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Hayek(TD88137)西方飲食模型飼料介紹
Hayek Diet(TD88137)for Western Diet Model

一、Hayek模型飼料


請注意
西方飲食模型飼料是一個大的概念,只要是高脂、高糖、高膽固醇等其中某2項或三項都稱為西方飲食模型飼料。本頁介紹的TD88137雖然被命名為西方飲食模型飼料,但只是西方飲食模型飼料中的一種。

Hayek等早在90年代早期研究時進行人類脂蛋白轉基因鼠的研究,所設計的西方飲食模型飼料主要是脂肪21.2%,碳水化合物49.1%,蛋白質19.8%,膽固醇0.2%。這個模型飼料的特點是脂肪全部是奶油,雖然也是高膽固醇,但是膽固醇含量只有0.2%,不像Paigen飼料中用到1.25%,而且其中不添加膽鹽。所采用的這個模型飼料在Harlan(Teklad)公司生產,編號為TD88137。

很顯然,基于對這個模型飼料的最大貢獻,應該叫做Hayek模型飼料,但是,文獻中都叫做TD88137。

與ResearchDiets公司相比,Harlan公司的做法有些欠妥。ResearchDiet公司在與van Heek等研究者合作時誕生的45%高脂肥胖飼料(D12451),后來又在此基礎上制作的60%高脂肥胖飼料(D12492)都是以van Heek來稱呼的,叫做van Heek系列模型飼料,這顯然是肯定了van Heek的貢獻。然而,Harlan公司與Hayek等研究者合作的西方飲食模型飼料(TD88137),在介紹TD88137時只是說他們公司與某某某大學的研究者們合作,沒有具體說明哪些研究者。這也許是至今很少有論文中提及Haylek(甚至很多研究中沒有引用Haylek等的研究論文)的原因。

Hayek西方飲食模型飼料的用途、缺點
Hayek西方飲食模型飼料的用途:

廣泛應用于大小鼠肥胖模型高血脂模型高膽固醇血癥模型胰島素抵抗模型II型糖尿病模型代謝綜合癥模型非酒精性脂肪肝模型動脈粥樣硬化模型高同型半胱氨酸血癥模型,等等。請注意不同種系和品系的差異。

Hayek西方飲食模型飼料的缺點:

(1)營養素不合理,需要優化;

二、Hayek模型飼料的用途和缺點


Hayek模型飼料已經在大鼠和小鼠等不同動物中使用,廣泛應用于多種西方飲食疾病的研究,見右圖。

當今很多著名實驗動物飼料企業都生產Hayek模型飼料。除了Harlan(Teklad)公司生產的TD88137,其他公司的情況是:ResearchDiets是D12079B。

在國內,特洛菲飼料科技有限公司采取了優化(TP26301, TP26302)、不優化(TP26300)和重新設計(TP26302和TP26304)三種策略提供不同的高脂肥胖模型飼料供研究者選用,并且提供了各種匹配的對照飼料供研究者根據研究的具體情況選擇。

如果讀者準備使用Hayek飼料開展研究,請閱讀“Hayek(TD88137)西方飲食模型飼料存在的問題和糾正”。

 

References:

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[11] Cash JG, Kuhel DG, Basford JE, Jaeschke A, Chatterjee TK, Weintraub NL, Hui DY. Apolipoprotein E4 Impairs Macrophage Efferocytosis and Potentiates Apoptosis by Accelerating Endoplasmic Reticulum Stress. J Biol Chem. 2012 August 10; 287(33): 27876–27884.

[12] Szeto FL, Reardon CA, Yoon D, Wang Y, Wong KE, Chen Y, Kong J, Liu SQ, Thadhani R, Getz GS, Li YC. Vitamin D Receptor Signaling Inhibits Atherosclerosis in Mice. Mol Endocrinol. 2012 July; 26(7): 1091–1101.

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[14] Kraja AT, Lawson HA, Arnett DK, Borecki IB, Broeckel U, de las Fuentes L, Hunt SC, Province MA, Cheverud J, Rao DC. Obesity–insulin targeted genes in the 3p26-25 region in human studies and LG/J and SM/J mice. Metabolism. Metabolism. 2012 August; 61(8): 1129–1141.

[15] Rohwedder I, Montanez E, Beckmann K, Bengtsson E, Dunér P, Nilsson J, Soehnlein O, F?ssler R. Plasma fibronectin deficiency impedes atherosclerosis progression and fibrous cap formation. EMBO Mol Med. 2012 July; 4(7): 564–576.

[16] Lee J, Seok S, Yu P, Kim K, Smith Z, Rivas-Astroza M, Zhong S, Kemper JK. Genomic analysis of hepatic Farnesoid X Receptor (FXR) binding sites reveals altered binding in obesity and direct gene repression by FXR Hepatology. Hepatology. 2012 July; 56(1): 108–117.

[17] Ding L, Biswas S, Morton RE, Smith JD, Hay N, Byzova TV, Febbraio M, Podrez EA. Akt3 Deficiency in Macrophages Promotes Foam Cell Formation and Atherosclerosis in Mice.Cell Metab. 2012 June 6; 15(6): 861–872

[18] Navab M, Reddy ST, Anantharamaiah GM, Hough G, Buga GM, Danciger J, Fogelman AM. D-4F-mediated reduction in metabolites of arachidonic and linoleic acids in the small intestine is associated with decreased inflammation in low-density lipoprotein receptor-null mice. J Lipid Res. 2012 March; 53(3): 437–445.

[19] Zhang X, Thatcher SE, Rateri DL, Bruemmer D, Charnigo R, Daugherty A, Cassis LA. Transient Exposure of Neonatal Female Mice to Testosterone Abrogates the Sexual Dimorphism of Abdominal Aortic Aneurysms. Circ Res. 2012 May 25; 110(11): e73–e85

[20] Fox RG, Magness S, Kujoth GC, Prolla TA, Maeda N. Mitochondrial DNA polymerase editing mutation, PolgD257A, disturbs stem-progenitor cell cycling in the small intestine and restricts excess fat absorption. Am J Physiol Gastrointest Liver Physiol. 2012 May 1; 302(9): G914–G924

[21] Elias I, Franckhauser S, Ferré T, Vilà L, Tafuro S, Mu?oz S, Roca C, Ramos D, Pujol A, Riu E, Ruberte J, Bosch F. Adipose Tissue Overexpression of Vascular Endothelial Growth Factor Protects Against Diet-Induced Obesity and Insulin Resistance. Diabetes. 2012 July; 61(7): 1801–1813.

[22] Liang CP, Han S, Li G, Tabas I, Tall AR.Impaired MEK Signaling and SERCA Expression Promote ER Stress and Apoptosis in Insulin-Resistant Macrophages and Are Reversed by Exenatide Treatment. Diabetes. 2012 October; 61(10): 2609–2620.

[23] Thorp E, Iwawaki T, Miura M, Tabas I. A reporter for tracking the UPR in vivo reveals patterns of temporal and cellular stress during atherosclerotic progression. J Lipid Res. 2011 May; 52(5): 1033–1038.

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[25] Yoshino J, Mills KF, Yoon MJ, Imai S. Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metab. 2011 October 5; 14(4): 528–536.

[26] Rahaman SO, Swat W, Febbraio M, Silverstein RL. Vav Family Rho Guanine Nucleotide Exchange Factors Regulate CD36-mediated Macrophage Foam Cell Formation. J Biol Chem. 2011 March 4; 286(9): 7010–7017.

[27] Maher JJ. New Insights from Rodent Models of Fatty Liver Disease. Antioxid Redox Signal. 2011 July 15; 15(2): 535–550.

[28] Wan W, Lim JK, Lionakis MS, Rivollier A, McDermott DH, Kelsall BL, Farber JM, Murphy PM. Genetic Deletion of Chemokine Receptor Ccr6 Decreases Atherogenesis in ApoE-deficient Mice. Circ Res. 2011 August 5; 109(4): 374–381.

[29] Li J, Wang Q, Chai W, Chen MH, Liu Z, Shi W. Hyperglycemia in apolipoprotein E-deficient mouse strains with different atherosclerosis susceptibility. Cardiovasc Diabetol. 2011; 10: 117.

[30] Qiang L, Lin HV, Kim-Muller JY, Welch CL, Gu W, Accili D. Proatherogenic Abnormalities Of Lipid Metabolism In SirT1 Transgenic Mice Are Mediated Through Creb Deacetylation.Cell Metab. 2011 December 7; 14(6): 758–767

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[34] Paik J, Fierce Y, Mai PO, Phelps SR, McDonald T, Treuting P, Drivdahl R, Brabb T, LeBoeuf R, O'Brien KD, Maggio-Price L. Murine Norovirus Increases Atherosclerotic Lesion Size and Macrophages in Ldlr?/? Mice. Comp Med. 2011 August; 61(4): 330–338.



有困惑?那就商量唄!

高脂肥胖、代謝綜合癥、胰島素抵抗、高血脂(高甘油三酯血癥、高膽固醇血癥)、糖尿病、動脈粥樣硬化、非酒精性脂肪肝,等模型飼料

南通特洛菲飼料科技有限公司提供各種動物、各種類型的肥胖及其并發癥的模型飼料。以下介紹與TD88137相當或者優化、重新設計的西方飲食模型飼料。

---------《》-------

大鼠小鼠西方飲食模型飼料:

markerTP26300

與Harlan公司TD88137相當。為追求與原作者使用的TD88137的研究者設計。用于未成年。

markerTP26301

由于TD88137的必需脂肪酸過少, TP26301進行了優化,與ResearchDiets公司D12079B相當。用于未成年。

markerTP26302

TD88137的營養素不科學、不合理, TP26302進行了優化。用于未成年期。

markerTP26303

TP26303針對TD88137進行了全面優化,用于未成年期。

markerTP26304

由于TD88137不適合成年期喂養, TP26304在TD88137基礎上專為成年期設計。營養素符合成年期要求。

markerTP26305

TP26305專為成年期設計,避免必需脂肪酸過低,又營養素合理。

 詳細情況,請瀏覽Hayek西方飲食模型飼料(Hayek Western-type Diet)選擇指南




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