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不同宏量营养素组成饮食引发的血管功能差异:一项现象学研究

Differential vascular dysfunction in response to diets of differing macronutrient composition: a phenomenonological study.

作者信息

Fatani Sameer, Pickavance Lucy C, Sadler Claire J, Harrold Joanne A, Cassidy Roslyn, Wilding John Ph, Naderali Ebrahim K

机构信息

School of Clinical Sciences, University of Liverpool, Liverpool, UK.

Department of Veterinary Preclinical Sciences, University of Liverpool, Liverpool, UK.

出版信息

Nutr Metab (Lond). 2007 Jun 14;4:15. doi: 10.1186/1743-7075-4-15.

DOI:10.1186/1743-7075-4-15
PMID:17570846
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1910600/
Abstract

BACKGROUND

Vascular dysfunction can develop from consumption of an energy-rich diet, even prior to the onset of obesity. However, the roles played by different dietary components remain uncertain. While attempting to develop models of obesity in a separate study, we observed that two high-energy diets of differing macronutrient compositions affected vascular function differently in overweight rats.

METHODS

Male Wistar rats (n = 6/group) were fed diets providing varying percentages of energy from fat and carbohydrate (CHO). For 10 weeks, they were fed either chow, as control diet (10% of energy from fat; 63% from CHO), chow supplemented with chocolate biscuit (30% fat; 56% CHO) or a high-fat diet (45% fat; 35% CHO). Blood concentrations of biochemical markers of obesity were measured, and epididymal fat pads weighed as a measure of adiposity. Mesenteric arteries were dissected and their contractile and relaxant properties analysed myographically. Data were tested by analysis of variance (ANOVA).

RESULTS

Weight gain and plasma concentrations of glucose, insulin and leptin were similar in all groups. However, biscuit-fed animals showed increased food intake (+27%; p < 0.01) and elevated concentrations of TGs and NEFAs (+41% and +17%; both p < 0.05). High-fat-fed animals showed an increase only in NEFAs (+38%; p < 0.01). Arterial vasoconstriction in response to NA and KCl increased only in biscuit-fed rats (both p < 0.01), while vasorelaxation in response to CCh and SNP, but not histamine, was attenuated in both groups (both p < 0.01). Furthermore, whereas the effect of the high-fat diet was most pronounced in endothelium-dependent vasorelaxation, the biscuit diet had the greater effect on endothelium-independent vasorelaxation.

CONCLUSION

Vascular dysfunction resulting from consumption of a high-fat or combined relatively high-fat/high-CHO diet occurs through different physiological processes, which may be attributable to their differing macronutrient compositions. Combining potentially atherogenic macronutrients induces more extensive vascular impairment than that of high-fat alone, and may be attributable to the more marked dyslipidaemia observed with such a diet. Thus, these findings help clarify the role of dietary components in vascular impairment, which has implications for clinical approaches to preventing cardiovascular disease.

摘要

背景

即使在肥胖症发作之前,食用富含能量的饮食也可能导致血管功能障碍。然而,不同饮食成分所起的作用仍不明确。在另一项试图建立肥胖模型的研究中,我们观察到两种宏量营养素组成不同的高能量饮食对超重大鼠的血管功能影响不同。

方法

将雄性Wistar大鼠(每组n = 6只)喂食从脂肪和碳水化合物(CHO)中提供不同能量百分比的饮食。持续10周,分别喂食普通饲料作为对照饮食(10%的能量来自脂肪;63%来自CHO)、添加巧克力饼干的普通饲料(30%脂肪;56% CHO)或高脂饮食(45%脂肪;35% CHO)。测量肥胖生化标志物的血液浓度,并称重附睾脂肪垫作为肥胖程度的指标。解剖肠系膜动脉,通过肌动描记法分析其收缩和舒张特性。数据通过方差分析(ANOVA)进行检验。

结果

所有组的体重增加以及血糖、胰岛素和瘦素的血浆浓度相似。然而,喂食饼干的动物食物摄入量增加(+27%;p < 0.01),甘油三酯(TGs)和非酯化脂肪酸(NEFAs)浓度升高(分别为+41%和+17%;均p < 0.05)。喂食高脂饮食的动物仅非酯化脂肪酸增加(+38%;p < 0.01)。仅在喂食饼干的大鼠中,对去甲肾上腺素(NA)和氯化钾(KCl)的动脉血管收缩增加(均p < 0.01),而在两组中,对乙酰胆碱(CCh)和硝普钠(SNP)的血管舒张反应(而非对组胺的反应)减弱(均p < 0.01)。此外,虽然高脂饮食的影响在内皮依赖性血管舒张中最为明显,但饼干饮食对非内皮依赖性血管舒张的影响更大。

结论

食用高脂或相对高脂/高碳水化合物组合饮食导致的血管功能障碍是通过不同的生理过程发生的,这可能归因于它们不同的宏量营养素组成。将潜在致动脉粥样硬化的宏量营养素组合在一起会比单独的高脂饮食诱导更广泛的血管损伤,这可能归因于这种饮食观察到的更明显的血脂异常。因此,这些发现有助于阐明饮食成分在血管损伤中的作用,这对预防心血管疾病的临床方法具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a0e/1910600/21874eb0795b/1743-7075-4-15-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a0e/1910600/1d2a9788b513/1743-7075-4-15-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a0e/1910600/21874eb0795b/1743-7075-4-15-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a0e/1910600/1d2a9788b513/1743-7075-4-15-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a0e/1910600/21874eb0795b/1743-7075-4-15-2.jpg

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