Prenatal High-Salt Diet-Induced Metabolic Disorders via Decreasing Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1α in Adult Male Rat Offspring
Prenatal High-Salt Diet-Induced Metabolic Disorders via Decreasing Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1α in Adult Male Rat Offspring
复制标题
产前高盐饮食通过减少成年雄性大鼠后代的过氧化物酶体增殖物诱导代谢紊乱 - 激活受体伽马共激活物 1α
DOI：
10.1002/mnfr.202000196
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发表时间：
2020-06-22
影响因子：
5.2
通讯作者：
Lu，Xiyuan
中科院分区：
文献类型：
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作者：
Liu，Yanping;Yang，Chunli;Lu，Xiyuan
虽然产前高盐（HS）摄入会导致后代的生理并发症，但关于其对后代葡萄糖代谢的影响知之甚少。因此，本研究的目的是确定产前HS饮食对后代的代谢的后果，并测试潜在的therapeutic.Methods和ResultsPregnant rats喂养无论是正常盐（1%氯化钠）或高盐（8%氯化钠）饮食在整个怀孕期间。实验在5个月大的雄性后代中进行。结果发现，产前HS饮食降低了后代的葡萄糖耐量和胰岛素敏感性。此外，过氧化物酶体增殖物激活受体γ共激活因子1 α（Ppargc 1a/PPARGC 1A）在转录物和蛋白质水平下调，导致骨骼肌线粒体生物合成和氧化呼吸减少。此外，Ppargc 1a的下调伴随着葡萄糖转运蛋白4（Glut 4）表达的降低。耐力运动训练，这些变化是减轻，最终导致改善insulin resistance.ConclusionThese研究结果表明，产前HS摄入诱导代谢紊乱通过降低表达的Ppargc 1a在骨骼肌的成年后代，提供新的信息有关的机制和早期预防胎儿起源的代谢疾病。
ScopeAlthough prenatal high‐salt (HS) intake leads to physiological complications in the offspring, little is known regarding its effects on the offspring's glucose metabolism. Therefore, the objectives of this study are to determine the consequences of prenatal HS diet on the offspring's metabolism and to test a potential therapy.Methods and ResultsPregnant rats are fed either a normal‐salt (1% NaCl) or high‐salt (8% NaCl) diet during the whole pregnancy. Experiments are conducted in five‐month‐old male offspring. It is found that the prenatal HS diet reduced the glucose tolerance and insulin sensitivity of the offspring. Additionally, there is down‐regulation of peroxisome proliferator‐activated receptor gamma coactivator 1 alpha (Ppargc1a/PPARGC1A) at the transcript and protein level, which leads to decreased mitochondrial biogenesis and oxidative respiration in skeletal muscle. Moreover, the down‐regulation of Ppargc1a is accompanied by decreases in the expression of glucose transporter type 4 (Glut4). With endurance exercise training, these changes are mitigated, which ultimately resulted in improved insulin resistance.ConclusionThese findings suggest that prenatal HS intake induces metabolic disorders via the decreased expression of Ppargc1a in the skeletal muscle of adult offspring, providing novel information concerning the mechanisms and early prevention of metabolic diseases of fetal origins.