Bazzano María Victoria, Paz Dante Agustín, Elia Evelin Mariel
Laboratorio de Biología del Desarrollo, Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-CONICET-UBA), Pabellón 2, Cdad. Universitaria, Buenos Aires, Argentina.
Laboratorio de Biología del Desarrollo, Instituto de Fisiología, Biología Molecular y Neurociencias (IFIBYNE-CONICET-UBA), Pabellón 2, Cdad. Universitaria, Buenos Aires, Argentina; Departamento de Biodiversidad y Biología Experimental, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Pabellón 2. Cdad. Universitaria, Buenos Aires, Argentina.
J Nutr Biochem. 2017 Apr;42:194-202. doi: 10.1016/j.jnutbio.2017.01.003. Epub 2017 Jan 23.
Obesity constitutes a health problem of increasing worldwide prevalence related to many reproductive problems such as infertility, ovulation dysfunction, preterm delivery, fetal growth disorders, etc. The mechanisms linking obesity to these pathologies are not fully understood. Cafeteria diet (CAF) is the animal model used for the study of obesity that more closely reflects western diet habits. Previously we described that CAF induces obesity associated to hyperglycemia, reduced ovarian reserve, presence of follicular cysts and ovulatory impairments. The aim of the present study was to contribute in the understanding of the physiological mechanisms altered as consequence of obesity. For that purpose, female Wistar rats were fed ad libitum with a standard diet (control group) or CAF (Obese group). We found that CAF fed-rats developed obesity, glucose intolerance and insulin resistance. Ovaries from obese rats showed decreased glucose uptake and became insulin resistant, showing decreased ovarian expression of glucotransporter type 4 and insulin receptor gene expression respect to controls. These animals showed an increased follicular nitric oxyde synthase expression that may be responsible for the ovulatory disruptions and for inflammation, a common feature in obesity. Obese rats resulted subfertile and their pups were macrosomic. We conclude that obesity alters the systemic and the ovarian glucidic homeostasis impairing the reproductive outcome. Since macrosomia is a risk factor for metabolic and obstetric disorders in adult life, we suggest that obesity is impacting not only on health and reproduction but it is also impacting on health and reproduction of the offspring.
肥胖是一个在全球范围内患病率不断上升的健康问题，与许多生殖问题相关，如不孕、排卵功能障碍、早产、胎儿生长发育障碍等。肥胖与这些病理状况之间的联系机制尚未完全明确。自助餐式饮食（CAF）是用于研究肥胖的动物模型，它更能反映西方饮食习惯。此前我们描述过，CAF会导致肥胖，并伴有高血糖、卵巢储备减少、卵泡囊肿的出现以及排卵障碍。本研究的目的是有助于理解因肥胖而改变的生理机制。为此，对雌性Wistar大鼠随意喂食标准饮食（对照组）或CAF（肥胖组）。我们发现，喂食CAF的大鼠出现了肥胖、葡萄糖不耐受和胰岛素抵抗。肥胖大鼠的卵巢显示葡萄糖摄取减少，并产生胰岛素抵抗，相对于对照组，其卵巢中葡萄糖转运蛋白4的表达以及胰岛素受体基因的表达均降低。这些动物的卵泡一氧化氮合酶表达增加，这可能是排卵紊乱和炎症的原因，而炎症是肥胖的一个常见特征。肥胖大鼠生育能力下降，其幼崽为巨大儿。我们得出结论，肥胖会改变全身和卵巢的糖代谢稳态，损害生殖结局。由于巨大儿是成年后代谢和产科疾病的一个风险因素，我们认为肥胖不仅影响健康和生殖，还会影响后代的健康和生殖。
