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最新研究顯示，碳水化合物限制飲食（CRD）在改善代謝綜合症（MetS）方面優於傳統低脂飲食（LFD）。CRD組在減少葡萄糖、胰島素水平、提高胰島素敏感性、減輕體重及降低心血管風險方面表現更佳。研究強調，調整飲食中碳水化合物的比例對於改善MetS和心血管風險具有重要意義。

碳水化合物限制對代謝綜合症的影響比低脂飲食更有利。

Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet

Jeff S Volek 1, Stephen D Phinney, Cassandra E Forsythe, Erin E Quann, Richard J Wood, Michael J Puglisi, William J Kraemer, Doug M Bibus, Maria Luz Fernandez, Richard D Feinman
Affiliations expand
PMID: 19082851 DOI: 10.1007/s11745-008-3274-2

https://pubmed.ncbi.nlm.nih.gov/19082851/

摘要

我們最近提出，由碳水化合物限制改善的生物標記恰好是定義代謝綜合症（MetS）的生物標記，而其中的共同主題是將胰島素作為控制元素進行調節。我們通過一項為期12週的研究，對40名具有動脈粥樣硬化脂質異常的受試者進行了測試，比較了兩種低熱量飲食（約1500千卡）：碳水化合物限制飲食（CRD）（%碳水化合物：脂肪：蛋白質 = 12:59:28）和低脂飲食（LFD）（56:24:20）。兩種干預均導致多個代謝標記的改善，但遵循CRD的受試者一致性地降低了葡萄糖（-12％）和胰島素（-50％）濃度，胰島素敏感性（-55％），體重減輕（-10％），脂肪含量降低（-14％），並且甘油三酸酯（TAG）（-51％），HDL-C（13％）和總膽固醇/HDL-C比值（-14％）的反應更有利。除了這些MetS的標誌外，CRD受試者對心血管風險的替代指標也呈現更有利的反應：餐後脂質血症（-47％），Apo B/Apo A-1比值（-16％）和LDL粒子分佈。儘管在CRD期間膳食飽和脂肪攝入量高出三倍，但TAG和膽固醇酯中的飽和脂肪酸顯著降低，與食用LFD的受試者相比，棕櫚油酸（16:1n-7）也降低，這是一種內源性脂肪生成標誌。與胰島素抵抗狀態有關的血清視黃醇結合蛋白4唯有CRD降低了該標誌（-20％）。這些發現支持將MetS的不同標誌統一起來，並支持其與膳食碳水化合物的密切聯繫的提議。結果支持使用膳食碳水化合物限制作為改善MetS和心血管風險特徵的有效方法。

Abstract

We recently proposed that the biological markers improved by carbohydrate restriction were precisely those that define the metabolic syndrome (MetS), and that the common thread was regulation of insulin as a control element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (approximately 1,500 kcal): a carbohydrate-restricted diet (CRD) (%carbohydrate:fat:protein = 12:59:28) and a low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced glucose (-12%) and insulin (-50%) concentrations, insulin sensitivity (-55%), weight loss (-10%), decreased adiposity (-14%), and more favorable triacylglycerol (TAG) (-51%), HDL-C (13%) and total cholesterol/HDL-C ratio (-14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk: postprandial lipemia (-47%), the Apo B/Apo A-1 ratio (-16%), and LDL particle distribution. Despite a threefold higher intake of dietary saturated fat during the CRD, saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum retinol binding protein 4 has been linked to insulin-resistant states, and only the CRD decreased this marker (-20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with dietary carbohydrate. The results support the use of dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk.