Symonds M E, Mostyn A, Pearce S, Budge H, Stephenson T
Academic Division of Child Health, School of Human Development, University Hospital, Nottingham NG7 2UH, UK.
J Endocrinol. 2003 Dec;179(3):293-9. doi: 10.1677/joe.0.1790293.
In the fetus, adipose tIssue comprises both brown and white adipocytes for which brown fat is characterised as possessing the unique uncoupling protein (UCP)1. The dual characteristics of fetal fat reflect its critical role at birth in providing lipid that is mobilised rapidly following activation of UCP1 upon cold exposure to the extra-uterine environment. A key stage in the maturation of fetal fat is the gradual rise in the abundance of UCP1. For species with a mature hypothalamic-pituitary axis at birth there is a gradual increase in the amount and activity of UCP1 during late gestation, in conjunction with an increase in the plasma concentrations of catecholamines, thyroid hormones, cortisol, leptin and prolactin. These may act individually, or in combination, to promote UCP1 expression and, following the post-partum surge in each hormone, UCP1 abundance attains maximal amounts. Adipose tIssue grows in the fetus at a much lower rate than in the postnatal period. However, its growth is under marked nutritional constraints and, in contrast to many other fetal organs that are unaffected by nutritional manipulation, fat mass can be significantly altered by changes in maternal and, therefore, fetal nutrition. Fat deposition in the fetus is enhanced during late gestation following a previous period of nutrient restriction up to mid gestation. This is accompanied by increased mRNA abundance for the receptors of IGF-I and IGF-II. In contrast, increasing maternal nutrition in late gestation results in less adipose tIssue deposition but enhanced UCP1 abundance. The pronounced nutritional sensitivity of fetal adipose tIssue to both increased and decreased maternal nutrition may explain why the consequences of an adverse nutritional environment persist into later life.
在胎儿期，脂肪组织包含棕色和白色脂肪细胞，其中棕色脂肪的特征是拥有独特的解偶联蛋白（UCP）1。胎儿脂肪的双重特性反映了其在出生时的关键作用，即在暴露于宫外环境寒冷刺激时，UCP1被激活后能迅速提供可动员的脂质。胎儿脂肪成熟的一个关键阶段是UCP1丰度的逐渐上升。对于出生时具有成熟下丘脑 - 垂体轴的物种，在妊娠后期，UCP1的量和活性会逐渐增加，同时儿茶酚胺、甲状腺激素、皮质醇、瘦素和催乳素的血浆浓度也会增加。这些激素可能单独或联合作用以促进UCP1的表达，并且在产后每种激素激增后，UCP1丰度达到最大值。胎儿期脂肪组织的生长速度远低于出生后。然而，其生长受到显著的营养限制，与许多其他不受营养操纵影响的胎儿器官不同，脂肪量会因母体营养进而胎儿营养的变化而显著改变。在妊娠中期之前经历一段营养限制后，妊娠后期胎儿的脂肪沉积会增加。这伴随着IGF - I和IGF - II受体的mRNA丰度增加。相反，妊娠后期增加母体营养会导致脂肪组织沉积减少，但UCP1丰度增加。胎儿脂肪组织对母体营养增加和减少均具有显著的营养敏感性，这可能解释了不良营养环境的后果为何会持续到成年期。
