一箭三雕!吃“全谷物”改变代谢、肠道微生物和免疫反应
2017/02/10
日前,塔夫茨大学的科学家们发表在同一杂志上的两项研究成果分别证实,吃全谷物能够增加卡路里消耗,同时还能够轻微改善肠道微生物群和免疫反应。


2月8日,在线发表于The American Journal of Clinical Nutrition杂志上题为“Substituting whole grains for refined grains in a 6-wk randomized trial favorably affects energy-balance metrics in healthy men and postmenopausal women”的一项研究表明,在饮食中用全谷物(whole grains)替代细粮(refined grains)通过在消化过程中降低卡路里的保留以及加速新陈代谢增加了热量损失。

先前,很多流行病学研究提出了摄入全谷物和高膳食纤维的健康益处,包括血糖控制等。然而,全谷物和纤维对体重管理是否是有益的一直存在争议。这项新研究可能会帮助解释为什么摄入全谷物对体重管理是有益的。

吃全谷物增加卡路里消耗

具体来说,研究小组进行了一项为期8周的随机单盲比较研究,参与者是81名年龄在40岁到65岁之间的男性和女性。研究的前两周,所有的参与者吃相同类型的食物。2周后,参与者被随机分配到吃全谷物或吃细粮的小组。研究期间,科学家们测量了参与者的体重、代谢率、血糖、粪便卡路里、饥饿和饱腹感。

结果发现,与吃细粮的人相比,吃全谷物的人由于静息代谢率增加,且粪便能量损失更大,每天额外消耗近100卡路里。该研究的通讯作者Susan B. Roberts博士说:“吃全谷物的人额外消耗的卡路里相当于快步走30分钟产生的作用。”

吃全谷物改善肠道微生物群和免疫反应

同日,一项相关的结果以“Substituting whole grains for refined grains in a 6-wk randomized trial has a modest effect on gut microbiota and immune and inflammatory markers of healthy adults”为题发表在同一杂志上。研究结果显示,吃全谷物能够适度改善健康的肠道微生物群以及某些免疫反应。

先前,科学家们推测,全谷物饮食是通过减少炎症降低心脏病、2型糖尿病和某些癌症的风险。在这一研究中,研究小组分析了富含全谷物的饮食对免疫反应、炎症反应、肠道微生物群以及排便频率的影响。

肠道微生物群和短链脂肪酸被认为是健康的免疫和炎症功能的重要贡献者。为了弄清楚全谷物饮食如何影响肠道微生物群,研究小组检测了粪便中细菌的组成和短链脂肪酸的浓度。结果发现,吃全谷物的参与者粪便中产生短链脂肪酸的毛螺菌属(Lachnospira)增加了,而促炎细菌Enterbacteriaceae减少了。

此外,研究中,血液样本分析揭示了不同饮食的参与者在记忆T细胞水平和TNF-α产生上的差异。具体来说,吃全谷物导致了记忆T细胞水平增加,而吃细粮导致了TNF-α产生的降低。其它炎性细胞因子水平未发生变化。不过,研究人员强调,这些差异并不大。

参考资料:

New study finds that eating whole grains increases metabolism and calorie loss

Eating whole grains led to modest improvements in gut microbiota and immune response

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  • Substituting whole grains for refined grains in a 6-wk randomized trial favorably affects energy-balance metrics in healthy men and postmenopausal women

    Background: The effect of whole grains on the regulation of energy balance remains controversial. Objective: We aimed to determine the effects of substituting whole grains for refined grains, independent of body weight changes, on energy-metabolism metrics and glycemic control. Design: The study was a randomized, controlled, parallel-arm controlled-feeding trial that was conducted in 81 men and postmenopausal women [49 men and 32 women; age range: 40–65 y; body mass index (in kg/m2): <35.0]. After a 2-wk run-in period, participants were randomly assigned to consume 1 of 2 weight-maintenance diets for 6 wk. Diets differed in whole-grain and fiber contents [mean ± SDs: whole grain–rich diet: 207 ± 39 g whole grains plus 40 ± 5 g dietary fiber/d; refined grain–based diet: 0 g whole grains plus 21 ± 3 g dietary fiber/d] but were otherwise similar. Energy metabolism and body-composition metrics, appetite, markers of glycemic control, and gut microbiota were measured at 2 and 8 wk. Results: By design, body weight was maintained in both groups. Plasma alkylresorcinols, which are biomarkers of whole-grain intake, increased in the whole grain–rich diet group (WG) but not in the refined grain–based diet group (RG) (P-diet-by-time interaction < 0.0001). Beta ± SE changes (ΔWG compared with ΔRG) in the resting metabolic rate (RMR) (43 ± 25 kcal/d; P = 0.04), stool weight (76 ± 12 g/d; P < 0.0001), and stool energy content (57 ± 17 kcal/d; P = 0.003), but not in stool energy density, were higher in the WG. When combined, the favorable energetic effects in the WG translated into a 92-kcal/d (95% CI: 28, 156-kcal/d) higher net daily energy loss compared with that of the RG (P = 0.005). Prospective consumption (P = 0.07) and glycemia after an oral-glucose-tolerance test (P = 0.10) trended toward being lower in the WG than in the RG. When nonadherent participants were excluded, between-group differences in stool energy content and glucose tolerance increased, and between-group differences in the RMR and prospective consumption were not statistically significant. Conclusion: These findings suggest positive effects of whole grains on the RMR and stool energy excretion that favorably influence energy balance and may help explain epidemiologic associations between whole-grain consumption and reduced body weight and adiposity. This trial was registered at clinicaltrials.gov as NCT01902394.

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  • Substituting whole grains for refined grains in a 6-wk randomized trial has a modest effect on gut microbiota and immune and inflammatory markers of healthy adults

    Background: Observational studies suggest an inverse association between whole-grain (WG) consumption and inflammation. However, evidence from interventional studies is limited, and few studies have included measurements of cell-mediated immunity. Objective: We assessed the effects of diets rich in WGs compared with refined grains (RGs) on immune and inflammatory responses, gut microbiota, and microbial products in healthy adults while maintaining subject body weights. Design: After a 2-wk provided-food run-in period of consuming a Western-style diet, 49 men and 32 postmenopausal women [age range: 40–65 y, body mass index (in kg/m2) <35] were assigned to consume 1 of 2 provided-food weight-maintenance diets for 6 wk. Results: Compared with the RG group, the WG group had increased plasma total alkyresorcinols (a measure of WG intake) (P < 0.0001), stool weight (P < 0.0001), stool frequency (P = 0.02), and short-chain fatty acid (SCFA) producer Lachnospira [false-discovery rate (FDR)-corrected P = 0.25] but decreased pro-inflammatory Enterobacteriaceae (FDR-corrected P = 0.25). Changes in stool acetate (P = 0.02) and total SCFAs (P = 0.05) were higher in the WG group than in the RG group. A positive association was shown between Lachnospira and acetate (FDR-corrected P = 0.002) or butyrate (FDR-corrected P = 0.005). We also showed that there was a higher percentage of terminal effector memory T cells (P = 0.03) and LPS-stimulated ex vivo production of tumor necrosis factor-α (P = 0.04) in the WG group than in the RG group, which were positively associated with plasma alkylresorcinol concentrations. Conclusion: The short-term consumption of WGs in a weight-maintenance diet increases stool weight and frequency and has modest positive effects on gut microbiota, SCFAs, effector memory T cells, and the acute innate immune response and no effect on other markers of cell-mediated immunity or systemic and gut inflammation. This trial was registered at clinicaltrials.gov as NCT01902394.

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