Porcine leptin inhibits protein breakdown and stimulates fatty acid oxidation in C2C12 myotubes.
Porcine leptin inhibits protein breakdown and stimulates fatty acid oxidation in C2C12 myotubes.
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猪瘦素可抑制 C2C12 肌管中的蛋白质分解并刺激脂肪酸氧化。
DOI：
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发表时间：
2003
影响因子：
3.3
通讯作者：
T. Ramsay
中科院分区：
文献类型：
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作者：
T. Ramsay
本研究评估了瘦素治疗抑制空腹肌肉质量损失的潜在机制。在Dulbecco改良Eagle’s培养基/F12中加入5% （vol/vol）马血清，将C2C12成肌细胞分化为肌管。这些肌管在与重组猪瘦素（0 ~ 500 ng/mL）孵育后，用于评估3h -酪氨酸的掺入和释放。以3h -酪氨酸掺入量测定，肌管蛋白合成不受瘦素处理的影响（P < 0.05）。通过3h -酪氨酸释放来测量C2C12肌管中的蛋白质分解，瘦素处理抑制了蛋白质分解。0.5 ng/mL瘦素浓度足以抑制3.5%的3h -酪氨酸释放（P < 0.05）；50 ng/mL最大抑菌率为10.2% （P < 0.05）。地塞米松（1微米）最大限度地刺激蛋白质分解。50 ng/mL瘦素可使地塞米松诱导的3h -酪氨酸释放降低32% （P < 0.05）。对C2C12肌管中3h -酪氨酸释放的抑制表明瘦素通过抑制蛋白质分解在体外产生蛋白质节约作用。脂肪酸代谢也被研究，因为脂肪酸是肌肉在减少摄入期间的主要能量来源，正如瘦素治疗所发生的那样。急性（4小时）和慢性（24小时）暴露于猪瘦素（0至500 ng/mL）来评估14c -棕榈酸酯氧化。急性瘦素治疗对棕榈酸盐代谢无影响（P < 0.05）。慢性瘦素暴露导致棕榈酸酯氧化增加26% （P < 0.05）。慢性瘦素治疗对脂肪酸氧化的刺激表明，在瘦素引起的采食量减少期间，瘦素使肌肉中的其他能量来源免于氧化。
This study evaluated the potential mechanism(s) by which leptin treatment inhibits loss of muscle mass with fasting. Cultures of C2C12 myoblasts were differentiated into myotubes with 5% (vol/vol) horse serum in Dulbecco's modified Eagle's medium/F12. These myotubes were used to assess 3H-tyrosine incorporation and release following incubation with recombinant porcine leptin (0 to 500 ng/mL). Protein synthesis in myotubes, as measured by 3H-tyrosine incorporation, was not affected by leptin treatment (P > 0.05). Protein breakdown in C2C12 myotubes, as measured by 3H-tyrosine release, was inhibited by leptin treatment. A leptin concentration of 0.5 ng/mL was sufficient to inhibit 3H-tyrosine release by 3.5% (P < 0.05); 50 ng/mL produced a maximal inhibition of 10.2% (P < 0.05). Dexamethasone (1 microM) was used to maximally stimulate protein breakdown. Leptin (50 ng/mL leptin) decreased dexamethasone-induced 3H-tyrosine release by 32% (P < 0.05). The inhibition of 3H-tyrosine release in C2C12 myotubes suggests that leptin produces a protein-sparing effect in vitro by inhibiting protein breakdown. Fatty acid metabolism also was investigated because fatty acids are a major energy source for muscle during periods of reduced intake, as occurs with leptin treatment. Acute (4 h) and chronic (24 h) exposures to porcine leptin (0 to 500 ng/mL) were used to evaluate 14C-palmitate oxidation. Acute leptin treatment had no effect (P > 0.05) on palmitate metabolism. Chronic leptin exposure resulted in up to a 26% increase in palmitate oxidation (P < 0.05). The stimulation of fatty acid oxidation with chronic leptin treatment suggests that leptin spares other energy sources in muscle from oxidation during periods of a leptin-induced decrease in feed intake.
饮食肥胖大鼠饥饿期间体脂肪优先减少。
影响因子：
6.1
作者：
Hill,JO;DiGirolamo,M
通讯作者：
DiGirolamo,M