Mcd diet

Manufactured by MP Biomedicals

Sourced in United States

The MCD diet is a specialized laboratory equipment designed to facilitate the induction and maintenance of a methionine-choline-deficient (MCD) diet in animal studies. This dietary intervention is commonly used to model liver disease and non-alcoholic fatty liver disease (NAFLD) in rodents. The MCD diet equipment enables researchers to precisely control the nutritional composition of the animal's diet, allowing for the study of the physiological and pathological effects of methionine and choline deficiency.

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Lab products found in correlation

Hydroxypropyl methylcellulose, by Merck Group (1 mentions) C57bl 6, by Jackson ImmunoResearch (1 mentions) Perhexiline maleate, by Cayman Chemical (1 mentions) C57bl 6 mice, by Charles River Laboratories (1 mentions) C57bl 6j mice, by MP Biomedicals (1 mentions)

4 protocols using mcd diet

Compound 1 Reduces Liver Fibrosis in NASH Model

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Example 2

Male wild-type (WT) mice C57Bl/6 were obtained from Jackson Laboratory and fed either with MCD diet (MP Biomedicals, #960439) or a lean control diet at 8 week of age for 8 weeks. Compound 1 was formulated as a solution in 1% hydroxypropyl methylcellulose (Sigma-Aldrich, St. Louis, USA). Mice were dosed subcutaneously once per day with 30 mg/kg Compound 1 or vehicle for 8 weeks. Compound 1 was administered subcutaneously to maintain high systemic levels. The CVC compound (cenicriviroc) was formulated as a solution in 1% hydroxypropyl methylcellulose, and tested at 30 mg/kg orally. For both compound 1 and CVC, trough drug level was over IC₅₀. FIG. 5 shows that compound 1 significantly reduces serum ALT levels whereas CVC does not. FIG. 6 shows that compound 1 reduces Sirius red-positive staining and, therefore, liver fibrosis, whereas CVC does not.

US11357760B2. Method of treating liver fibrosis (2022-06-14). ChemoCentryx, Inc. [US]. Inventors: Zhenhua Miao [US], Israel Charo [US].

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Nutritional Induction of Liver Cancer

Cited 3 times

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C57BL/6 mice were purchased from Charles River Laboratories (VA, USA) at 8–10 weeks of age. NAFLD was induced by feeding mice the MCD diet (catalog number 960439, MP Biomedicals), or custom made high C18:2 (12%) or low C18:2 (2%) diet (Research Diets) as previously described^{8 (link)}. Liver-specific inducible MYC oncogene transgenic mice (MYC-ON) have been previously used by our group where MYC expression in the liver was activated by removing doxycycline treatment from the drinking water of 4-week-old double transgenic mice for TRE-MYC and LAP-tTA^{8 (link), 38 (link), 39 (link)}. The CPT inhibitor, perhexiline maleate (Cayman Chemical, MI, USA) was given intraperitoneally to MYC-ON mice at 8 mg/kg in 100 µL 50/50 solution of PBS/DMSO three times per week from week 6 to week 11, during which time the mice were fed with the MCD diet^{27 (link)}. MYC-ON mice were injected i.p. with 100 µL of vehicle without perhexiline as control. Mice were approximately 20 g at time of injections. Upon removal of the liver, sections of the liver were fixed with 10% formaldehyde and sent to Histoserv (Germantown, MD, USA) for hematoxylin and eosin (H&E) staining. All animal experiments were performed according to the institutional guidelines and approved by a NCI-Bethesda (Bethesda, MD, USA) Institutional Animal Care and Use protocol.

Brown Z.J., Fu Q., Ma C., Kruhlak M., Zhang H., Luo J., Heinrich B., Yu S.J., Zhang Q., Wilson A., Shi Z.D., Swenson R, & Greten T.F. (2018). Carnitine palmitoyltransferase gene upregulation by linoleic acid induces CD4+ T cell apoptosis promoting HCC development. Cell Death & Disease, 9(6), 620.

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Methionine Choline-Deficient Diet Model

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Mice were fed with a methionine choline-deficient (MCD) diet (MP Biomedicals) for 2 weeks (short term) or 8 weeks (long term). Livers from these mice were collected, fixed in 4% PFA, and embedded in paraffin for histological evaluation. Intraperitoneal injection of the JNK-Inhibitor SP600125 (15 μl/1 mg) (Absource Diagnostics) or vehicle (DMSO) was performed twice a day over 2 weeks of MCD feeding.

Gautheron J., Vucur M., Reisinger F., Cardenas D.V., Roderburg C., Koppe C., Kreggenwinkel K., Schneider A.T., Bartneck M., Neumann U.P., Canbay A., Reeves H.L., Luedde M., Tacke F., Trautwein C., Heikenwalder M, & Luedde T. (2014). A positive feedback loop between RIP3 and JNK controls non-alcoholic steatohepatitis. EMBO Molecular Medicine, 6(8), 1062-1074.

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Mouse Models of Colitis and NASH

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For acute colitis, 6-week-old male C57BL/6J mice (InVivos, Singapore) were grouped randomly and given 3.5% DSS (colitis grade, 36 to 50 kDa, MP Biomedicals, USA) in drinking water for 7 days. B-mEVs (0.6 mg/kg per day, low dose; 3.0 mg/kg per day, high dose) were orally administered to mice for 1 week before DSS feeding. Chronic colitis was induced by intermittent administration of 3.5% DSS. Body weight and DAI (body weight loss, stool consistency, and bleeding) were assessed in both acute and chronic models of colitis. For NASH, 7-week-old C57BL/6J mice were fed on the MCD diet (MP Biomedicals, USA) for 8 weeks. At 4 weeks of MCD diet feeding, mice were randomly grouped for different treatments. Mice were orally administered with B-mEVs starting at 4 weeks feeding on MCD diet 1.2 mg/kg every other day for 4 weeks. Saline or EV-depleted supernatant (1.2 mg/kg every other day) were used as negative control. Mice were kept on a 12-hour light and dark cycle. All animal experiments were approved by the Institutional Animal Care and Use Committee of the National University of Singapore or Ocean University of China and conformed to the Guide for the Care and Use of Laboratory Animals published by the U.S. National Institutes of Health (NIIH Publication, 8th Edition, 2011).

Tong L., Zhang S., Liu Q., Huang C., Hao H., Tan M.S., Yu X., Lou C.K., Huang R., Zhang Z., Liu T., Gong P., Ng C.H., Muthiah M., Pastorin G., Wacker M.G., Chen X., Storm G., Lee C.N., Zhang L., Yi H, & Wang J.W. (2023). Milk-derived extracellular vesicles protect intestinal barrier integrity in the gut-liver axis. Science Advances, 9(15), eade5041.

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