Metabolic and ovarian consequences of perinatal sex steroid programming

作者: Camilla Alexanderson

DOI:

关键词:

摘要: Endocrine and metabolic disturbances in adulthood may stem from insults such as nutritional hormonal alterations that occur at critical periods pre- or postnatal life – a process known programming. This means suboptimal conditions utero early contribute to adult reproductive impairments type 2 diabetes, insulin resistance, dyslipidemia. The aims of this thesis were 1) identify the potential ovarian programming effects sex steroid exposure female rats, 2) utilize data collected by Swedish Twin Registry investigate, large cohort dizygotic twins, prenatal androgen on metabolism anthropometry women with male twin. main findings were: A single dose testosterone estradiol caused resistance an increase mesenteric adipocyte size rats. Testosterone also resulted dyslipidemia elevated triglyceride levels. Rats exposed displayed more pronounced than rats dihydrotestosterone. Testosterone-injected exhibited increased adipose tissue. Dihydrotestosterone-injected reduced sensitivity only. Estradiol administration directly after birth altered morphology expression genes involved follicle development. decreased weight parametrial tissue, tissue lipoprotein lipase activity, metabolism. In addition, estradiol-exposed was accompanied serum levels inflammatory markers, skeletal muscle immune-related regulation glucose lipid Adult twin brother BMI, higher risk being overweight compared same-sex pairs. differences BMI between groups observed 60 years older, but not those below age. Dyslipidemia, diabetes mellitus, common summary, perinatal steroids affected developing organism, predisposing endocrine abnormalities features syndrome Changes sensitivity, profile, distribution, cellularity metabolism, well morphology, are factors can be programmed perinatally health consequences adulthood. Our observations body opposite-sex twins consistent results animal experiments, indicating relevance for humans.

参考文章(180)
Bryce C Ryan, John G Vandenbergh, Intrauterine position effects. Neuroscience & Biobehavioral Reviews. ,vol. 26, pp. 665- 678 ,(2002) , 10.1016/S0149-7634(02)00038-6
T Sir-Petermann, L Devoto, M Maliqueo, P Peirano, SE Recabarren, L Wildt, Resumption of ovarian function during lactational amenorrhoea in breastfeeding women with polycystic ovarian syndrome: endocrine aspects Human Reproduction. ,vol. 16, pp. 1603- 1610 ,(2001) , 10.1093/HUMREP/16.8.1603
P. Mauriège, C. Martel, D. Langin, M. Lacaille, J.P. Després, A. Bélanger, F. Labrie, Y. Deshaies, Chronic effects of dehydroepiandrosterone on rat adipose tissue metabolism. Metabolism-clinical and Experimental. ,vol. 52, pp. 264- 272 ,(2003) , 10.1053/META.2003.50043
C Gilling-Smith, D S Willis, R W Beard, S Franks, Hypersecretion of androstenedione by isolated thecal cells from polycystic ovaries. The Journal of Clinical Endocrinology and Metabolism. ,vol. 79, pp. 1158- 1165 ,(1994) , 10.1210/JCEM.79.4.7962289
Dana C. Dolinoy, Jennifer R. Weidman, Robert A. Waterland, Randy L. Jirtle, Maternal genistein alters coat color and protects Avy mouse offspring from obesity by modifying the fetal epigenome Environmental Health Perspectives. ,vol. 114, pp. 567- 572 ,(2006) , 10.1289/EHP.8700
R A DeFronzo, J D Tobin, R Andres, Glucose clamp technique: a method for quantifying insulin secretion and resistance. American Journal of Physiology. ,vol. 237, pp. 214- 223 ,(1979) , 10.1152/AJPENDO.1979.237.3.E214
R B Barnes, R L Rosenfield, D A Ehrmann, J F Cara, L Cuttler, L L Levitsky, I M Rosenthal, Ovarian hyperandrogynism as a result of congenital adrenal virilizing disorders: evidence for perinatal masculinization of neuroendocrine function in women. The Journal of Clinical Endocrinology and Metabolism. ,vol. 79, pp. 1328- 1333 ,(1994) , 10.1210/JCEM.79.5.7962325
L. C. Groop, Insulin resistance: the fundamental trigger of type 2 diabetes. Diabetes, Obesity and Metabolism. ,vol. 1, pp. 1- 7 ,(1999) , 10.1046/J.1463-1326.1999.0010S1001.X
C. N. Hales, D. J. P. Barker, Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia. ,vol. 35, pp. 595- 601 ,(1992) , 10.1007/BF00400248