This study evaluates the protective role of oyster peptide (OP) on the occurrence of Exercise‐Hypogonadal Male Condition. Male rats were given heavy‐load swimming training and / or OP was supplemented for 6 consecutive weeks. After heavy‐load training, sperm count, sperm viability and sperm motility in epididymis, testosterone in serum and testis, glutathione peroxidase (GSH‐px) and androgen receptor (AR) in testis and mating times were remarkably decreased, malondialdehyde (MDA), capture latency and mating latency were significantly increased, mRNA expression of steroidogenic acute regulatory (StAR) and P450 cholesterol side‐chain cleavage enzyme (P450scc) were obviously down‐regulated, but serum follicle‐stimulating hormone (FSH) and luteinising hormone (LH) were not statistically changed. Conversely, when OP was supplemented at heavy‐load training, sperm count, sperm viability and sperm motility in epididymis, serum FSH, LH, testosterone, GSH‐px, superoxide dismutase (SOD), testosterone, AR in testis and mating times were dramatically increased, while testicular MDA, capture latency and mating latency were significantly decreased, and mRNA expression of StAR, StARD7, P450scc and 3β‐hydroxysteroid dehydrogenase (3β‐HSD) were significantly up‐regulated. In conclusion, heavy‐load training causes testicular spermatogenic and steroidogenic disorders by enhancing the generation of reactive oxygen species (ROS), which can be protected by the co‐administration of OP by enhancing the function of pituitary gonad axis and lowering ROS generation.
Aim The aim of this study was to investigate the effect of oyster oligopeptide (OOP) at different doses on testosterone secretion and its regulating mechanism in partial androgen deficiency syndrome of aging male. Methods The cyclophosphamide‐induced partial androgen deficiency syndrome of the aging male rats were treated with a low, medium and high dose of OOP for 6 weeks. Results Cyclophosphamide could decrease levels of total testosterone and luteinizing hormone in serum, and testosterone and glutathione peroxidase in testis, and increase malondialdehyde, and downregulate the mRNA expression of steroidogenic acute regulatory protein, steroidogenic acute regulatory‐related lipid transfer domain 7 and P450 cholesterol side chain cleavage enzyme in testis (P < 0.05). All these changes were reversed by OOP co‐administration with different doses, although, OOP at a low dose did not increase serum testosterone, luteinizing hormone and testicular glutathione peroxidase levels. Conclusions OOP treatment with different doses can effectively reduce oxidative stress in testicular tissue, promote the synthesis of testosterone and then prevent the formation of partial androgen deficiency syndrome of the aging male, with optimal effect at medium dose. Geriatr Gerontol Int 2021; 21: 268–275.
Objective Objective: To explore the effects of alanyl-glutamine(Ala-Gln)or glutamine(Gln) supplementation on protein metabolism in rat skeletal muscle during simulated altitude training,and compare the intervention of Gln or Ala-Gln to provide the necessary experimental basis for finding nutritional interventions to inhibit skeletal muscle protein degradation during altitude training. Methods Methods: Forty SD rats aged 6 weeks were randomly divided into normoxic control group(NC group,n=10),hypoxic exercise group(HE group, n=10),hypoxic exercise + glutamine + alanine group(HEG group,n=10), hypoxic exercise + alanyl glutamine group(HEAG group,n=10). Rats were subjected to 6 weeks of 13.6% hypoxic exposure and 90% lactic acid threshold intensity weight-bearing swimming(load weight of 2.1% of body weight)exercise training,30 minutes after the end of each training,the mixed solution of Ala and Gln was administered according to the dose of 0.75g/Kg body weight in HEG group,and the solution of Ala-Gln was administered in the HEAG group at a dose of 1.5 g/kg body weight. After 6 weeks,the contents of rat skeletal muscle total protein(Pro),myosin heavy chain(Myo),tumor necrosis factor-α(TNF-α),nuclear transcription factor-κB (NF-κB),NF-κB inhibitory protein α(IkBα),and mRNA expression of muscle atrophy box F gene(MAFbx),muscle ring finger gene 1(MuRF1),and inhibitor of kappa B kinase complex-beta(IKKβ)were measured. Results Results:(1)Compared with NC group,the content of Pro and Myo in skeletal muscle in HE group was significantly decreased(P<0.05,P<0.01),and the mRNA expression of MAFbx and MuRF1 in skeletal muscle was significantly increased(P<0.05,P< 0.01),the levels of TNF-α and NF-κB were significantly increased(P<0.05),the content of IkBα was significantly decreased(P<0.05),and the expression of IKKβ mRNA was significantly increased(P<0.01). (2)Compared with HE group,the content of Pro and Myo in skeletal muscle in HEG group increased,but there was no significant difference(P>0.05). The expression of MuRF1 mRNA and the content of TNF-α and NF-κB in skeletal muscle decreased,IkBα content increased,there were no significant difference,but mRNA expression of MAFbx and IKKβ was significantly decreased(P<0.05, P<0.01). (3)Compared with HE group,the content of Pro and Myo in skeletal muscle in HEAG group increased significantly(P<0.05),mRNA expression of IKKβ,MuRF1 and MAFb(P<0.01)and TNF-α,NF-κB content(P<0.05)in skeletal muscle was significantly decreased,and the IkBα content was significantly increased(P<0.05). Conclusions Conclusion:(1)Simulated altitude training can activate TNF-α/NF-κB/MuRF1 pathway and enhance the catabolism of skeletal muscle protein,which is one of the important mechanisms for the reduction of skeletal muscle protein content caused by altitude training. (2)Supplementation of Ala-Gln during altitude training can significantly reduce the activation of TNF-α/NF-κB/MuRF1 pathway in skeletal muscle,and reduce the catabolism of skeletal muscle protein during altitude training,which plays a very important role in preventing the loss of skeletal muscle protein caused by altitude training. supplementation of Gln monomer during altitude training has little inhibitory effect on the activation of TNF-α/NF-κB/MuRF1 pathway in skeletal muscle.
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