Is it time to revisit the Pedersen hypothesis in the face of the obesity epidemic?

Is it time to revisit the Pedersen hypothesis in the face of the obesity epidemic?
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DOI:
10.1016/j.ajog.2010.11.039
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发表时间:
2011-06
影响因子:
9.8
通讯作者:
Hauguel-De Mouzon S
Hauguel-De Mouzon S
中科院分区:
医学1区
文献类型:
--
作者:
Catalano PM;Hauguel-De Mouzon S

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彼得森假说是在50多年前提出的。Jorgen Pedersen主要照顾患有1型糖尿病的女性。他认为胎儿过度生长与葡萄糖经胎盘转移增加有关,葡萄糖经胎盘转移刺激胎儿β细胞释放胰岛素,导致巨大儿。最佳的母亲血糖控制降低围产期死亡率和发病率。然而,在随后的几十年里,孕产妇肥胖症以及随后的妊娠期(GDM)和2型糖尿病有所增加。1型和GDM/2型糖尿病的基础病理生理学是根本不同的:1型糖尿病主要是β细胞衰竭的病症,而2型糖尿病/GDM包括胰岛素抵抗和β细胞功能障碍。因此,1型糖尿病和肥胖症的胎儿所处的代谢环境可能完全不同。在这篇综述中,我们研究了肥胖糖尿病妇女的代谢环境和影响胎儿肥胖的脂质代谢。了解这些问题的重要性与全球范围内肥胖症的增加趋势以及后代围产期代谢功能障碍的规划有关。
The Pedersen hypothesis was formulated over 50 years ago. Jorgen Pedersen primarily cared for women with type-1 diabetes. He suggested that fetal overgrowth was related to increased transplacental transfer of glucose stimulating the release of insulin by the fetal beta cell and subsequent macrosomia. Optimal maternal glucose control decreased perinatal mortality and morbidity. However, over the ensuing decades, there have been increases in maternal obesity and subsequently gestational (GDM) and type-2 diabetes. The underlying pathophysiology of type- 1 and GDM/type-2 diabetes are fundamentally different: type-1 diabetes being primarily a disorder of beta cell failure and type-2 diabetes/GDM including both insulin resistance and beta cell dysfunction. As such the metabolic milieu in which the developing fetus is exposed may be quite different in type-1 diabetes and obesity. In this review we examine the metabolic environment of obese diabetic women and lipid metabolism affecting fetal adiposity. The importance of understanding these issues relates to the increasing trends of obesity worldwide with perinatal programming of metabolic dysfunction in the offspring.
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