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Surwit模型饲料介绍
Surwit Diet formulas

Surwit饲料的种类
【1】Surwit 58%高脂高糖饲料:

脂肪58%,糖约25%,饲料热量大约是5.5千卡/g

【2】Surwit 58%高脂低糖饲料:

脂肪约58%。饲料热量大约是5.5千卡/g。

【3】Surwit 11%低脂高糖饲料:

脂肪热量11%,糖61%。

【4】Surwit 11%低脂低糖饲料:

脂肪热量11%。

Surwit等在研究高脂肥胖及其并发症方面,可谓是元老级和权威学者,他们的两个关键性研究所用的模型饲料至今被广为采用,并且后来有些学者和有些实验动物饲料企业在此基础上设计出了其他模型饲料。

一、Surwit diet介绍


Surwit等研究者在80年代已经设计了高脂高糖饲料用于研究饮食所致肥胖和糖尿病的研究。所用的模型饲料就是右图中所列的58%高脂高糖饲料。下图是用Surwit的这种模型饲料喂养的效果比较。

随着他们继续深入研究,到了90年代,他们又进一步观察比较了高脂高糖和高脂低糖分别对体重(肥胖)的作用,糖与脂肪之间对体脂的相互作用。为了达到研究目的,他们设计了2种高脂饲料,即高脂高糖饲料和高脂低糖饲料,以及2种低脂饲料,即低脂高糖饲料和低脂低糖饲料,从而形成了2个水平的脂肪含量(高脂、低脂)、2个水平的糖含量(高糖、低糖)的4种组合,也就是4种饲料。

他们获得的关键性发现是,高脂高糖饲料和高脂低糖都能让动物肥胖,但是,高脂高糖饲料比高脂低糖饲料的肥胖程度更大,更重要的是,高脂高糖和高脂无糖虽然都能升高血糖和空腹胰岛素水平,但是,两者之间并没有差别,也就是,高脂情况下,糖含量高低对于血糖和空腹胰岛素水平没有起作用。

那么,两种高脂饲料喂养的动物之间,为什么高脂高糖饲料引起的肥胖程度更大?关键是动物对高脂高糖饲料的食物利用率(FE)增大。更有趣的是,在体重和体脂两项指标方面,他们发现低脂高糖喂养的动物比低脂低糖的动物明显降低(变瘦)。呵呵,“减肥”?确实,后来Surwit等研究者又进一步在人体研究了低脂高糖的减体重的效果。

Surwit等研究者在这些研究中所用的4种饲料后来被称为,称为Surwit diet。

由于第4种饲料是低脂对照饲料,因此,前3种被后来作为模型饲料。

Surwit饲料的用途、缺点
Surwit高脂模型饲料的用途:

广泛应用于大小鼠肥胖模型高血脂模型高胆固醇血症模型胰岛素抵抗模型II型糖尿病模型代谢综合症模型非酒精性脂肪肝模型。请注意不同种系和品系的差异。

Suiwit饲料的缺点:

(1)营养素不合理,需要优化;

Surwit模型饲料的用途即为广泛,见右图。

如今广为采用的van Heek系列的45%高脂肥胖模型饲料60%高脂肥胖模型饲料就是基于Surwit模型饲料基础上延伸而来。

二、Surwit diet应用的注意点


Surwit模型也存在缺点:营养素不合理,需要优化。

南通特洛菲饲料科技有限公司对4种模型饲料分别采取了优化(产品代码TP24200)和不优化(产品代码TP24220)的策略,甚至重新设计(产品代码TP24000和TP24100)。

如果读者准备使用Surwit饲料开展研究,请阅读“Surwit高脂高糖和高脂低糖模型饲料存在的问题与纠正”。

 

References:

[1] Bilal Omar, Giovanni Pacini, Bo Ahrén. Differential Development of Glucose Intolerance and Pancreatic Islet Adaptation in Multiple Diet Induced Obesity Models. Nutrients. 2012 October; 4(10): 1367–1381.

[2] Surwit RS, Wang S, Petro AE, Sanchis D, Raimbault S, Ricquier D, Collins S. Diet-induced changes in uncoupling proteins in obesity-prone and obesity-resistant strains of mice. Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):4061-5.

[3] Lan H, Hoos LM, Liu L, Tetzloff G, Hu W, Abbondanzo SJ, Vassileva G, Gustafson EL, Hedrick JA, Davis HR.Lack of FFAR1/GPR40 does not protect mice from high-fat diet-induced metabolic disease.Diabetes. 2008 Nov;57(11):2999-3006.

[4] Collins S, Daniel KW, Petro AE, Surwit RS. Strain-specific response to beta 3-adrenergic receptor agonist treatment of diet-induced obesity in mice.Endocrinology. 1997 Jan;138(1):405-13.

[5] Lenhard JM, Croom DK, Weiel JE, Spaltenstein A, Reynolds DJ, Furfine ES. Dietary fat alters HIV protease inhibitor-induced metabolic changes in mice.J Nutr. 2000 Sep;130(9):2361-6.

[6] Delmée E, Cani PD, Gual G, Knauf C, Burcelin R, Maton N, Delzenne NM. Relation between colonic proglucagon expression and metabolic response to oligofructose in high fat diet-fed mice.Life Sci. 2006 Aug 1;79(10):1007-13.

[7] Kenerson HL, Yeh MM, Yeung RS. Tuberous sclerosis complex-1 deficiency attenuates diet-induced hepatic lipid accumulation.PLoS One. 2011 Mar 29;6(3):e18075.

[8] Ahrén B, Simonsson E, Scheurink AJ, Mulder H, Myrsén U, Sundler F. Dissociated insulinotropic sensitivity to glucose and carbachol in high-fat diet-induced insulin resistance in C57BL/6J mice. Metabolism. 1997 Jan;46(1):97-106.

[9] Tschöp J, Nogueiras R, Haas-Lockie S, Kasten KR, Castañeda TR, Huber N, Guanciale K, Perez-Tilve D, Habegger K, Ottaway N, Woods SC, Oldfield B, Clarke I, Chua S Jr, Farooqi IS, O'Rahilly S, Caldwell CC, Tschöp MH. CNS leptin action modulates immune response and survival in sepsis.J Neurosci. 2010 Apr 28;30(17):6036-47.

[10] Lelliott CJ, Medina-Gomez G, Petrovic N, Kis A, Feldmann HM, Bjursell M, Parker N, Curtis K, Campbell M, Hu P, Zhang D, Litwin SE, Zaha VG, Fountain KT, Boudina S, Jimenez-Linan M, Blount M, Lopez M, Meirhaeghe A, Bohlooly-Y M, Storlien L, Strömstedt M, Snaith M, Oresic M, Abel ED, Cannon B, Vidal-Puig A. Ablation of PGC-1beta results in defective mitochondrial activity, thermogenesis, hepatic function, and cardiac performance.PLoS Biol. 2006 Nov;4(11):e369.

[11] Dokmanovic-Chouinard M, Chung WK, Chevre JC, Watson E, Yonan J, Wiegand B, Bromberg Y, Wakae N, Wright CV, Overton J, Ghosh S, Sathe GM, Ammala CE, Brown KK, Ito R, LeDuc C, Solomon K, Fischer SG, Leibel RL. Positional cloning of "Lisch-Like", a candidate modifier of susceptibility to type 2 diabetes in mice.PLoS Genet. 2008 Jul 25;4(7):e1000137.

[12] Simoncic M, Horvat S, Stevenson PL, Bünger L, Holmes MC, Kenyon CJ, Speakman JR, Morton NM.Divergent physical activity and novel alternative responses to high fat feeding in polygenic fat and lean mice.Behav Genet. 2008 May;38(3):292-300.

[13] Karlsson EA, Sheridan PA, Beck MA. Diet-induced obesity impairs the T cell memory response to influenza virus infection. J Immunol. 2010 Mar 15;184(6):3127-33.

[14] Ahrén B, Scheurink AJ. Marked hyperleptinemia after high-fat diet associated with severe glucose intolerance in mice. Eur J Endocrinol. 1998 Oct;139(4):461-7.

[15] Collins S, Surwit RS. Pharmacologic manipulation of ob expression in a dietary model of obesity.J Biol Chem. 1996 Apr 19;271(16):9437-40.

[16] Yu XX, Mao W, Zhong A, Schow P, Brush J, Sherwood SW, Adams SH, Pan G. Characterization of novel UCP5/BMCP1 isoforms and differential regulation of UCP4 and UCP5 expression through dietary or temperature manipulation.FASEB J. 2000 Aug;14(11):1611-8.

[17] Winzell MS, Ahrén B. The high-fat diet-fed mouse: a model for studying mechanisms and treatment of impaired glucose tolerance and type 2 diabetes. Diabetes. 2004 Dec;53 Suppl 3:S215-9.

[18] Kohli R, Kirby M, Xanthakos SA, Softic S, Feldstein AE, Saxena V, Tang PH, Miles L, Miles MV, Balistreri WF, Woods SC, Seeley RJ. High-fructose, medium chain trans fat diet induces liver fibrosis and elevates plasma coenzyme Q9 in a novel murine model of obesity and nonalcoholic steatohepatitis.Hepatology. 2010 Sep;52(3):934-44.

[19] Rong JX, Qiu Y, Hansen MK, Zhu L, Zhang V, Xie M, Okamoto Y, Mattie MD, Higashiyama H, Asano S, Strum JC, Ryan TE. Adipose mitochondrial biogenesis is suppressed in db/db and high-fat diet-fed mice and improved by rosiglitazone.Diabetes. 2007 Jul;56(7):1751-60.

[20] Paul DS, Walton FS, Saunders RJ, Stýblo M. Characterization of the impaired glucose homeostasis produced in C57BL/6 mice by chronic exposure to arsenic and high-fat diet.Environ Health Perspect. 2011 Aug;119(8):1104-9.

[21] Diab I, Abdelaziz H and Aboheif H. Nuclear Factor- κB (NF-κB) Expression in High Fat Diet-Induced Obesity and Insulin Resistance in Rats. J Am Sci 2012;8(5):479-486.

[22] Cao J, Sodhi K, Puri N, Monu SR, Rezzani R, Abraham NG. High fat diet enhances cardiac abnormalities in SHR rats: Protective role of heme oxygenase-adiponectin axis.Diabetol Metab Syndr. 2011 Dec 23;3(1):37.

[23] Colleen Croniger. An Unbiased Approach to Discover Novel Therapies for Liver Disease. J Metabonomics Metabolites 2012, 1:1

[24] Liu X, Rossmeisl M, McClaine J, Riachi M, Harper ME, Kozak LP. Paradoxical resistance to diet-induced obesity in UCP1-deficient mice.J Clin Invest. 2003 Feb;111(3):399-407.

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有困惑?那就商量呗!

高脂肥胖、代谢综合症、胰岛素抵抗、高血脂(高甘油三酯血症、高胆固醇血症)、糖尿病、动脉粥样硬化、非酒精性脂肪肝,等模型饲料

南通特洛菲饲料科技有限公司提供各种动物、各种类型的肥胖及其并发症的模型饲料。以下介绍Surwit模型饲料。

---------《》-------

大鼠小鼠Surwit模型饲料:

markerTP24220, TP24221

TP24220和TP24221分别与Surwit高脂高糖模型饲料、高脂低糖模型饲料一致,与ResearchDiets公司D12331和D12330相当,或者与TestDiet公司58R3和58R2相当。为追求与Surwit饲料相当的研究者设计。用于未成年(接近成年),建议不用于幼年、妊娠哺乳期。

markerTP24200

由于Surwit模型饲料营养素不合理,TP24200将营养素优化到合理水平。用于未成年,建议不用于幼年、妊娠、哺乳期。

markerTP24100

基于Surwit模型饲料重新设计,用于成年动物。

markerTP24000

基于Surwit模型饲料重新设计,适用于未成年(任何阶段)、妊娠、哺乳期。

60%高脂肥胖模型饲料选择指南

45%高脂肥胖模型饲料选择指南




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