Saito Misato, Lessard S J, Rivas Donato A, Reeder Donald W, Hawley John A, Yaspelkis Ben B
Exercise Biochemistry Laboratory, Department of Kinesiology, California State University Northridge, CA 91330-8287, USA.
Metabolism. 2008 Sep;57(9):1173-80. doi: 10.1016/j.metabol.2008.03.023.
We determined whether sustained aerobic exercise reverses high-fat diet-induced impairments in the c-Cbl associated protein (CAP)/Casitas b-lineage lymphoma (c-Cbl) signaling cascade in rodent skeletal muscle. Sprague-Dawley rats were placed into either control (n = 16) or high-fat-fed (n = 32) diet groups for 4 weeks. During a subsequent 4-week experimental period, 16 high-fat-fed rats remained sedentary, 16 high-fat-fed rats completed 4 weeks of exercise training, and control animals were sedentary and remained on the control diet. After the intervention period, animals were subjected to hind limb perfusions in the presence (n = 8 per group) or absence (n = 8 per group) of insulin. In the plasma membrane fractions, neither high-fat feeding nor exercise training altered adaptor protein with PH and SH2 domains, (APS), c-Cbl, or TC10 protein concentrations. In contrast, CAP protein concentration and insulin-stimulated plasma membrane c-Cbl tyrosine phosphorylation were reduced by high-fat feeding; but exercise training reversed these impairments. Of note was that insulin-stimulated atypical protein kinase Czeta kinase activity toward TC10 was reduced by high-fat feeding but normalized by exercise training. We conclude that sustained (4 weeks) exercise training can reverse high-fat diet-induced impairments on the CAP/c-Cbl pathway in high-fat-fed rodent skeletal muscle. We also provide the first evidence that the CAP/c-Cbl insulin signaling cascade in skeletal muscle may directly interact with components of the classic (phosphoinositide 3-kinase dependent) insulin signaling cascade.
我们研究了持续有氧运动是否能逆转高脂饮食诱导的啮齿动物骨骼肌中与c-Cbl相关蛋白(CAP)/Casitas b系淋巴瘤(c-Cbl)信号级联的损伤。将Sprague-Dawley大鼠分为对照组(n = 16)或高脂饮食组(n = 32),持续4周。在随后的4周实验期内,16只高脂饮食大鼠保持 sedentary,16只高脂饮食大鼠完成4周的运动训练,而对照动物保持 sedentary 并维持对照饮食。干预期结束后,在有胰岛素(每组n = 8)或无胰岛素(每组n = 8)的情况下对动物进行后肢灌注。在质膜组分中,高脂喂养和运动训练均未改变含PH和SH2结构域的衔接蛋白(APS)、c-Cbl或TC10蛋白浓度。相比之下,高脂喂养降低了CAP蛋白浓度和胰岛素刺激的质膜c-Cbl酪氨酸磷酸化;但运动训练逆转了这些损伤。值得注意的是,高脂喂养降低了胰岛素刺激的非典型蛋白激酶Czeta激酶对TC10的活性,但运动训练使其恢复正常。我们得出结论,持续(4周)的运动训练可以逆转高脂饮食诱导的高脂喂养啮齿动物骨骼肌中CAP/c-Cbl途径的损伤。我们还提供了首个证据,即骨骼肌中的CAP/c-Cbl胰岛素信号级联可能直接与经典(磷酸肌醇3激酶依赖性)胰岛素信号级联的成分相互作用。