| 284 | 19 | 61 |
| 下载次数 | 被引频次 | 阅读次数 |
目的通过高脂高糖饮食诱导雌性大鼠多囊卵巢综合征(PCOS),探讨其生殖和代谢特征。方法将23天断奶雌性大鼠随机分成两组:对照组接受正常饮食(对照组,n=18),实验组接受高脂高糖饮食(HFHS组,n=18),连续喂养14周。观察两组体重、动情周期和卵巢组织学变化,检测两组空腹血糖、空腹胰岛素、计算胰岛素抵抗指数(HOMA-IR)、血脂水平、性激素水平。结果 HFHS组大鼠体重至第3周起显著高于对照组(P<0.001),但两组卵巢重量无显著差异[(0.041±0.006)g vs.(0.045±0.005)g,P>0.05]。HFHS组动情周期失去规律变化,发情期持续时间占整个发情周期时间的比例显著长大对照组[(0.46±0.06)vs.(0.27±0.03),P<0.001]。HFHS组卵巢组织学检查发现多个囊状扩张卵泡、黄体数量下降。HFHS组空腹胰岛素、HOMA-IR、总胆固醇水平显著高于对照组(P<0.001);发情间期HFHS组LH和E2水平显著低于对照组(P<0.05),睾酮(T)水平显著高于对照组(P<0.001);发情前期HFHS组LH和P水平显著低于对照组(P<0.05),T和E2水平显著高于对照组(P<0.001)。结论高脂高糖饮食诱导雌性大鼠PCOS,并产生代谢紊乱和卵巢改变,与PCOS患者临床观察到的相似。
Abstract:Objective:To establish a polycystic ovary syndrome(PCOS)animal model of female rats induced by high fat and high sugar diet,and the reproductive and metabolic characteristics of the PCOS rats were also explored.Methods:The female rats with 23 days old were randomly divided into two groups:the rats received a normal diet in control group(n=18),and the rats received a high-fat and high sugar diet in HFHS group(n=18),continuous feeding for 14 weeks.The body weight,estrus cycle and histology of ovary in the two groups were observed.The fasting glucose,fasting insulin,Insulin resistance index(HOMA-IR),lipid profile,hormonal levels were also measured.Results:The body weight of HFHS group increased significantly from the third weeks than that of control group(P<0.001).However,there were no significant differences in ovarian weight between two groups[(0.041±0.006)g vs.(0.045±0.005)g,P>0.05].The estrous cycle of HFHS group lost regular changes.The proportion of estrus duration to the time of total estrus cycle in HFHS group(0.46±0.06)was significantly longer than that of the control group(0.27±0.03)(P<0.001).The results of ovarian histological examination showed multiple cystic expansion follicles and decrease of the number of corpus luteum.The levels of fasting insulin,HOMA-IR and total cholesterol in the HFHS group were significantly higher than those in the control group(P<0.001).In diestrus,thelevels of LH and E2 in the HFHS group were significantly lower than those in the control group(P<0.05),and testosterone(T)level was significantly higher than that in the control group(P<0.001).In proestrus,LH and progesterone levels in the HFHS group were significantly lower than the control group(P<0.05),and the levels of T and E2 were significantly higher than the control group(P<0.001).Conclusions:High fat and high sugar diets can induce PCOS in female rats,and produce metabolic disorders and ovarian changes which were similar to those observed in patients with PCOS.
[1] Silvestris E,de Pergola G,Rosania R,et al.Obesity as disruptor of the female fertility[J].Reprod Biol Endocrinol,2018,16:22.
[2]王哲蔚,徐韶华,孙莉,等.成年妇女体重增加速度与多囊卵巢综合征发病关系的研究[J].生殖医学杂志,2017,26:1136-1141.
[3] Tziomalos K,Dinas K.Obesity and outcome of assisted reproduction in patients with polycystic ovary syndrome[J].Front Endocrinol(Lausanne),2018,9:149.
[4] Foroozanfard F,Rafiei H,Samimi M,et al.The effects of dietary approaches to stop hypertension diet on weight loss,anti-Müllerian hormone and metabolic profiles in women with polycystic ovary syndrome:A randomized clinical trial[J].Clin Endocrinol(Oxf),2017,87:51-58.
[5] Tain YL,Lin YJ,Sheen JM,et al.High fat diets sexspecifically affect the renal transcriptome and program obesity,kidney injury,and hypertension in the offspring[J].Nutrients,2017,9(4).pii:E357.doi:10.3390/nu9040357.
[6] Khadilkar SS.Polycystic ovarian syndrome:Is it time to rename PCOS to HA-PODS?[J].J Obstet Gynaecol India,2016,66:81-87.
[7] Walters KA,Bertoldo MJ,Handelsman DJ.Evidence from animal models on the pathogenesis of PCOS[J].Best Pract Res Clin Endocrinol Metab,2018,32:271-281.
[8] Kauffman AS,Thackray VG,Ryan GE,et al.A novel letrozole model recapitulates both the reproductive and metabolic phenotypes of polycystic ovary syndrome in female mice[J].Biol Reprod,2015,93:69.
[9] Zhang B,Wang J,Shen S,et al.Association of androgen excess with glucose intolerance in women with polycystic ovary syndrome[J].Biomed Res Int,2018,2018:6869705.
[10] Chen MJ,Chou CH,Chen SU,et al.The effect of androgens on ovarian follicle maturation:Dihydrotestosterone suppress FSH-stimulated granulosa cell proliferation by upregulating PPARγ-dependent PTEN expression[J].Sci Rep,2015,5:18319.
[11] Wang RS, ChangHY, KaoSH, et al. Abnormal mitochondrialfunctionandimpairedgranulosacell differentiation in androgen receptor knockout mice[J].Int J Mol Sci,2015,16:9831-9849.
[12] Reis AM,Honorato-Sampaio K.C-type natriuretic peptide:a link between hyperandrogenism and anovulation in a mouse model of polycystic ovary syndrome[J].Clin Sci(Lond),2018,132:905-908.
[13] Pierre A,Taieb J,Giton F,et al.Dysregulation of the antimüllerian hormone system by steroids in women with polycystic ovary syndrome[J].J Clin Endocrinol Metab,2017,102:3970-3978.
[14] Zhang Y,Hu M,Meng F,et al.Metformin ameliorates uterine defects in a rat model of polycystic ovary syndrome[J].EBioMedicine,2017,18:157-170.
[15] Xu N,Geller DH,Jones MR,et al. Comprehensive assessment of expression of insulin signaling pathway components in subcutaneous adipose tissue of women with and without polycystic ovary syndrome[J].J Clin Transl Endocrinol,2015,2:99-104.
[16] Crha I,Ventruba P,FilipinskáE,et al.Medroxyprogesteron acetate use to block LH surge in oocyte donor stimulation[J].Ceska Gynekol,2018,83:11-16.
基本信息:
中图分类号:R711.75
引用信息:
[1]古兰·托合提木拉提,叶尔努尔·吐苏甫汗,马玉兰,等.高脂高糖饮食暴露诱导大鼠多囊卵巢综合征研究[J].生殖医学杂志,2019,28(02):169-173.
基金信息:
新疆自治区自然科学基金(2011211C184)
2019-02-15
2019-02-15