School of Natural Sciences, University of California, Merced, CA, United States of America.
Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO, United States of America.
PLoS One. 2021 Nov 2;16(11):e0252360. doi: 10.1371/journal.pone.0252360. eCollection 2021.
Caloric restriction (CR) is one of the most important behavioral interventions to reduce excessive abdominal adiposity, which is a risk factor for the development of insulin resistance. Previous metabolomics studies have characterized substrate metabolism during healthy conditions; however, the effects of CR and subsequent mass recovery on shifts in substrate metabolism during insulin resistance (IR) have not been widely investigated. To assess the effects of acute CR and the subsequent mass recovery on shifts in substrate metabolism, a cohort of 15-week old Long Evans Tokushima Otsuka (LETO) and Otsuka Long Evans Tokushima Fatty (OLETF) rats were calorie restricted (CR: 50% × 10 days) with or without partial body mass recovery (PR; 73% x 7 days), along with their respective ad libitum controls. End-of-study plasma samples were analyzed for primary carbon metabolites by gas chromatography (GC) time-of-flight (TOF) mass spectrometry (MS) data acquisition. Data analysis included PCA, Pearson correlation vs previously reported variables (adipose and body masses, and insulin resistance index, IRI), and metabolomics maps (MetaMapp) generated for the most significant group comparisons. All treatments elicited a significant group differentiation in at least one principal component. CR improved TCA cycle in OLETF, and increased lipolysis and proteolysis. These changes were reversed after PR except for gluconeogenesis. Plasma lipid concentrations were inversely correlated to IRI in LETO, but not OLETF. These shifts in substrate metabolism suggest that the CR-induced decreases in adipose may not be sufficient to more permanently alter substrate metabolism to improve IR status during metabolic syndrome.
热量限制(CR)是减少过多腹部肥胖的最重要行为干预措施之一,而腹部肥胖是胰岛素抵抗发展的一个风险因素。以前的代谢组学研究已经描述了健康状态下的底物代谢;然而,CR 及其随后的体重恢复对胰岛素抵抗(IR)期间底物代谢的转变的影响尚未得到广泛研究。为了评估急性 CR 及其随后的体重恢复对底物代谢转变的影响,对一组 15 周龄的长野津田大冢(LETO)和大冢长野津田肥胖(OLETF)大鼠进行了热量限制(CR:50%×10 天),并进行了部分体重恢复(PR;73%×7 天),以及各自的随意进食对照。通过气相色谱(GC)飞行时间(TOF)质谱(MS)数据采集分析研究结束时的血浆样本中的主要碳代谢物。数据分析包括 PCA、与以前报道的变量(脂肪和体重,以及胰岛素抵抗指数,IRI)的 Pearson 相关性,以及为最显著的组比较生成的代谢组图谱(MetaMapp)。所有处理方法至少在一个主成分中引起了显著的组分化。CR 改善了 OLETF 的 TCA 循环,并增加了脂肪分解和蛋白水解。这些变化在 PR 后除了糖异生外都得到了逆转。血浆脂质浓度与 LETO 中的 IRI 呈负相关,但与 OLETF 无关。这些底物代谢的变化表明,CR 引起的脂肪减少可能不足以更永久地改变底物代谢,以改善代谢综合征期间的 IR 状态。