脂肪細胞素表現調控之探討：
1.富含三酸甘油酯脂蛋白對脂肪細胞ob基因表現之影響
2.LPS和H2O2對巨噬細胞和單核球細胞resistin mRNA表現之影響

張美鈴

doi:10.6342/NTU.2005.02148

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脂肪細胞素表現調控之探討： 1.富含三酸甘油酯脂蛋白對脂肪細胞ob基因表現之影響 2.LPS和H2O2對巨噬細胞和單核球細胞resistin mRNA表現之影響

Studies on the expression and regulation of adipokines： 1. Triacylglycerol-rich lipoproteins effects on ob gene expression in adipose cells. 2. LPS and H2O2 effects on resistin mRNA expression in macrophages and monocytes.

張美鈴 , Ph.D　　Advisor：呂紹俊　　

繁體中文 DOI： 10.6342/NTU.2005.02148

脂肪細胞素；脂肪細胞； ob 基因；瘦素；脂多醣；過氧化氫；胰島素阻抗素, 巨噬細胞, 單核球細胞； adipokines ； adipocyte ； TRL ； ob gene ； leptin ； LPS ； H2O2 ； resistin ； macrophage ； monocyte

Abstract │ Reference (409) │ Altmetrics

Abstract 〈TOP〉

肥胖引起之胰島素抗性是造成代謝性症候群的主要因子，而adipokines在胰島素抗性扮演重要的角色。Leptin具『抗肥胖荷爾蒙』的角色，參與能量恆定調節，本論文欲探討，攝取高油飲食，餐後之TRL（triacyglycerol-rich lipoproteins）是否影響ob基因表現。由於發炎反應和氧化壓力參與胰島素抗性發生，故探討發
炎誘發劑LPS和氧化壓力來源H2O2對具有抗胰島素特性之resistin的影響及其可能調節機制。
在TRL 對ob 基因影響的實驗中，因為長期攝取高油飲食易造成肥胖，攝食高油飲食後，血液中會出現高濃度的TG（triacylglycerol），TG 主要利用TRL運送至周邊組織，所以探討高油飲食後之TRL 是否影響ob 基因表現。雄性Wistar大鼠經過禁食48 小時後，分別給予高油飼料或無油高醣飼料，復食30 分鐘移走
飼料，分別在復食後第2、4 和8 小時犧牲。結果，高油組大鼠的血漿TG 濃度顯著較高（p < 0.05），血漿中leptin 濃度和脂肪組織之ob mRNA 表現顯著低於無油高醣組（p < 0.05）；兩組之血漿葡萄糖和胰島素濃度沒有顯著差異。高油組血漿TRL 濃度顯著高於無油高醣組，推測TRL 可能參與調節ob mRNA 表現。收集大鼠管餵5mL 大豆油3 小時後之血漿TRL，處理已分化之3T3-L1 脂肪細胞，結果顯示，TRL 顯著抑制3T3-L1 脂肪細胞之ob mRNA 表現，呈現劑量和時間效應，並且可抑制胰島素所提高之ob mRNA 表現。從結果得知，高油飲食餐後有較低ob mRNA 表現和血漿leptin 濃度，可能是因為TRL 抑制ob 基因表現所致。
在囓齒科動物，resistin主要在脂肪組織表現，且參與胰島素抗性之作用。人類resistin mRNA在單核球細胞表現最高，推測resistin在發炎反應和氧化壓力引起之胰島素抗拒扮演重要的角色。於是利用LPS誘發發炎反應，以及H2O2當氧化壓力來源，探討單核球細胞和巨噬細胞在模擬生物體之發炎反應和氧化壓力環境下，其resistin mRNA表現之變化，並探討其可能之調節機制。在LPS引起發炎反
應之實驗，LPS顯著提高RAW264.7 巨噬細胞和小鼠肝臟巨噬細胞resistin mRNA表現。抗發炎試劑dexametasone、genistein和PPARγ 之agonists（ciglitazone、pioglitazone和15d-PGJ2），顯著地抑制經由LPS刺激提高resistin mRNA的作用。從actinomycin D降低LPS刺激所提高之resistin RNA表現量，可知LPS在轉錄層次調控resistin RNA表現。PI3K、ERK1/2 和NF-κB之各別抑制劑Ly293002（25 nM）、U0126（2.5 μM）和CAPE（10 μg/mL）阻斷LPS對resistin mRNA的活化，且免疫螢光染色分析可見NF-κB之p50 subunit大量轉位至細胞核。綜合以上結果，PI3K、ERK和NF-κB參與LPS對巨噬細胞之resistin mRNA的活化作用。
當以H2O2處理，THP-1 和人類PBMC（peripheral blood mononuclear cells）resistin mRNA的表現量明顯增加。由actinomycin D抑制H2O2對resistin mRNA的活化，可知H2O2經由轉錄層次驅動resistin mRNA表現。在THP-1 細胞，NF-κB之抑制劑CAPE（10 μg/mL）顯著地降低H2O2所增加之resistin mRNA含量，且p50 subunit因H2O2處理而大量轉位至細胞核，得知NF-κB參與H2O2以促進resistin mRNA表現。此外，H2O2並不影響TNF-α之表現，因此H2O2提高resistin mRNA表現之機制，有別於LPS的活化作用。

Parallel Abstract 〈TOP〉

Obesity is the most common cause of metabolic syndrome. Adipocytes produce a variety of biologically active molecules, collectively known as adipokines,including leptin, resistin, TNF-α and adiponectin. These adipokines participates in the metablic syndrome. Leptin acts as an satiety factor and anti-obesity hormone, to control appetite and energy expenditure. The present studies, examine the possible role of triacylglycerol-rich lipoproteins in the down-regulation of adipose obese gene
expression in rats re-fed a high-fat diet. Because inflammation and oxidative stress are also believed to be implicated in the pathophysiology of insulin resistance in
metabolic diseases, the effect of LPS and H2O2 on resistin mRNA expression was studied in monocytes and macrophages.
The large amount of absorbed dietary lipid after feeding a high-fat diet is mainly transported as triacylglycerol (TG)-rich lipoproteins (TRL) in the post-prandial blood
and is subsequently distributed to peripheral tissues including adipose and muscle tissues. An in vivo and an in vitro study were conducted to investigate the possible
role of post-prandial TRL after high fat feeding in the regulation of obese (ob) gene expression. Adult male Wistar rats were fasted for 48 h and re-fed with either a
fat-free/high-carbohydrate diet or a high-fat diet for 2, 4, or 8 h. Rats re-fed the high-fat diet had significantly higher plasma TG (p < 0.05) and lower plasma leptin
and adipose ob mRNA (p < 0.05) than those fed the fat-free/high-carbohydrate diet; however, plasma glucose and insulin concentrations were not significantly different
between the two groups. Plasma lipid analysis found large amount of TRL in rats fed with the high-fat diet; however, only very small amount of the TRL was found in
rats fed with the fat-free/high-carbohydrate diet. We speculated that TRL might be involved in regulation of ob gene expression. To further examine the after of TRL on ob mRNA expression, differentiated 3T3-L1 adipocytes were treated with TRL collected from rats fed 5 mL soybean oil by gastric intubations. TRL down-regulated ob mRNA not only in a dose and time dependent manner but also in
the presence of insulin in 3T3-L1 adipocytes. These results suggest a possible role of TRL in the down-regulation of adipose ob mRNA expression and may account, at least in part, for the previous observations that short-term high fat feeding resulted in lower plasma leptin.
Adipocyte-derived resistin is a circulating protein implicated in insulin resistance in rodents, but the role of human resistin is uncertain. In human, resistin
is mainly expressed in monocytes, it may be involved in insulin resistance which induced by inflammation and oxidative stress. Therefore the effect of LPS and H2O2
on resistin mRNA expression was examined in monocytes and macrophages. 
LPS led to a significant increase of resistin mRNA in a dose and time dependent manner in RAW264.7 cells and Kuffer’s cells. Induction of resistin mRNA was attenuated by anti-inflammatory reagents, such as dexametasone, genistein and PPARγ agonists (ciglitazone, pioglitazone and 15d-PGJ2), which suggest that resistin is involved in inflammation process. Actinomycin D inhibit the resistin mRNA activation by LPS, indicated that the LPS increased resistin mRNA through the transcriptional activation. LPS-induced increase of resistin mRNA was blocked by U0126 (2.5 μM) and Ly294002 (25 nM). These results suggest that the MEK and PI3K are involved in the LPS-induced increase of resistin mRNA. NF-κB translocation inhibitor, CAPE (10 μg/mL), inhibited translocation of NF-κB to nucleus and blocked LPS-induced increase of resistin mRNA. These results suggest that NF-κB activation is necessary for resistin induction by LPS.
Resistin mRNA expression was induced by H2O2 treatment in THP-1 cells and human’s PBMC. Induction of resistin was also attenuated by transcriptional inhibitor drugs, actinomycin D. Treatment of the cells with NF-κB inhibitor, CAPE (10 μg/mL), prevented increase of resistin mRNA upon H2O2 treatment. The p50 subunit was translocated to nucleus after H2O2 administration. These results suggest
that the NF-κB is involved in the H2O2-induced increase of resistin mRNA expression. TNF-α is not involved in H2O2 induction of resistin mRNA, but involved in LPS induction process.

Reference ( 409 ) 〈TOP〉

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