Clinical Mass Spectrometry Laboratory, Clinical Research Institute, Affiliated Nanhua Hospital, University of South China, Hengyang, PR China.
Endocrine Department, Affiliated Nanhua Hospital, University of South China, Hengyang, PR China.
Hum Exp Toxicol. 2023 Jan-Dec;42:9603271231217992. doi: 10.1177/09603271231217992.
: Adipose tissue is a dynamic endocrine organ that plays a key role in regulating metabolic homeostasis. Previous studies confirmed that bisphenol A (BPA) or fructose can interfere with the function of adipose tissue. Nonetheless, knowledge on how exposure to BPA and fructose impacts energy metabolism in adipose tissue remains limited.: To determine impact of combined chronic exposure to low-dose bisphenol A and fructose on serum adipocytokines and the energy target metabolome in white adipose tissue.: 57 energy metabolic intermediates in adipose tissue and 7 adipocytokines in serum from Sprague Dawley rats were examined after combined exposure to two levels of BPA (lower dose: 0.25, and higher dose: 25 μg/kg every other day) and 5% fructose for 6 months.: combined exposure to lower-dose BPA and fructose significantly increased omentin-1, pyruvic acid, adenosine triphosphate (ATP), adenosine monophosphate (AMP), inosine monophosphate (IMP), inosine, and l-lactate; however, these parameters were not significantly affected by higher-dose BPA combined with fructose. Interestingly, the level of succinate (an intermediate of the citric acid cycle) increased dose-dependently in adipose tissue, and the level of apelin 13 (a versatile adipocytokine) decreased dose-dependently in serum after combined exposure to BPA and fructose. Phosphoenolpyruvic acid, phenyl-lactate, and ornithine were significantly correlated with asprosin, omentin-1, apelin, apelin 13, and adiponectin, while l-tyrosine was significantly correlated with irisin and a-FABP under combined exposure to BPA and fructose.: these findings indicated that lower-dose BPA combined with fructose could amplify the impact on glycolysis, energy storage, and purine nucleotide biosynthesis in adipose tissue, and adipocytokines, such as omentin-1 and apelin 13, may be related to metabolic interference induced by BPA and fructose exposure.
脂肪组织是一个动态的内分泌器官，在调节代谢平衡方面起着关键作用。先前的研究证实，双酚 A（BPA）或果糖会干扰脂肪组织的功能。尽管如此，关于 BPA 和果糖暴露如何影响脂肪组织的能量代谢知之甚少。
确定慢性低剂量 BPA 和果糖联合暴露对白色脂肪组织血清脂肪细胞因子和能量靶代谢组的影响。
对 Sprague Dawley 大鼠在联合暴露于两种剂量的 BPA（低剂量：0.25μg/kg，每隔一天；高剂量：25μg/kg，每隔一天）和 5%果糖 6 个月后，检测脂肪组织中的 57 种能量代谢中间产物和血清中的 7 种脂肪细胞因子。
联合暴露于低剂量 BPA 和果糖显著增加了网膜素-1、丙酮酸、三磷酸腺苷（ATP）、一磷酸腺苷（AMP）、次黄嘌呤单磷酸（IMP）、次黄嘌呤和 l-乳酸；然而，高剂量 BPA 联合果糖联合暴露对这些参数没有显著影响。有趣的是，琥珀酸（柠檬酸循环的中间产物）的水平在脂肪组织中呈剂量依赖性增加，而血清中阿立新 13（一种多功能脂肪细胞因子）的水平在 BPA 和果糖联合暴露后呈剂量依赖性降低。磷酸烯醇丙酮酸、苯乳酸和鸟氨酸与胰高血糖素原、网膜素-1、阿立新、阿立新 13 和脂联素显著相关，而 l-酪氨酸与 BPA 和果糖联合暴露下的鸢尾素和 a-FABP 显著相关。
低剂量 BPA 联合果糖可放大对脂肪组织糖酵解、能量储存和嘌呤核苷酸生物合成的影响，而脂肪细胞因子，如网膜素-1 和阿立新 13，可能与 BPA 和果糖暴露引起的代谢干扰有关。
