Polycystic ovary syndrome(PCOS) is a common endocrine disorder that affects up to 6.8% of reproductive age women.Experimental research and clinical observations suggest that PCOS may originate in the very early stages...Polycystic ovary syndrome(PCOS) is a common endocrine disorder that affects up to 6.8% of reproductive age women.Experimental research and clinical observations suggest that PCOS may originate in the very early stages of development,possibly even during intrauterine life.This suggests that PCOS is either genetically-transmittedor is due to epigenetic alterations that develop in the intrauterine microenvironment.Although familial cases support the role of genetic factors,no specific genetic pattern has been defined in PCOS.Several candidate genes have been implicated in its pathogenesis,but none can specifically be implicated in PCOS development.Hypotheses based on the impact of the intrauterine environment on PCOS development can be grouped into two categories.The first is the "thrifty" phenotype hypothesis,which states that intrauterine nutritional restriction in fetuses causes decreased insulin secretion and,as a compensatory mechanism,insulin resistance.Additionally,an impaired nutritional environment can affect the methylation of some specific genes,which can also trigger PCOS.The second hypothesis postulates that fetal exposure to excess androgen can induce changes in differentiating tissues,causing the PCOS phenotype to develop in adult life.This review aimed to examine the role of fetal programming in development of PCOS.展开更多
Protein restriction in utero may give rise to restricted growth as well as induce metabolically related diseases. In order to determine the suitability of mink as an animal model for metabolism studies, the effects of...Protein restriction in utero may give rise to restricted growth as well as induce metabolically related diseases. In order to determine the suitability of mink as an animal model for metabolism studies, the effects of protein restriction during gestation on dam and kit performance must first be determined. Mink dams were fed an adequate protein (AP;crude protein:fat:carbohydrate ratio of 31:55:14% of metabolizable energy, ME) or a low protein diet (LP;19%:49%: 32% of ME) during the last 21.2 ± 3.3 days of gestation, followed by an adequate diet during lactation. Respiration and balance experiments were performed during late gestation and twice during lactation. The dietary treatment only affected energy metabolism traits significantly during the treatment period in late gestation, such that LP dams oxidized less protein (12% vs 23% of heat production, HE, P = 0.001) but more carbohydrate (37% vs 26% of HE, P -0.75.day-1, P < 0.05) than AP dams. Reproductive performance and kit organ growth were not affected by diet. Kit losses up to weaning were higher in LP than AP dams (2.0 vs 1.4, P < 0.05). LP fetuses weighed less (8.3 vs 11.6 g, P < 0.001) and were shorter (6.2 vs 7.6 cm, P < 0.001) than AP fetuses, however, differences might have been due to different implantation times. LP kits weighed 8.5% less than AP kits at birth, and remained lighter until 21 days of age. The LP diet caused growth restriction and increased kit mortality indicating that the dietary protein supply during late gestation was suboptimal to re-quirements. The long-term consequences of protein restriction in utero in terms of permanent metabolic changes in adulthood now need to be investigated.展开更多
文摘Polycystic ovary syndrome(PCOS) is a common endocrine disorder that affects up to 6.8% of reproductive age women.Experimental research and clinical observations suggest that PCOS may originate in the very early stages of development,possibly even during intrauterine life.This suggests that PCOS is either genetically-transmittedor is due to epigenetic alterations that develop in the intrauterine microenvironment.Although familial cases support the role of genetic factors,no specific genetic pattern has been defined in PCOS.Several candidate genes have been implicated in its pathogenesis,but none can specifically be implicated in PCOS development.Hypotheses based on the impact of the intrauterine environment on PCOS development can be grouped into two categories.The first is the "thrifty" phenotype hypothesis,which states that intrauterine nutritional restriction in fetuses causes decreased insulin secretion and,as a compensatory mechanism,insulin resistance.Additionally,an impaired nutritional environment can affect the methylation of some specific genes,which can also trigger PCOS.The second hypothesis postulates that fetal exposure to excess androgen can induce changes in differentiating tissues,causing the PCOS phenotype to develop in adult life.This review aimed to examine the role of fetal programming in development of PCOS.
文摘Protein restriction in utero may give rise to restricted growth as well as induce metabolically related diseases. In order to determine the suitability of mink as an animal model for metabolism studies, the effects of protein restriction during gestation on dam and kit performance must first be determined. Mink dams were fed an adequate protein (AP;crude protein:fat:carbohydrate ratio of 31:55:14% of metabolizable energy, ME) or a low protein diet (LP;19%:49%: 32% of ME) during the last 21.2 ± 3.3 days of gestation, followed by an adequate diet during lactation. Respiration and balance experiments were performed during late gestation and twice during lactation. The dietary treatment only affected energy metabolism traits significantly during the treatment period in late gestation, such that LP dams oxidized less protein (12% vs 23% of heat production, HE, P = 0.001) but more carbohydrate (37% vs 26% of HE, P -0.75.day-1, P < 0.05) than AP dams. Reproductive performance and kit organ growth were not affected by diet. Kit losses up to weaning were higher in LP than AP dams (2.0 vs 1.4, P < 0.05). LP fetuses weighed less (8.3 vs 11.6 g, P < 0.001) and were shorter (6.2 vs 7.6 cm, P < 0.001) than AP fetuses, however, differences might have been due to different implantation times. LP kits weighed 8.5% less than AP kits at birth, and remained lighter until 21 days of age. The LP diet caused growth restriction and increased kit mortality indicating that the dietary protein supply during late gestation was suboptimal to re-quirements. The long-term consequences of protein restriction in utero in terms of permanent metabolic changes in adulthood now need to be investigated.
