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Prenatal High-Salt Diet Induced Metabolic Disorders Via Decreasing Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1α in Adult Male Rat Offspring.

SCOPE
Although prenatal high salt (HS) intake leads to physiological complications in the offspring, little is known regarding its effects on the offspring's glucose metabolic. 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 RESULTS
Pregnant rats fed either normal-salt (1% NaCl) or high-salt (8% NaCl) diet during the whole pregnancy. Experiments conducted in 5-month-old male offspring. found that prenatal HS diet reduced the glucose tolerance and insulin sensitivity of the offspring. Additionally, there down-regulation of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (Ppargc1a/PPARGC1A) at the transcript and protein level, which led to decreased mitochondrial biogenesis and oxidative respiration in skeletal muscle. Moreover, the down-regulation of Ppargc1a was accompanied by decreases in the expression of glucose transporter type 4 (Glut4). With endurance exercise training, these changes mitigated, which ultimately resulted in improved insulin resistance.


CONCLUSION
These findings suggest that prenatal HS intake induces metabolic disorders via the decreased expression of Ppargc1a in skeletal muscle of adult offspring, providing novel information concerning the mechanisms and early prevention of metabolic diseases of fetal origins. This article is protected by copyright. All rights reserved.