D12331

Manufactured by Research Diets

Sourced in United States, United Kingdom

D12331 is a specialized laboratory equipment designed for research purposes. It serves as a precision tool for controlled environmental conditions within a laboratory setting. The core function of this product is to maintain and regulate specific environmental parameters, such as temperature and humidity, to facilitate accurate and consistent experimental procedures.

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Lab products found in correlation

D12329, by Research Diets (8 mentions) C57bl 6j mice, by Jackson ImmunoResearch (8 mentions) D12328, by Research Diets (4 mentions) C57bl 6j mice, by Janvier Labs (4 mentions) Lm 485, by Inotiv (4 mentions) High fat diet (hfd), by Research Diets (3 mentions) B6 cg lepob j, by Jackson ImmunoResearch (3 mentions) Td 88137, by Research Diets (2 mentions) Minispec, by Bruker (2 mentions) C57bl 6 mice, by Jackson ImmunoResearch (2 mentions) C57bl 6j mice, by Charles River Laboratories (2 mentions) C57bl 6j mice, by Research Diets (2 mentions) Leprdb db db mice, by Jackson ImmunoResearch (2 mentions) Wild type c57bl 6 mice, by Jackson ImmunoResearch (1 mentions) Standard mouse chow diet, by Research Diets (1 mentions) Td 2916, by Inotiv (1 mentions) C57bl 6j strain, by Jackson ImmunoResearch (1 mentions) D12331, by Ssniff (1 mentions) D12450ji, by Research Diets (1 mentions) Db db mice, by Jackson ImmunoResearch (1 mentions)

98 protocols using d12331

Dietary Manipulation and PCSK9 Virus Injection

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Apoe^−/− mice were fed a high-fat diet (HFD, Harlan Teklad, TD.88137) and Ldlr^−/− mice were fed a high-cholesterol diet (HCD, Research Diets D12331). 5 × 10¹¹U of adv-PCSK9 virus was injected i.v and mice began consuming a high-cholesterol diet (HCD, Research Diets D12331) immediately after virus injection. Unless otherwise indicated, mice were fed a regular chow diet.

McAlpine C.S., Kiss M.G., Rattik S., He S., Vassalli A., Valet C., Anzai A., Chan C.T., Mindur J.E., Kahles F., Poller W.C., Frodermann V., Fenn A.M., Gregory A.F., Halle L., Iwamoto Y., Hoyer F.F., Binder C.J., Libby P., Tafti M., Scammell T.E., Nahrendorf M, & Swirski F.K. (2019). Sleep modulates hematopoiesis and protects against atherosclerosis. Nature, 566(7744), 383-387.

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Dietary Effects on Glp1r-Knockout Mice

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All studies were approved and performed following the guidelines of the institutional animal care and use committees of the University of Cincinnati.Glp1r-knockout (KO) and age-matched wild-type (WT) male mice on a C57/BL6J background were generated as previously described [16 ] and bred at the University of Cincinnati. Mice were maintained on a 12:12 h light–dark cycle at 22°C with free access to water and to either a stan dard chow control diet (CD; 5.6% fat; LM-485, Teklad, Harlan; Indianapolis, IN, USA) or a high-sucrose diet containing 58% energy from fat (HFD; Research Diets #D12331, New Brunswick, NJ, USA), as indicated. Mice were 12–14 weeks and 16–18 weeks of age for CD and HFD diet experiments, respectively.
Male C57BL/6J mice (The Jackson Laboratory; Bar Harbor, ME, USA) were fed HFD (Research Diets #D12331, New Brunswick) starting at 10 weeks of age and were then maintained on the diet for 24 weeks prior to liraglutide treatment. Mice were randomly assigned to groups using Microsoft Excel. Experimenters were not blind to group assignment and outcome assessment. All the data collected are presented. In the case of the gene expression analysis, a subset of samples per group was randomly chosen using Microsoft Excel.

Heppner K.M., Marks S., Holland J., Ottaway N., Smiley D., Dimarchi R, & Perez-Tilve D. (2015). Contribution of brown adipose tissue activity to the control of energy balance by GLP-1 receptor signalling in mice. Diabetologia, 58(9), 2124-2132.

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Dietary Manipulation and PCSK9 Virus Injection

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High-Fat, High-Sugar Diet Induces Obesity in Mice

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Six- to eight-week-old male C57Bl/6 mice were given ad libitum access to a high-fat, high-sugar diet comprising 58% kcal fat (D12331; Research Diets, New Brunswick, NJ). The mice had free access to water and were maintained at 23 ± 1°C, constant humidity and on a 12-h light–dark cycle. Mice were maintained under these conditions for a minimum of 20 weeks before study initiation. At study start, mice were randomized into groups matched for body weight and body composition, with similar variance. No animals were excluded due to illness or outlier results; therefore, no exclusion determination was required. All animal studies were approved by the Animal Ethics Committee of the government of Upper Bavaria, Germany, and all experiments were performed according to the guidelines of the Institutional Animal Care and Use Committee of the Helmholtz Center Munich, Bavaria, Germany.

Clemmensen C., Finan B., Fischer K., Tom R.Z., Legutko B., Sehrer L., Heine D., Grassl N., Meyer C.W., Henderson B., Hofmann S.M., Tschöp M.H., Van der Ploeg L.H, & Müller T.D. (2015). Dual melanocortin-4 receptor and GLP-1 receptor agonism amplifies metabolic benefits in diet-induced obese mice. EMBO Molecular Medicine, 7(3), 288-298.

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Long-term selection of diverse mouse lines

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The long term selection and further development of the F, L and congenic lines are described elsewhere^{5 (link)–6 (link)}. Animals were fed pelleted diet (Special Diets Services, Witham, Essex, UK) or defined low (11% calories as fat with sucrose; D12329) or high fat (58% calories as fat with sucrose; D12331) diets (Research Diets, New Brunswick, New Jersey).

Morton N.M., Beltram J., Carter R.N., Michailidou Z., Gorjanc G., Fadden C.M., Barrios-Llerena M.E., Rodriguez-Cuenca S., Gibbins M.T., Aird R.E., Moreno-Navarrete J.M., Munger S.C., Svenson K.L., Gastaldello A., Ramage L., Naredo G., Zeyda M., Wang Z.V., Howie A.F., Saari A., Sipilä P., Stulnig T.M., Gudnason V., Kenyon C.J., Seckl J.R., Walker B.R., Webster S.P., Dunbar D.R., Churchill G.A., Vidal-Puig A., Fernandez-Real J.M., Emilsson V, & Horvat S. (2016). Genetic identification of thiosulfate sulfurtransferase as an adipocyte-expressed anti-diabetic target in mice selected for leanness. Nature medicine, 22(7), 771-779.

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High-Fat Diet Induced Metabolic Changes

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Wild type C57BL/6 mice were purchased from the Jackson Laboratory and housed in a 12-hour light/dark cycle (lights on 7 am-7 pm). The mice were first treated with a high fat diet (Research Diets D12331, 5.56 kcal/gm) for 12 weeks. An MRI was performed for the baseline body composition. The mice were then treated with PBS control, T3 (200 μg/kg) or ASO-T3 (25 mg/kg) twice a week. The metabolic cage studies were started from day 7 when there was no difference in body weight. A repeat MRI was performed three weeks after the treatment. Mouse studies were conducted in accordance with federal guidelines and were approved by the Institutional Animal Care and Use Committee of University of California Irvine and East Carolina University.

Cao Y., Matsubara T., Zhao C., Gao W., Peng L., Shan J., Liu Z., Yuan F., Tang L., Li P., Guan Z., Fang Z., Lu X., Huang H, & Yang Q. (2017). Antisense oligonucleotide and thyroid hormone conjugates for obesity treatment. Scientific Reports, 7, 9307.

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Effects of ActRII Variant on Diet-Induced Obesity

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Example 7

Adult male C57BL/6 mice are assigned to weight-matched treatment groups (n=10/group). All animals are maintained on either regular chow diet (Chow; Purina LabDiet 5001; St. Louis, Mo.) or high fat diet (HFD; Research Diets D12331; New Brunswick, N.J.). Chow- and HFD-fed groups are further divided into groups that are dosed twice weekly with either ActRII variant or vehicle for a period of 60 d. Body weights are measured twice per week at the time of treatment. Body composition is measured using the MiniSpec LF50 at baseline (before administration of treatments and transfer to HFD) and then every other week until the end of the study. At the study termination date, tissues of interest (serum, plasma, muscles and fat depots) are surgically removed and weighed. Serum samples are subsequently evaluated for biomarkers of adiposity and plasma was evaluated for Hba1c levels.

US11013785B2. Activin receptor type IIA variants and methods of use thereof (2021-05-25). Keros Therapeutics, Inc. [US]. Inventors: Jasbir S. Seehra [US], Jennifer Lachey [US].

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Genetic mouse models for metabolic studies

Cited 2 times

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Mc4r^flox/flox, Chat-cre, and Phox2B-cre mice on a C57BL/6J background have been previously described^{3 (link), 4 (link)}. Mice were group housed (1–5 mice per cage) in a barrier facility at 23°C unless otherwise noted. Mice were provided Harlan Teklad 2016 chow diet and water ad libitum unless otherwise noted. High-fat/high-sucrose (HFHS; Research Diets D12331) diet, if applicable, was removed and refilled weekly. Mice losing >10% of body weight during the acclimation period for metabolic cage studies (see below) or post-surgery prior to clamp studies (see below) were not studied. Body composition was measured using NMR (Bruker Mini-Spec).

Berglund E.D., Liu T., Kong X., Sohn J.W., Vong L., Deng Z., Lee C.E., Lee S., Williams K.W., Olson D.P., Scherer P.E., Lowell B.B, & Elmquist J.K. (2014). Melanocortin 4 receptors in autonomic neurons regulate thermogenesis and glycemia. Nature neuroscience, 17(7), 911-913.

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High-fat, high-carb diet in mice

Cited 1 time

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C57Bl/6 mice pups (37 of each sex) were obtained from Harlan Laboratories S.R.L. (S.Piero al Natisone, Italy). Immediately after weaning, animals were randomly group-housed in cages in a temperature-controlled environment (22±2°C) and on a 12 hours light/dark schedule, and fed ad-libitum with control diet (CTRL, D12328, Research Diets, New Brunswick, NJ) or HFHC diet (HFHC: D12331, Research Diets, New Brunswick, NJ), plus 42g/L fructose/sucrose in drinking water, for a total of 16 weeks [25 (link)]. Four experimental checkpoints were established (4, 8, 12 and 16 weeks of diet), in which part of the animals was sacrificed. Animal care and procedures were conducted in accordance with the Italian Law (decree 116–92) and by European Community directive 86-609-EEC. All experimental protocol were approved by the local committee of the Medical Research Institute and by the National Authority (Ministero della Salute—Direzione generale della sanità animale e dei farmaci veterinari—Ufficio VI, Rome, Italy, under the Article 7, D.lgs 116/92). The maximal effort was done to reduce the number of animals used and their sufferance in the respect of the 3R rule.

Marin V., Rosso N., Dal Ben M., Raseni A., Boschelle M., Degrassi C., Nemeckova I., Nachtigal P., Avellini C., Tiribelli C, & Gazzin S. (2016). An Animal Model for the Juvenile Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis. PLoS ONE, 11(7), e0158817.

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Conditional Deletion of Mcu in Beta Cells

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Two to five C57BL/6 J mice were housed per individually ventilated cage in a pathogen-free facility with a 12 h light-dark cycle and were fed ad libitum with a standard mouse chow diet (Research Diets, New Brunswick, NJ, USA) unless otherwise stated. For high-fat high-sucrose diet (HFHS) treatment (58% [wt/wt] fat and sucrose content; D12331; Research Diets), mice were placed on the diet at 5–6 weeks of age for 4 weeks prior to analysis. All in vivo procedures were approved by the UK Home Office, according to the Animals (Scientific Procedures) Act 1986.
In brief, C57BL/6 J mice bearing Mcu alleles with floxP sites flanking exons 11 and 12 were generated by GenOway (strain B6-Mcu^tm1Geno; Grenoble, France) and bred to animals carrying Cre recombinase inserted at the Ins1 locus (Ins1^Cre), allowing efficient and beta cell-selective deletion of both Mcu splice variants, without recombination in the brain or confounding expression of human growth hormone. Mice bearing floxed Mcu alleles but lacking Cre recombinase were used as wild-type (WT) littermate controls. Possession of Ins1Cre alleles alone exerted no effect on glycaemic phenotype (data not shown).

Georgiadou E., Haythorne E., Dickerson M.T., Lopez-Noriega L., Pullen T.J., da Silva Xavier G., Davis S.P., Martinez-Sanchez A., Semplici F., Rizzuto R., McGinty J.A., French P.M., Cane M.C., Jacobson D.A., Leclerc I, & Rutter G.A. (2020). The pore-forming subunit MCU of the mitochondrial Ca2+ uniporter is required for normal glucose-stimulated insulin secretion in vitro and in vivo in mice. Diabetologia, 63(7), 1368-1381.

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