Exercise Interventions in Diabetic Kidney Disease
Summary
Diabetic kidney disease (DKD) affects up to one third of individuals with diabetes and constitutes a leading cause of end-stage renal failure worldwide. Exercise interventions have emerged as a safe, low-cost adjunct to pharmacological therapy, offering improvements in glycaemic control, blood pressure regulation and lipid metabolism. Regular physical activity mitigates albuminuria, preserves glomerular filtration rate and attenuates renal fibrosis by modulating inflammatory and oxidative pathways. Mechanistic studies reveal that moderate-intensity aerobic exercise enhances mitochondrial function, stimulates fatty acid β-oxidation through PPARδ-CPT1α signalling and upregulates SIRT1 to suppress pro-inflammatory transcription factors. High-intensity interval training (HIIT) further demonstrates benefits in animal models by reducing circulating fetuin-A and bolstering endogenous antioxidant defences. Collectively, exercise programmes tailored to individual capacity hold global significance in delaying DKD progression and reducing cardiovascular comorbidity.
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Exercise Interventions in Diabetic Kidney Disease publication trend
The graph below shows the total number of articles in exercise interventions in diabetic kidney disease across all publications each year (not limited to Nature Index journals).
Technical terms
Diabetic kidney disease (DKD): a chronic complication of diabetes characterised by progressive albuminuria, declining glomerular filtration rate and renal fibrosis.
eGFR (estimated glomerular filtration rate): a calculated measure of kidney function based on serum creatinine and demographic factors.
UACR (urinary albumin–creatinine ratio): a ratio used to detect and quantify albuminuria, an early marker of renal damage.
PPARδ (peroxisome proliferator-activated receptor delta): a nuclear receptor that regulates genes involved in fatty acid metabolism and energy homeostasis.
CPT1α (carnitine palmitoyltransferase 1 alpha): the rate-limiting mitochondrial enzyme for long-chain fatty acid β-oxidation.
HIIT (high-intensity interval training): an exercise protocol alternating brief bouts of intense activity with periods of rest or low intensity.
Oxidative stress: an imbalance between reactive oxygen species production and antioxidant defences, contributing to cellular injury.
Fibrosis: excessive deposition of extracellular matrix proteins, leading to tissue scarring and loss of organ function.
References
- Exercise alleviates diabetic kidney disease through PPARδ-CPT1α pathway-dependent fatty acid β-oxidation. The Innovation Life (2024).
- Exercise in Diabetic Nephropathy: Protective Effects and Molecular Mechanism. International Journal of Molecular Sciences (2024).
- Exercise training improves diabetic renal injury by reducing fetuin-A, oxidative stress and inflammation in type 2 diabetic rats. Heliyon (2024).
- Exercise training upregulates SIRT1 to attenuate inflammation and metabolic dysfunction in kidney and liver of diabetic db/db mice. Nutrition & Metabolism (2019).
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