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肥胖兔子肌肉甘油三酯而非磷脂的合成速率增加。

The synthetic rate of muscle triglyceride but not phospholipid is increased in obese rabbits.

作者信息

Zhang Xiao-jun, Chinkes David L, Wu Zhanpin, Herndon David N, Wolfe Robert R

机构信息

Metabolism Unit, Shriners Hospital for Children, Galveston, TX 77550, USA.

出版信息

Metabolism. 2009 Nov;58(11):1649-56. doi: 10.1016/j.metabol.2009.05.021. Epub 2009 Jul 15.

DOI:10.1016/j.metabol.2009.05.021
PMID:19608209
Abstract

Fat is a major energy source for skeletal muscle, and disruption of normal trafficking of fatty acids in muscle is linked to insulin resistance. We quantified muscle triglyceride (TG) and phospholipid (PL) synthesis in lean and obese rabbits by means of l-[U-(13)C(16)]palmitate infusion. Intramyocellular palmitoyl-coenzyme A was used as the precursor for rates of TG and PL synthesis, which were compared with the rates calculated using plasma nonesterified palmitate as the precursor. The muscle of obese rabbits had a greater (P < .05) combined pool of fatty acyl-coenzyme A plus fatty acyl-carnitine than lean rabbits (40.9 +/- 3.7 vs 28.6 +/- 5.3 nmol/g). Although the fractional synthetic rates of muscle TG were almost identical (0.095%/h +/- 0.016%/h vs 0.092%/h +/- 0.019%/h), the absolute synthetic rates were greater (P < .01) in the obese than in lean rabbits (39.7 +/- 9.5 vs 10.1 +/- 2.5 nmol g(-1) h(-1)) because of greater TG content in the muscle of obese rabbits. Plasma nonesterified fatty acids and TG accounted for 51% to 55% of the true precursor pool for muscle lipid synthesis in both groups, and the rest was derived from fatty acids recycled within the muscle. In contrast, the fractional and absolute synthetic rates of muscle PL as well as PL contents were comparable in the 2 groups. In conclusion, the content and synthetic rate of muscle TG rather than PL were increased in obese rabbits, which might be linked to insulin resistance. Plasma lipids and muscle lipolysis were the 2 predominate contributors to the intramyocellular fatty acyl-coenzyme A pool for lipid synthesis.

摘要

脂肪是骨骼肌的主要能量来源,肌肉中脂肪酸正常转运的破坏与胰岛素抵抗有关。我们通过输注l-[U-(13)C(16)]棕榈酸酯来定量瘦兔和肥胖兔肌肉甘油三酯(TG)和磷脂(PL)的合成。细胞内棕榈酰辅酶A用作TG和PL合成速率的前体,并与使用血浆非酯化棕榈酸作为前体计算的速率进行比较。肥胖兔的肌肉中脂肪酰辅酶A加脂肪酰肉碱的合并池比瘦兔更大(P < 0.05)(40.9 +/- 3.7对28.6 +/- 5.3 nmol/g)。尽管肌肉TG的分数合成速率几乎相同(0.095%/小时 +/- 0.016%/小时对0.092%/小时 +/- 0.019%/小时),但由于肥胖兔肌肉中TG含量更高,其绝对合成速率在肥胖兔中比瘦兔更大(P < 0.01)(39.7 +/- 9.5对10.1 +/- 2.5 nmol g(-1) h(-1))。两组中血浆非酯化脂肪酸和TG占肌肉脂质合成真正前体池的51%至55%,其余来自肌肉内循环的脂肪酸。相比之下,两组中肌肉PL的分数和绝对合成速率以及PL含量相当。总之,肥胖兔肌肉TG的含量和合成速率而非PL增加,这可能与胰岛素抵抗有关。血浆脂质和肌肉脂解是细胞内脂肪酰辅酶A脂质合成池的两个主要贡献者。

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