棕榈硬脂
餐后
酯交换脂肪
化学
棕榈酸
交叉研究
食品科学
棕榈仁
脂蛋白
胆固醇
内科学
脂肪酸
生物化学
医学
棕榈油
安慰剂
胰岛素
替代医学
脂肪酶
酶
病理
作者
Charlotte Mills,Scott Harding,Mariam Bapir,Giuseppina Mandalari,Louise J. Salt,Robert Gray,Barbara A. Fielding,Peter J. Wilde,Wendy L. Hall,Sarah Berry
摘要
Interesterified (IE) fats are widely used in place of trans fats; however, little is known about their metabolism. To test the impact of a commonly consumed IE compared with a non-IE equivalent fat on in vivo postprandial and in vitro lipid metabolism, compared with a reference oil [rapeseed oil (RO)]. A double-blinded, 3-phase crossover, randomized controlled trial was performed in healthy adults (n = 20) aged 45–75 y. Postprandial plasma triacylglycerol and lipoprotein responses (including stable isotope tracing) to a test meal (50 g fat) were evaluated over 8 h. The test fats were IE 80:20 palm stearin/palm kernel fat, an identical non-IE fat, and RO (control). In vitro, mechanisms of digestion were explored using a dynamic gastric model (DGM). Plasma triacylglycerol 8-h incremental area under the curves were lower following non-IE compared with RO [−1.7 mmol/L⋅h (95% CI: –3.3, –0.0)], but there were no differences between IE and RO or IE and non-IE. LDL particles were smaller following IE and non-IE compared with RO (P = 0.005). Extra extra large, extra large, and large VLDL particle concentrations were higher following IE and non-IE compared with RO at 6–8 h (P < 0.05). No differences in the appearance of [13C]palmitic acid in plasma triacylglycerol were observed between IE and non-IE fats. DGM revealed differences in phase separation of the IE and non-IE meals and delayed release of SFAs compared with RO. Interesterification did not modify fat digestion, postprandial lipemia, or lipid metabolism measured by stable isotope and DGM analysis. Despite the lower lipemia following the SFA-rich fats, increased proatherogenic large triacylglycerol-rich lipoprotein remnant and small LDL particles following the SFA-rich fats relative to RO adds a new postprandial dimension to the mechanistic evidence linking SFAs to cardiovascular disease risk.
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