We evaluated effects of calorie restriction (CR: consuming 60-65% of ad libitum [AL] intake) initiated late-in-life with or without acute exercise on insulin-stimulated glucose uptake (ISGU) of skeletal muscle by studying four groups of 26-month-old rats: sedentary-AL, sedentary-CR (8-week duration), 3 hours post-exercise (3hPEX)-AL and 3hPEX-CR. ISGU was determined in isolated epitrochlearis muscles incubated ± insulin. Muscles were assessed for signaling proteins (immunoblotting) and lipids (mass spectrometry). ISGU from sedentary-CR and 3hPEX-AL exceeded sedentary-AL; 3hPEX-CR exceeded all other groups. Akt (Ser473, Thr308) and Akt substrate of 160 kDa (AS160; Ser588, Thr642, Ser704) phosphorylation levels tracked with ISGU. Among the 477 lipids detected, 114 were altered by CR (including reductions in 15 of 25 acylcarnitines), and 27 were altered by exercise (including reductions in 18 of 22 lysophosphatidylcholines) with only six lipids overlapping between CR and exercise. ISGU significantly correlated with 23 lipids, including: acylcarnitine 20:1 (r = .683), lysophosphatidylethanolamine19:0 (r = -.662), acylcarnitine 24:0 (r = .611), and plasmenyl-phosphatidylethanolamine 37:5 (r = -.603). Muscle levels of ceramides (a lipid class previously linked to insulin resistance) were not altered by CR and/or exercise nor significantly correlated with ISGU, implicating other mechanisms (which potentially involve other lipids identified in this study) for greater ISGU and Akt and AS160 phosphorylation with these interventions.

中文翻译：

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急性运动结合热量限制开始的寿命后期对老年大鼠骨骼肌中胰岛素信号，脂质和葡萄糖摄取的影响。

我们通过研究四组糖尿病患者，评估了无论是否进行急性运动，在生命后期开始的卡路里限制（CR：摄入60-65％的[AL]摄入量）对骨骼肌的胰岛素刺激的葡萄糖摄取（ISGU）的影响。 26个月大的大鼠：久坐的AL，久坐的CR（持续8周），运动后3小时（3hPEX）-AL和3hPEX-CR。在孤立的上睑肌中孵育±胰岛素来测定ISGU。评估肌肉的信号蛋白（免疫印迹）和脂质（质谱）。久坐的CR和3hPEX-AL的ISGU超过久坐的AL；3hPEX-CR超过所有其他组。用ISGU跟踪的Akt（Ser473，Thr308）和160 kDa的Akt底物（AS160; Ser588，Thr642，Ser704）磷酸化水平。在检测到的477种脂质中，有114种被CR改变（包括减少了25种酰基肉碱中的15种），运动后改变了27和27（包括减少22个溶血磷脂酰胆碱中的18个），而CR和运动之间只有6个脂质重叠。ISGU与23种脂质显着相关，包括：酰基肉碱20：1（r = .683），溶血磷脂酰乙醇胺19：0（r = -.662），酰基肉碱24：0（r = .611）和plasmenyl-磷脂酰乙醇胺37：5（ r = -.603）。CR和/或运动不会改变神经酰胺（以前与胰岛素抵抗相关的脂质类别）的肌肉水平，也不与ISGU显着相关，这暗示了更大ISGU和Akt和AS160的其他机制（可能涉及本研究中确定的其他脂质）这些干预的磷酸化。ISGU与23种脂质显着相关，包括：酰基肉碱20：1（r = .683），溶血磷脂酰乙醇胺19：0（r = -.662），酰基肉碱24：0（r = .611）和plasmenyl-磷脂酰乙醇胺37：5（ r = -.603）。CR和/或运动不会改变神经酰胺（以前与胰岛素抵抗相关的脂质类别）的肌肉水平，也不与ISGU显着相关，这暗示了更大ISGU和Akt和AS160的其他机制（可能涉及本研究中确定的其他脂质）这些干预的磷酸化。ISGU与23种脂质显着相关，包括：酰基肉碱20：1（r = .683），溶血磷脂酰乙醇胺19：0（r = -.662），酰基肉碱24：0（r = .611）和plasmenyl-磷脂酰乙醇胺37：5（ r = -.603）。CR和/或运动不会改变神经酰胺（以前与胰岛素抵抗相关的脂质类别）的肌肉水平，也不与ISGU显着相关，这暗示了更大ISGU和Akt和AS160的其他机制（可能涉及本研究中确定的其他脂质）这些干预的磷酸化。