Parenteral and enteral metabolism of anaplerotic triheptanoin in normal rats. II. Effects on lipolysis, glucose production, and liver acyl-CoA profile
Parenteral and enteral metabolism of anaplerotic triheptanoin in normal rats. II. Effects on lipolysis, glucose production, and liver acyl-CoA profile
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DOI：
10.1152/ajpendo.00384.2009
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发表时间：
2010-02-01
影响因子：
5.1
通讯作者：
Brunengraber, Henri
中科院分区：
文献类型：
--
作者：
Gu, Lei;Zhang, Guo-Fang;Brunengraber, Henri
顾丽，张国荣，Kombu RS, Allen F, Kutz G, Brewer WU, Roe CR, Brunengraber H.正常大鼠肠外和肠内三庚酸代谢的研究。2。对脂肪分解、葡萄糖生成和肝脏酰基辅酶a谱的影响。[J] .中国生物医学工程学报，2016,31(2):369 - 371。首次发表于2009年11月10日；doi: 10.1152 / ajpendo.00384.2009。-异中链甘油三酯三heptanoin在临床试验中用于长链脂肪酸氧化障碍患者的慢性饮食治疗。我们之前的研究表明（Kinman RP, Kasumov T, Jobbins KA, Thomas KR, Adams JE, Brunengraber LN, Kutz G, Brewer WU, Roe CR, Brunengraber H. Am J Physiol Endocrinol Metab 291: e86 - e866, 2006）静脉输注三庚烷酸会增加由甘油转化引起的脂肪分解。在这项研究中，我们测试了三庚酸输注诱导的脂肪分解是否伴随着潜在有害的长链脂肪酸的释放。给大鼠注射庚酸+/-甘油或三庚酸。静脉输注热量需要量40%的三庚酸显著增加甘油内源性R-a，但不增加油酸内源性R-a。因此，脂肪分解的激活在相同的细胞中被脂肪酸再酯化所平衡。肝脏酰基辅酶a谱显示庚酸β -氧化和c -5生酮的中间产物积累，游离辅酶a减少，但没有证据表明肝脏代谢紊乱，如丙酰超载。我们的数据表明，静脉或十二指肠内给药三庚酸可用于代谢失代偿的长链脂肪酸氧化障碍的重症监护和营养支持。
Gu L, Zhang GF, Kombu RS, Allen F, Kutz G, Brewer WU, Roe CR, Brunengraber H. Parenteral and enteral metabolism of anaplerotic triheptanoin in normal rats. II. Effects on lipolysis, glucose production, and liver acyl-CoA profile. Am J Physiol Endocrinol Metab 298: E362-E371, 2010. First published November 10, 2009; doi:10.1152/ajpendo.00384.2009.-The anaplerotic odd-medium-chain triglyceride triheptanoin is used in clinical trials for the chronic dietary treatment of patients with long-chain fatty acid oxidation disorders. We previously showed (Kinman RP, Kasumov T, Jobbins KA, Thomas KR, Adams JE, Brunengraber LN, Kutz G, Brewer WU, Roe CR, Brunengraber H. Am J Physiol Endocrinol Metab 291: E860-E866, 2006) that the intravenous infusion of triheptanoin increases lipolysis traced by the turnover of glycerol. In this study, we tested whether lipolysis induced by triheptanoin infusion is accompanied by the potentially harmful release of long-chain fatty acids. Rats were infused with heptanoate +/- glycerol or triheptanoin. Intravenous infusion of triheptanoin at 40% of caloric requirement markedly increased glycerol endogenous R-a but not oleate endogenous R-a. Thus, the activation of lipolysis was balanced by fatty acid reesterification in the same cells. The liver acyl-CoA profile showed the accumulation of intermediates of heptanoate beta-oxidation and C-5-ketogenesis and a decrease in free CoA but no evidence of metabolic perturbation of liver metabolism such as propionyl overload. Our data suggest that triheptanoin, administered either intravenously or intraduodenally, could be used for intensive care and nutritional support of metabolically decompensated long-chain fatty acid oxidation disorders.