POMC基因敲除对高脂饮食诱导的肥胖雄性幼鼠睾丸功能的影响机制OA
The mechanism of POMC gene knockout to affect testicular function in obese male young mice induced by high-fat diet obesity
目的 探究阿黑皮素原(POMC)基因敲除对高脂饮食诱导的肥胖雄性幼鼠睾丸功能的影响机制.方法 将20 只野生型C57BL/6 雄性幼鼠随机均分为对照组(普通饲料喂养)与高脂饮食组(高脂饲料喂养),另10 只POMC-/-幼鼠设为敲除POMC高脂组(高脂饲料喂养).比较各组同时间幼鼠体质量,测量睾丸容积.采用HE、油红O染色检测各组睾丸组织病理结构与脂肪含量;Western blotting、qRT-PCR检测睾丸组织POMC、可卡因-苯丙胺调节转录肽(CART)蛋白及其mRNA水平;试剂盒检测血清睾酮与血脂[甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDLC)、高密度脂蛋白胆固醇(HDLC)]水平;TUNEL染色检测各组睾丸组织细胞凋亡水平.结果 与对照组比较,高脂饮食组、敲除POMC高脂组在第8、第12 周时的体质量、睾丸组织红染的中性脂肪增加(P<0.05),睾丸组织生精小管生殖细胞层减少(P<0.05),睾丸容积、睾酮、HDLC和POMC、CART蛋白及其mRNA表达水平降低(P<0.05),TC、TG、LDLC水平及细胞凋亡水平升高(P<0.05).与高脂饮食组比较,敲除POMC高脂组幼鼠在第8、第12 周时的体质量、睾丸组织红染的中性脂肪增加(P<0.05),睾丸组织生精小管生殖细胞层减少(P<0.05),睾丸容积、睾酮、HDLC和POMC、CART蛋白及其mRNA水平降低(P<0.05),TC、TG、LDLC及细胞凋亡水平升高(P<0.05).结论 POMC基因敲除显著加重高脂饮食诱导的肥胖雄性幼鼠睾丸功能损伤,其机制可能与POMC/CART信号通路受到抑制,进而导致代谢失调与细胞凋亡增加有关.
Aim To explore the mechanism of pro-opiomelanocortin(POMC)gene knockout to affect testicular function in obse young mice induced by high-fat diet obesity.Methods Twenty wild-type C57BL/6 male offspring mice were randomly and equally divided into a control group(fed a standard diet)and a high-fat diet group(fed a high-fat diet),while another ten POMC-/-pups were used as the knockout POMC high-fat group(fed a high-fat diet).The body weight of neonatal mice among different groups at the same time were compared,the testicular volume was measured.HE staining and oil red O staining were used to detect the his-topathological structure and fat content of testicular tissues in each group;Western blotting and qRT-PCR were used to detect the pro-tein and mRNA expression levels of POMC and cocaine-and amphetamine-regulated transcript(CART)in testicular tissues.The re-agent kit is used to detect the levels of serum testosterone and blood lipids[triglyceride(TG),total cholesterol(TC),low-density lipoprotein cholesterol(LDLC),and high-density lipoprotein cholesterol(HDLC)];TUNEL staining was used to detect the apoptosis level of testicular tissue cells in each group.Results Compared with the control group,the high-fat diet group and the knockout POMC high-fat group showed an increase in body weight at weeks 8 and 12,and red-stained neutral fat in testicular tissue(P<0.05),while a decrease in germ cell layer of seminiferous tubules in testicular tissue(P<0.05),a decrease in testicular volume,testoster-one,HDLC,and POMC,CART protein and their mRNA expression levels(P<0.05),and an increase inTC,TG,LDLClevels and cell apoptosis levels(P<0.05).Compared with the high-fat diet group,the weight at weeks 8 and 12,and red-stained neutral fat in testicular tissue of the knockout POMC high-fat group were increased(P<0.05),while the germ cell layer of seminiferous tubules in testicular tissue were decreased(P<0.05),and testicular volume,testosterone,HDLC,and POMC,CART protein and their mRNA levels were also decreased(P<0.05),in addition,TC,TG,LDLC and cell apoptosis levels were increased(P<0.05).Conclu-sion Knockout of POMC gene significantly exacerbates testicular dysfunction induced by high-fat diet in obese male young mice,and its mechanism may be related to the inhibition of POMC/CART signaling pathway,leading to metabolic disorders and increased cell apoptosis.
龙海旭;詹红艳;狄雯雯;唐美美
湖南中医药大学第二附属医院儿科,湖南 长沙 410005湖南中医药大学第二附属医院儿科,湖南 长沙 410005湖南中医药大学第二附属医院儿科,湖南 长沙 410005湖南中医药大学第二附属医院儿科,湖南 长沙 410005
医药卫生
肥胖POMC基因敲除睾丸功能高脂饮食幼鼠
obesityPOMC gene knockouttesticular functionhigh-fat dietyoung mice
《中南医学科学杂志》 2026 (1)
25-29,5
湖南省卫生健康委卫生科研课题项目(W20243267)
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