| 摘要: | 本研究之目的爲探討肥胖者減重對發炎指標、細胞激素和血液脂肪酸之影
響，進一步再探討血液脂肪酸與發炎指標/細胞激素之相關性。本研究對象
分為肥胖組和非肥胖對照組，肥胖組23 位，接受為期2~3 個月的減重計畫
之介入，非肥胖者20 位做為正常對照組。結果顯示，肥胖組平均減重6%
(p<0.001)，且減重後收縮壓(p<0.001)、舒張壓(p<0.001)、麩氨基酸草醋酸
轉氨基酶(p=0.014)、麩氨基酸焦葡萄轉氨基酶(p=0.023)、總膽固醇(p<0.001)
和homeostasis model assessment of insulin resistance (HOMA-IR) (p=0.049)皆
有顯著下降。在發炎指標及細胞激素部份，減重後瘦體素下降23%
（p<0.001）、胃餓素增加10%（p=0.023），而C-反應蛋白質、腫瘤壞死因
子-α 和間白素-6 未有顯著差異。在血液脂肪酸部分，減重後紅血球之總飽
和脂肪酸下降3% (p=0.015)，總單元不飽和脂肪酸下降5% (p=0.033)，另一
方面，總n-6 多元不飽和脂肪酸增加4% (p=0.012)、C20:4 n-6 增加10%
(p=0.006)、C22:4 n-6 增加7% (p=0.018)、C22:5 n-6 增加15% (p=0.011)，C22:5
n-3 增加11% (p=0.037)，總n-3 多元不飽和脂肪酸及C22:6 n-3 分別增加
13%、14%，但呈現邊緣性的相關（p<0.1）。減重後血漿總n-3 多元不飽和
脂肪酸增加12%呈現邊緣性相關（p<0.1）。肥胖組減重前以及非肥胖對照
組經年齡校正後，瘦體素與HOMA-IR 呈現正相關（β=0.160，p=0.003），
胃餓素與HOMA-IR 呈現負相關（β=-0.004，p=0.016），紅血球總飽和脂肪酸與胃餓素呈負相關（β=-48.960，p=0.027），C20:4 n-6（β=51.234，p=0.041）、
總n-3 多元不飽和脂肪酸（β=45.818，p=0.043）、C22:5 n-3（β=298.282，
p=0.007）與胃餓素呈現正相關。血漿中總n-6 多元不飽和脂肪酸（β=26.514，
p=0.008）、C18:2 n-6（β=23.942，p=0.045）與胃餓素呈現正相關。總飽和
脂肪酸與C-反應蛋白呈現正相關（β=0.204，p=0.000），總n-6 多元不飽和
脂肪酸（β=-0.272，p=0.002）、C18:2 n-6（β=-0.370，p=0.000）與C-反應蛋
白呈現負相關。肥胖組之體重減輕，顯著改善血壓、麩氨基酸草醋酸轉氨
基酶、麩氨基酸焦葡萄轉氨基酶、膽固醇和HOMA-IR，瘦體素與HOMA-IR
呈現正相關，胃餓素與HOMA-IR 呈現負相關。此外，體重減輕也顯著降低
瘦體素以及提高胃餓素之濃度，也顯著改善n-6 多元不飽和脂肪酸及n-3 多
元不飽和脂肪酸濃度，多元不飽和脂肪酸或許對於瘦體素和胃餓素的改變
具有調節之作用。
This study was aimed to examine and effects of weight loss on changes of blood
fatty acid and clinical/inflammatory proxies in obese subjects. The intervention
group constituted twenty-three obese adults receiving nutrition-counseling-based
weight-loss programs by registered dietitians for 2-3 month and twenty lean
adults server as the control group. Obese group after weight loss with a
significant reduction systolic blood pressure (p<0.001), diastolic blood pressure
(p<0.001), glutamate oxaloacetate transaminase (p=0.014), glutamate pyruvate
transaminase (p=0.023), total cholesterol (p<0.001), and homeostasis model
assessment of insulin resistance (p=0.049). Fasting blood fatty acids and plasma
leptin/ ghrelin were measured before and after weight loss, and were then
compared with those obtained from the control lean subjects. After weight loss,
leptin was significantly reduced by 23% (p<0.001) and ghrelin was increased by
10% (p=0.023). Effects of weight loss were accompanied by decreases in
erythrocyte total saturates by 3% (p=0.015) and total monounsaturates by 5%
(p=0.033). On the other hand, concentrations of erythrocyte total n-6
polyunsaturates, C20:4 n-6, C22:4 n-6 and C22:5 n-6 were increased by 4%
(p=0.012), 10% (p=0.006), 7% (p=0.018) and 15% (p=0.011) as well as C22:5
n-3 by 11% (p=0.037), respectively. Erythrocyte total n-3 polyunsaturates and C22:6 n-3 were also significantly increased after weight loss, but only reached
marginally significance (p<0.1). Plasma total n-3 polyunsaturates and C22:5 n-3
were also increased after weight loss, but only reached marginally significance
(p<0.1). Combining data from obese subjects before weight loss and the lean
control after adjusting for confounding factors, leptin (β=0.160, p=0.003) were
positively, and ghrelin (β=-0.004, p=0.016) were negatively correlated with
homeostasis model assessment of insulin resistance, erythrocyte total saturates
were negatively (β=-48.960, p=0.027), and C20:4 n-6(β=51.234, p=0.041), total
n-3 polyunsaturates (β=45.818, p=0.043) and C22:5 n-3 (β=298.28, p=0.007)
were positively correlated with ghrelin. Marginal and negative associations with
ghrelin were also detected in total n-6 polyunsaturates, C20:5 n-3 and C22:6 n-3
(p<0.16). Plasma total n-6 polyunsaturates (β=26.514, p=0.008) and C18:2 n-6
(β=23.942, p=0.045) were positively correlated with ghrelin. However, different
classes of fatty acids did not appear to associate with leptin levels. In conclusion,
weight loss reduced leptin and elevated ghrelin levels, and ameliorated n-6 and
n-3 polyunsaturates status. Polyunsaturates may play roles in modulating of
leptin and ghrelin changes. |
