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Surwit模型飼料介紹
Surwit Diet formulas

Surwit飼料的種類
【1】Surwit 58%高脂高糖飼料:

脂肪58%,糖約25%,飼料熱量大約是5.5千卡/g

【2】Surwit 58%高脂低糖飼料:

脂肪約58%。飼料熱量大約是5.5千卡/g。

【3】Surwit 11%低脂高糖飼料:

脂肪熱量11%,糖61%。

【4】Surwit 11%低脂低糖飼料:

脂肪熱量11%。

Surwit等在研究高脂肥胖及其并發癥方面,可謂是元老級和權威學者,他們的兩個關鍵性研究所用的模型飼料至今被廣為采用,并且后來有些學者和有些實驗動物飼料企業在此基礎上設計出了其他模型飼料。

一、Surwit diet介紹


Surwit等研究者在80年代已經設計了高脂高糖飼料用于研究飲食所致肥胖和糖尿病的研究。所用的模型飼料就是右圖中所列的58%高脂高糖飼料。下圖是用Surwit的這種模型飼料喂養的效果比較。

隨著他們繼續深入研究,到了90年代,他們又進一步觀察比較了高脂高糖和高脂低糖分別對體重(肥胖)的作用,糖與脂肪之間對體脂的相互作用。為了達到研究目的,他們設計了2種高脂飼料,即高脂高糖飼料和高脂低糖飼料,以及2種低脂飼料,即低脂高糖飼料和低脂低糖飼料,從而形成了2個水平的脂肪含量(高脂、低脂)、2個水平的糖含量(高糖、低糖)的4種組合,也就是4種飼料。

他們獲得的關鍵性發現是,高脂高糖飼料和高脂低糖都能讓動物肥胖,但是,高脂高糖飼料比高脂低糖飼料的肥胖程度更大,更重要的是,高脂高糖和高脂無糖雖然都能升高血糖和空腹胰島素水平,但是,兩者之間并沒有差別,也就是,高脂情況下,糖含量高低對于血糖和空腹胰島素水平沒有起作用。

那么,兩種高脂飼料喂養的動物之間,為什么高脂高糖飼料引起的肥胖程度更大?關鍵是動物對高脂高糖飼料的食物利用率(FE)增大。更有趣的是,在體重和體脂兩項指標方面,他們發現低脂高糖喂養的動物比低脂低糖的動物明顯降低(變瘦)。呵呵,“減肥”?確實,后來Surwit等研究者又進一步在人體研究了低脂高糖的減體重的效果。

Surwit等研究者在這些研究中所用的4種飼料后來被稱為,稱為Surwit diet。

由于第4種飼料是低脂對照飼料,因此,前3種被后來作為模型飼料。

Surwit飼料的用途、缺點
Surwit高脂模型飼料的用途:

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。請注意不同種系和品系的差異。

Suiwit飼料的缺點:

(1)營養素不合理,需要優化;

Surwit模型飼料的用途即為廣泛,見右圖。

如今廣為采用的van Heek系列的45%高脂肥胖模型飼料60%高脂肥胖模型飼料就是基于Surwit模型飼料基礎上延伸而來。

二、Surwit diet應用的注意點


Surwit模型也存在缺點:營養素不合理,需要優化。

南通特洛菲飼料科技有限公司對4種模型飼料分別采取了優化(產品代碼TP24200)和不優化(產品代碼TP24220)的策略,甚至重新設計(產品代碼TP24000和TP24100)。

如果讀者準備使用Surwit飼料開展研究,請閱讀“Surwit高脂高糖和高脂低糖模型飼料存在的問題與糾正”。

 

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] Tsch?p J, Nogueiras R, Haas-Lockie S, Kasten KR, Casta?eda 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, Tsch?p 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, Str?mstedt 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, Styblo 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.

[25] Leavens KF, Easton RM, Shulman GI, Previs SF, Birnbaum MJ. Akt2 is required for hepatic lipid accumulation in models of insulin resistance.Cell Metab. 2009 Nov;10(5):405-18.



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Surwit模型飼料。

---------《》-------

大鼠小鼠Surwit模型飼料:

markerTP24220, TP24221

TP24220和TP24221分別與Surwit高脂高糖模型飼料、高脂低糖模型飼料一致,與ResearchDiets公司D12331和D12330相當,或者與TestDiet公司58R3和58R2相當。為追求與Surwit飼料相當的研究者設計。用于未成年(接近成年),建議不用于幼年、妊娠哺乳期。

markerTP24200

由于Surwit模型飼料營養素不合理,TP24200將營養素優化到合理水平。用于未成年,建議不用于幼年、妊娠、哺乳期。

markerTP24100

基于Surwit模型飼料重新設計,用于成年動物。

markerTP24000

基于Surwit模型飼料重新設計,適用于未成年(任何階段)、妊娠、哺乳期。

60%高脂肥胖模型飼料選擇指南

45%高脂肥胖模型飼料選擇指南




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