Effects of different exercise modes on relieving renal dysfunction in obese rats by regulating mitochondrial biogenesis and mitophagy
Objective To observe the effect of different exercises on relieving renal dysfunction in-duced by obesity,and explore their regulatory roles in mitochondrial biogenesis and mitophagy in this process.Methods Male Sprague-Dawley rats aged 5 weeks were selected as the experimental subjects.Among them,8 were randomly selected as normal diet quiet control group(NC group),while the rest were on high-fat diet to establish obesity-induced renal dysfunction.After successful modeling,they were randomly divided into a high-fat diet sedentary control group(HC group),an aerobic exercise group(AT group),a resistance training group(RT group),and a combined exercise group(AT+RT group),each of eight.The AT group underwent daily 60-minute aerobic exercise on a treadmill with an intensity of 55％-65％ of the maximum oxygen uptake,5 days/week,the RT group performed pro-gressive load resistance training using a ladder climbing method,3 days/week,8 sets/day,while the AT+RT group underwent aerobic and resistance exercise alternatingly,5 days/week,for 8 weeks suc-cessively.At the end of the intervention,24-hour urine samples were collected to test the microalbu-minuria(MAU),blood samples were taken to measure lipid profile,serum creatinine(SCR),and cys-tatin C(CysC).Moreover,epididymal and perirenal fat were weighed and recorded,and kidney tissues were examined the mitochondrial membrane potential.Meanwhile,hematoxylin and eosin staining was used to observe pathological changes in the kidney,and Western blotting was conducted to detect the protein expression levels of peroxisome proliferator-activated receptor gamma coactivator 1 alpha(PGC-1α),mitochondrial transcription factor A (Tfam),Bcl-2-interacting myosin like coiled-coil protein(Be-clin1),PTEN-induced kinase1 (PINK1),and Parkinson disease kinase(Parkin) in kidney tissues.Re-sults After 8-week exercise,the body weight in the AT,RT,and AT+RT groups was significantly low-er than the HC group(P<0.01).The Lee's index in the AT and RT groups was significantly lower than the HC group(P<0.01,P<0.05),and the adiposity ratio in the RT group was lower than the lat-ter(P<0.01).Moreover,the MAU level in the HC group was significantly higher than the other four groups(P<0.05).In addition,serum triglycerides(TG) and total cholesterol(TC) levels in the AT,RT,and AT+RT groups were significantly lower than the HC group(P<0.01,P<0.05),and the low-density lipoprotein cholesterol(LDL-C) level in the AT group was also significantly lower than the latter group (P<0.05).Meanwhile,SCR levels in the AT,RT,and AT+RT groups were significantly lower than the HC group(P<0.05,P<0.01),with the lowest SCR levels in the RT group and CysC levels in the AT and AT+RT groups significantly lower than the HC group(P<0.05).Besides,the glomerular area of the HC group was significantly larger than all the other groups(P<0.01).(6) The mitochondrial membrane potential of kidney cells was highest in the NC group,followed by the HC group,with that of the AT+RT group significantly lower than the NC group(P<0.01).Compared with the HC group,the expression levels of PGC-1α and Tfam protein were significantly higher in the AT,RT,and AT+RT groups(P<0.01) and that of Beclin1 protein was significantly higher in the AT group(P<0.05),while the expression levels of Parkin protein in the AT and RT groups were significantly high-er than the NC group(P<0.05).Conclusion Aerobic training,resistance training,or a combination of both interventions over 8 weeks can effectively reduce fat and weight,relieving the renal dysfunction in obese rats.Resistance training has a significant effect on delaying weight gain and reducing TG and SCR,while aerobic exercise effectively lowers LDL-C and CysC levels.All forms of exercise can en-hance the expression levels of key proteins associated with mitochondrial biogenesis,with aerobic exer-cise demonstrating a more pronounced intervention effect in upregulating the expression of mitophagy proteins.
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