Tuesday, May 04, 2010

鰻魚肌肉和肝臟基因表現之變化

鰻魚養殖與人工催熟過程中肌肉和肝臟代謝相關基因表現量之變化

證據指出鰻魚體脂肪累積到一定比率可能是促使鰻魚降海繁殖的因素。鰻魚攝取的能量經由肝臟轉換後以脂肪儲存在肌纖維之間的脂肪細胞,儲蓄的脂肪經由肝臟代謝後再運送至肌肉或卵巢提供禁食洄游與卵細胞發育之能量來源,為研究能量與生殖啟動或能量轉移之優良模式生物。挑選不同體型鰻魚(100~800克)進行調查,結果顯示隨著體重增加,在雌鰻的肝臟中aldolase b和h-FABP的表現量會上升,而PPARγ、RXR、EDF-1及NNT的表現量則有下降的趨勢;在肌肉組織中,PPARγ、RXR、EDF-1、PTEN、aldolase b、NNT、h-FABP和pyruvate carboxylase的表現量有下降的趨勢。若以卵巢發育的角度來看,卵巢GSI值越高的雌鰻,其肝臟中aldolase b和pyruvate carboxylase的表現量會隨GSI增加而上升;在肌肉組織中,隨著GSI增加,PPARγ和RXR的表現量有下降的趨勢。另外觀察體脂肪累積與脂肪代謝相關基因之表現的關聯,發現在雌鰻的肝臟中,隨著肌肉內的脂肪含量增加,PPARγ、RXR、EDF-1及NNT的表現量有下降的趨勢,而aldolase b和h-FABP的表現量則有上升的趨勢;在肌肉組織中,PPARγ、RXR、EDF-1、PTEN、aldolase b、NNT、h-FABP和pyruvate carboxylase的表現量有下降的趨勢。接著觀察人工催熟對脂肪代謝相關基因表現量之影響,以腦下垂體萃取物催熟雌鰻,發現隨著GSI增加,其肝臟中h-FABP的表現量有上升的趨勢,在肌肉組織中ACC b2的表現量則有明顯上升;施打腦下垂體萃取物加睪固酮的雌鰻,其肌肉組織內EDF-1和h-FABP的表現量相較於只施打腦下垂體萃取物的雌鰻有明顯下降,而ACC b2的表現量則有明顯上升。總合以上結果:推測體重較重以及脂肪含量較高的鰻魚,其肝臟和肌肉內的脂肪合成會減緩;隨著卵巢發育越好,肝臟中pyruvate carboxylase和h-FABP的表現量有上升的趨勢,肌肉中ACC b2的表現量則有明顯上升,肝臟中pyruvate carboxylase和h-FABP以及肌肉中的ACC b2和卵巢發育具較強之相關性。

關鍵字: 鰻魚、脂肪代謝、基因表現、成長、人工催熟

Science. 2001 Mar 30;291(5513):2613-6.

Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2.
Abu-Elheiga L, Matzuk MM, Abo-Hashema KA, Wakil SJ.

Abstract
Malonyl-coenzyme A (malonyl-CoA), generated by acetyl-CoA carboxylases ACC1 and ACC2, is a key metabolite in the regulation of energy homeostasis. Here, we show that Acc2-/- mutant mice have a normal life span, a higher fatty acid oxidation rate, and lower amounts of fat. In comparison to the wild type, Acc2-deficient mice had 10- and 30-fold lower levels of malonyl-CoA in heart and muscle, respectively. The fatty acid oxidation rate in the soleus muscle of the Acc2-/- mice was 30% higher than that of wild-type mice and was not affected by addition of insulin; however, addition of insulin to the wild-type muscle reduced fatty acid oxidation by 45%. The mutant mice accumulated 50% less fat in their adipose tissue than did wild-type mice. These results raise the possibility that pharmacological manipulation of ACC2 may lead to loss of body fat in the context of normal caloric intake.

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