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一种新型植物配方通过改善胰岛素抵抗来预防糖尿病。

A novel botanical formula prevents diabetes by improving insulin resistance.

作者信息

Kan Juntao, Velliquette Rodney A, Grann Kerry, Burns Charlie R, Scholten Jeff, Tian Feng, Zhang Qi, Gui Min

机构信息

Nutrilite Health Institute, 720 Cailun Road, Shanghai, 201203, China.

Nutrilite Health Institute, 7575 East Fulton Avenue, Ada, MI, 49355, USA.

出版信息

BMC Complement Altern Med. 2017 Jul 5;17(1):352. doi: 10.1186/s12906-017-1848-3.

DOI:10.1186/s12906-017-1848-3
PMID:28679380
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5499036/
Abstract

BACKGROUND

Type 2 diabetes mellitus (T2DM) is a major risk factor for cardiovascular disease, and the prevalence has increased significantly in recent decades to epidemic proportions in China. Individually, fenugreek (Trigonella foenum graecum) seed, mulberry (Morus alba L.) leaf and American ginseng (Panax quinquefolius) root can improve glycemia in various animal models and humans with impaired glucose metabolism and T2DM. The aim of this study was to design an optimized botanical formula containing these herbal extracts as a nutritional strategy for the prevention of insulin resistance and T2DM.

METHODS

Cell-free α-amylase and α-glucosidase enzyme assays were used to determine inhibitory potential of extracts. Glucose uptake was examined in differentiated human adipocytes using radiolabeled 2-deoxyglucose. Male Sprague Dawley rats were divided and glycemia balanced into 5 groups: two controls (naïve and model) and three doses of the botanical test formula containing standardized fenugreek seed, mulberry leaf and American ginseng extracts (42.33, 84.66 and 169.33 mg/kg BW). Insulin resistance and T2DM was induced by feeding animals a high fat diet and with an alloxan injection. Glucose tolerance was examined by measuring serum glucose levels following an oral glucose load.

RESULTS

Fenugreek seed and mulberry leaf dose dependently inhibited α-amylase (IC50 = 73.2 μg/mL) and α-glucosidase (IC50 = 111.8 ng/mL), respectively. All three botanical extracts improved insulin sensitivity and glucose uptake in human adipocytes, which lead to the design of an optimized botanical test formula. In a rat model of insulin resistance and T2DM, the optimized botanical test formula improved fasting serum glucose levels, fasting insulin resistance and the development of impaired glucose tolerance. The reduction in epididymal adipose tissue GLUT4 and PDK1 expression induced by high fat diet and alloxan was blunted by the botanical test formula.

CONCLUSIONS

A novel botanical formula containing standardized extracts of mulberry leaf, fenugreek seed and American ginseng at a ratio of 1:1.3:3.4 prevented the development of insulin resistance, impaired glucose tolerance and T2DM. Given the rising need for effective non-drug targeting of insulin resistance and progression to T2DM, complementary and alternative nutritional strategies without intolerable side effects could have meaningful impact on metabolic health and diabetes risks.

摘要

背景

2型糖尿病(T2DM)是心血管疾病的主要危险因素,近几十年来其患病率在中国显著上升至流行程度。单独来看,胡芦巴(Trigonella foenum graecum)种子、桑叶(Morus alba L.)和西洋参(Panax quinquefolius)根可改善各种动物模型以及葡萄糖代谢受损和T2DM患者的血糖水平。本研究的目的是设计一种优化的植物配方,包含这些草药提取物,作为预防胰岛素抵抗和T2DM的营养策略。

方法

采用无细胞α -淀粉酶和α -葡萄糖苷酶活性测定法来确定提取物的抑制潜力。使用放射性标记的2 -脱氧葡萄糖检测分化的人脂肪细胞中的葡萄糖摄取。将雄性Sprague Dawley大鼠分组并使血糖平衡,分为5组:两个对照组(未处理组和模型组)和三个剂量的植物测试配方组,该配方包含标准化的胡芦巴种子、桑叶和西洋参提取物(42.33、84.66和169.33mg/kg体重)。通过给动物喂食高脂肪饮食并注射四氧嘧啶诱导胰岛素抵抗和T2DM。通过测量口服葡萄糖负荷后的血清葡萄糖水平来检测葡萄糖耐量。

结果

胡芦巴种子和桑叶分别剂量依赖性地抑制α -淀粉酶(IC50 = 73.2μg/mL)和α -葡萄糖苷酶(IC50 = 111.8ng/mL)。所有三种植物提取物均改善了人脂肪细胞中的胰岛素敏感性和葡萄糖摄取,这促成了一种优化的植物测试配方的设计。在胰岛素抵抗和T2DM大鼠模型中,优化的植物测试配方改善了空腹血清葡萄糖水平、空腹胰岛素抵抗以及葡萄糖耐量受损的情况。植物测试配方减弱了高脂肪饮食和四氧嘧啶诱导的附睾脂肪组织中GLUT4和PDK1表达的降低。

结论

一种新型植物配方,包含按1:1.3:3.4比例的标准化桑叶、胡芦巴种子和西洋参提取物,可预防胰岛素抵抗、葡萄糖耐量受损和T2DM的发展。鉴于对有效非药物靶向胰岛素抵抗及进展为T2DM的需求不断增加,无难以忍受副作用的补充和替代营养策略可能对代谢健康和糖尿病风险产生有意义的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1a1/5499036/e49141961fd0/12906_2017_1848_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1a1/5499036/b0273e1c0231/12906_2017_1848_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1a1/5499036/a6d51955a5d4/12906_2017_1848_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1a1/5499036/e49141961fd0/12906_2017_1848_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1a1/5499036/b0273e1c0231/12906_2017_1848_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1a1/5499036/3097ba08f44b/12906_2017_1848_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1a1/5499036/65a02d403868/12906_2017_1848_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1a1/5499036/badda2466508/12906_2017_1848_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1a1/5499036/a6d51955a5d4/12906_2017_1848_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1a1/5499036/e49141961fd0/12906_2017_1848_Fig6_HTML.jpg

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