut | |
| 700 | 1 | |a Jafari, Elham |e verfasserin |4 aut | |
| 700 | 1 | |a Khoramipour, Kayvan |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Heliyon |d 2015 |g 10(2024), 6 vom: 30. März, Seite e27749 |w (DE-627)NLM255913095 |x 2405-8440 |7 nnns |
| 773 | 1 | 8 | |g volume:10 |g year:2024 |g number:6 |g day:30 |g month:03 |g pages:e27749 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.heliyon.2024.e27749 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 10 |j 2024 |e 6 |b 30 |c 03 |h e27749 | ||