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The “AIN” diets were published by the American Institute of Nutrition (now the American Society for Nutrition–ASN), based on extensive research and a broad collaboration of researchers. The number in the name indicates the year the formula was published, with the AIN-93M (Maintenance) and AIN-93G (Growth) formulated to be improvements upon the AIN-76A. These formulas are the founding purified diet formulas upon which countless customized research diets are based upon.
TestDiet® developed another purified diet formula, known as the Basal Purified Diet (5755), which has also been a baseline formula for numerous research-specific diets. Using purified diet formulas gives us the highest level of control over the nutrient composition, allowing for easy modification to delete or adjust targeted nutrients with little impact over the remainder of the diet. Selecting the proper control diet is of utmost importance for research integrity and the ability to publish your work. Please ask a nutritionist about the best control diet for your TestDiet custom product.
Reeves, P.G., F.H. Nielsen, and G.C. Fahey, Jr. 1993. AIN-93 purified diets for laboratory rodents: Final report of the American Institute of Nutrition and ad hoc writing committee on the reformulation of the AIN-76A diet. J. Nutr. 123:1939-1951
Purina TestDiet® can produce a multitude of formulas for research in obesity, diabetes, metabolic syndrome, and related diseases – and can produce custom variations to meet your specific research needs. We have created high fat diets for many species, including rodents, pigs, primates, and dogs.
Table: Fatty Acid Profiles of Commonly Used Fat Sources in Laboratory Animal Diets
This diet series was first introduced in 1997 by Van Heek et al. in the J. Clinical Investigation. The diets are based on the AIN-76A Semi-Purified Diet with lard as the predominate source of fat and no added fiber. Mineral and vitamin premixes are included in higher quantities in the high fat diets than the controls to promote adequate micronutrient intake during anticipated regulation of caloric intake.
Meakin P.J., Harper A.J., Hamilton D.L., et al. 2012. Reduction in BACE1 decreases body weight, protects against diet-induced obesity and enhances insulin sensitivity in mice. Biochem. J. 441; 285–296.
Mitsutake S., Date T., Yokota H., et al. 2012. Ceramide kinase deficiency improves diet-induced obesity and insulin resistance. FEBS Lett. 586; 1300–1305.
Salmon A.B., Flores L.C., Li Y., et al. 2012. Reduction of glucose intolerance with high fat feeding is associated with anti-inflammatory effects of thioredoxin 1 overexpression in mice. Pathobiology of Aging & Age-related Diseases 2; 10.3402/pba.v2i0.17101.
Zhang C., McFarlane C., Lokireddy S., et al. 2012. Inhibition of myostatin protects against diet-induced obesity by enhancing fatty acid oxidation and promoting a brown adipose phenotype in mice. Diabetologia 55; 183–193.
Martínez-Carrillo B.E., Zúñiga-Torres M.G., Jarillo-Luna R.A., et al. 2011. Effect of exercise and high carbohydrates diet in the T-lymphocytes of Peyer’s patches of Balb/c mice. Proceedings of the Nutrition Society 70; E39.
Tomada I., Tomada N., Almeida H., Neves D. 2011. Energy restriction and exercise modulate angiopoietins and vascular endothelial growth factor expression in the cavernous tissue of high-fat diet-fed rats. Asian J. Androl. 14; 635-642.
Zhang C., McFarlane C., Lokireddy S., et al. 2011. Myostatin-deficient mice exhibit reduced insulin resistance through activating the AMP-activated protein kinase signaling pathway. Diabetologia 54; 1491–1501.
Zúñiga-Torres M.G., Martínez-Carrillo B.E., Jarillo-Luna R.A., et al. 2011. Effect of high fat diet and moderate exercise on T-lymphocytes of Peyer’s patches mice. Proceedings of the Nutrition Society 70; E48.
Gaidhu M.P., Anthony N.M., Patel P., et al. 2010. Dysregulation of lipolysis and lipid metabolism in visceral and subcutaneous adipocytes by high-fat diet: role of ATGL, HSL, and AMPK. Am. J. Physiol. Cell Physiol. 298; C961–971.
Feher A., Rutkai I., Beleznai T., et al. 2010. Caveolin-1 limits the contribution of BK(Ca) channel to EDHF-mediated arteriolar dilation: implications in diet-induced obesity. Cardiovasc. Res. 87; 732–739.
Prieto D., Kaminski P.M., Bagi Z., et al. 2010. Hypoxic relaxation of penile arteries: involvement of endothelial nitric oxide and modulation by reactive oxygen species. Am. J. Physiol. Heart Circ. Physiol. 299; H915–924.
van den Broek N.M.A., Ciapaite J., De Feyter H.M.M.L., et al. 2010. Increased mitochondrial content rescues in vivo muscle oxidative capacity in long-term high-fat-diet-fed rats. FASEB J. 24; 1354–1364.
Yamada P.M., Mehta H.H., Hwang D., et al. 2010. Evidence of a role for insulin-like growth factor binding protein (IGFBP)-3 in metabolic regulation. Endocrinology 151; 5741–5750.
Developed in 1992 by Professor Richard Surwit at Duke University for diet-induced obesity and diabetic studies. This diet series is based on the AIN-76A Semi-Purified Diet to be high in saturated fat with hydrogenated coconut oil as the main fat source. It also contains no added fiber. Mineral and vitamin premixes are included in higher quantities in the high fat diets than the controls to promote adequate micronutrient intake during anticipated regulation of caloric intake.
Jheng H-F., Tsai P-J., Guo S-M., et al. 2012. Mitochondrial fission contributes to mitochondrial dysfunction and insulin resistance in skeletal muscle. Mol. Cell. Biol. 32; 309–319.
Lee R.K., Hittel D.S., Nyamandi V.Z., et al. 2012. Unconventional microarray design reveals the response to obesity is largely tissue specific: analysis of common and divergent responses to diet-induced obesity in insulin-sensitive tissues. Appl. Physiol. Nutr. Metab. 37; 257–268.
Meoli L. 2012. Comprehensive Phenotyping of Two Mouse Mutants Reveals a Potential Novel Role of G Protein-coupled Receptor 30. Ph.D thesis. Humboldt-Universität zu Berlin.
Caton P.W., Kieswich J., Yaqoob M.M., et al. 2011. Metformin opposes impaired AMPK and SIRT1 function and deleterious changes in core clock protein expression in white adipose tissue of genetically-obese db/db mice. Diabetes Obes. Metab. 13; 1097–1104.
Duggan G.E., Hittel D.S., Sensen C.W., et al. 2011. Metabolomic response to exercise training in lean and diet-induced obese mice. J. Appl. Physiol. 110; 1311–1318.
Duggan G.E., Hittel D.S., Hughey C.C., et al. 2011. Differentiating short- and long-term effects of diet in the obese mouse using (1) H-nuclear magnetic resonance metabolomics. Diabetes Obes. Metab. 13; 859–862.
Shearer J., Severson DL., Su L., et al. 2009. Partial A1 adenosine receptor agonist regulates cardiac substrate utilization in insulin-resistant rats in vivo. J. Pharmacol. Exp. Ther. 328; 306–311.
Tsai Y-S., Tsai P-J., Jiang M-J., et al. 2009. Decreased PPAR gamma expression compromises perigonadal-specific fat deposition and insulin sensitivity. Mol. Endocrinol. 23; 1787–1798.
Shearer J., Duggan G., Weljie A., et al. 2008. Metabolomic profiling of dietary-induced insulin resistance in the high fat-fed C57BL/6J mouse. Diabetes Obes. Metab. 10; 950–958.
This four-diet series is formulated with three of the diets providing similar kcal from fat as the Van Heek series but using the Basal Purified Diet (5755) as the base formula. This diet series contains fiber in the form of cellulose and fat primarily fromlard and corn oil. Mineral and vitamin premixes are included in higher quantities in the high fat diets than the controls to promote adequate micronutrient intake during anticipated regulation of caloric intake.
Hageman et al. 2010. High-fat diet leads to tissue-specific changes reflecting risk factors for diseases in DBA/2J mice Physiol Genomics. 42(1): 55–66.
Krisantis et al. 2022. Non-enzymatic glycoxidation linked with nutrition enhances the tumorigenic capacity of prostate cancer epithelia through AGE mediated activation of RAGE in cancer associated fibroblasts. Translational Oncology. 101350 pp 1-10
Liu Tzu-Wen. 2013. Changes in fatty acid profiles after three weeks of high-fat diet feeding in obesity prone rats. Masters Thesis. University of Missouri-Columbia. pp 1-110. Liu et al. 2017. Oval Cells Contribute to Fibrogenesis of Marginal Liver Grafts under Stepwise Regulation of Aldose Reductase and Notch Signaling. Theranostics Vol. 7 (19) 4879-4893.
Park et al. 2012. Physical activity opposes coronary vascular dysfunction induced during high fat feeding in mice. J Physiol 590.17 pp 4255–4268
Patel R, Baker SS, Liu W, Desai S, Alkhouri R, et al. (2012) Effect of Dietary Advanced Glycation End Products on Mouse Liver. PLoS ONE 7(4): e35143. doi:10.1371/journal.pone.0035143
Sekar and Chow. 2014. Secretin receptor-knockout mice are resistant to high-fat diet-induced obesity and exhibit impaired intestinal lipid absorption. FASEB J. 28: 2494-2505.
So et al. 2012. Silencing of lipid metabolism genes through IRE1α-mediated mRNA decay lowers plasma lipids in mice Cell Metab. 16(4): 487–499
Vingtdeux et al. 2011. Small-Molecule Activators of AMP-Activated Protein Kinase (AMPK), RSVA314 and RSVA405, Inhibit Adipogenesis. Mol Med 17(9-10)1022-1030
Zhao et al. 2013. Pubertal high fat diet: effects on mammary cancer development. Breast Cancer Research, 15:R100
There are numerous Western-type purified diets available. Western diets have moderate to high fat content and include added cholesterol with or without sodium cholate. Western diets have multiple uses such as inducing obesity, atherosclerosis, non-alcoholic steatohepatitis, osteoporosis, hypertension and other metabolic syndromes.
This four-diet series was introduced in 1999 and designed to evaluate the relationship between diet and genetics in atherogenic murine models. These diets were modified from the AIN-76A Semi-Purified Diet to contain cocoa butter in addition to corn oil and are free of fiber.
Lichtman A.H. et al. Hyperlipidemia and Atherosclerotic Lesion Development in LDL Receptor-Deficient Mice Fed Defined Semipurified Diets with and Without Cholate. Arterioscler Thromb Vasc Biol. 1999;19:1938-1944.
Zheng H., Zou H., Liu X., et al. 2012. Cholesterol level influences opioid signaling in cell models and analgesia in mice and humans. J. Lipid Res. 53; 1153–1162.
Stephens A.M., Dean L.L., Davis J.P., et al., 2010. Peanuts, peanut oil, and fat free peanut flour reduced cardiovascular disease risk factors and the development of atherosclerosis in Syrian golden hamsters. J. Food. Sci. 75; H116–122.
There are numerous Western-type purified diets available. Western diets have moderate to high fat content and include added cholesterol with or without sodium cholate. Western diets have multiple uses such as inducing obesity, atherosclerosis, non-alcoholic steatohepatitis, osteoporosis, hypertension and other metabolic syndromes.
Nuotio-Antar et al. FABP4-Cre Mediated Expression of Constitutively Active ChREBP Protects Against Obesity, Fatty Liver, and Insulin Resistance. Endocrinology. 2015 Nov; 156(11): 4020–4032.
Yang Y., Chang B., Chan L., Sustained expression of the transcription factor GLIS3 is required for normal beta cell function in adults. EMBO Mol Med (2013)5:92-104
There are numerous Western-type purified diets available. Western diets have moderate to high fat content and include added cholesterol with or without sodium cholate. Western diets have multiple uses such as inducing obesity, atherosclerosis, non-alcoholic steatohepatitis, osteoporosis, hypertension and other metabolic syndromes.
Shelly L., Royer L., Sand T., et al. 2008. Phospholipid transfer protein deficiency ameliorates diet-induced hypercholesterolemia and inflammation in mice. J. Lipid Res. 49; 773–781.
Evans M.J., Mahaney P.E., Borges-Marcucci L., et al. 2009. A synthetic farnesoid X receptor (FXR) agonist promotes cholesterol lowering in models of dyslipidemia. Am. J. Physiol. Gastrointest. Liver Physiol. 296; G543–552.
Luo Y., Warren L., Xia D., et al. 2009. Function and distribution of circulating human PCSK9 expressed extrahepatically in transgenic mice. J. Lipid Res. 50; 1581–1588.
Characteristics of a ketogenic diet includes higher fat levels than Western Diets to the extent that it replaces all carbohydrates and fiber. Fat sources are solid but soft at room temperature, so the high levels of fat make ketogenic diets extremely soft with the consistency of a dough. Most ketogenic diets are unable to be pelleted, and depending on what fat source is used, may need to be hand mixed prior to feeding. Ketogenic diets can be used for multiple research applications including cancer, neuroscience and metabolism. Ketogenic diets have been widely used to study neurological disorders and diseases such as Alzheimer’s, epilepsy and autism. Ketogenic diets are also used in studying metabolic diseases such as obesity, diabetes, and non-alcoholic fatty liver disease.
Amino Acid Defined Diets are chemically refined purified diets in which the protein fraction of the diet is completely made up of pure amino acids. This type of diet is important for research targeting specific amino acids, adjusting one or more individual amino acid, meanwhile keeping other amino acids or overall protein level constant. The Baker Amino Acid Diet is the most commonly used amino acid defined purified diet to use as a starting point for further modification. There are multiple ways to remove amino acids from the diet:
Caballero F., Fernández A., Matías N., et al. 2010. Specific contribution of methionine and choline in nutritional nonalcoholic steatohepatitis: impact on mitochondrial S-adenosyl-L-methionine and glutathione. J. Biol. Chem. 285; 18528–18536.
Gilbert E.R., Li H., Emmerson D.A., et al. 2010. Dietary protein composition influences abundance of peptide and amino acid transporter messenger ribonucleic acid in the small intestine of 2 lines of broiler chicks. Poult. Sci. 89; 1663–1676.
Hirakawa et al. 1984. Comparative utilization of a crystalline amino acid diet and a methionine fortified casein diet by young rats and mice. Nutrition Research. Vol. 4, pp. 891-895.
Kim H., Toyofuku Y., Lynn F.C., et al. 2010. Serotonin regulates pancreatic beta cell mass during pregnancy. Nat. Med. 16; 804–808.
Maddocks et al. 2013. Serine starvation induces stress and p53-dependent metabolic remodelling in cancer cells. Nature. Vol 493; 542-546.
Maddocks et al. 2017. Modulating the therapeutic response of tumors to dietary serine and glycine starvation. Nature. Vol 544; 372-378.