Hf diet

Manufactured by Research Diets

Sourced in United States

The HF diet is a laboratory animal diet formulated to provide a high-fat content. The diet is designed to support research studies that require a high-fat dietary regimen.

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Lab products found in correlation

Collagenase, by Merck Group (3 mentions) Nupage gel, by Thermo Fisher Scientific (3 mentions) Superscript 3 reverse transcriptase, by Thermo Fisher Scientific (3 mentions) Oligo dt 12 18 primer, by Thermo Fisher Scientific (3 mentions) Mouse diabetes multiplex assay kit, by Bio-Rad (2 mentions) Anti ucp1 antibody, by Abcam (2 mentions) Pe conjugated anti sca 1 or pdgfrα antibodies, by R&D Systems (2 mentions) Fitc conjugated antibody against cd29 or cd34, by Abcam (2 mentions) Mouse estradiol elisa kit, by Abcam (2 mentions) Anti gapdh antibody, by Santa Cruz Biotechnology (2 mentions) Insulin, by Merck Group (2 mentions) Dulbecco s modified eagle s medium dmem, by Merck Group (2 mentions) β actin protein, by Cell Signaling Technology (1 mentions) Anti sirt1, by Santa Cruz Biotechnology (1 mentions) Resveratrol rsv, by Merck Group (1 mentions) Lpl activity assay kit, by Cell Biolabs (1 mentions) F 12k medium, by Thermo Fisher Scientific (1 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (1 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (1 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (1 mentions)

6 protocols using hf diet

Evaluating Adipogenic Regulators in Cells

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Rosiglitazone (ROSI), GW9662, resveratrol (RSV), and 6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide (EX-527) were from Sigma (St. Louis, MO). Anti-LPL antibody was from GeneTex (Irvine, CA). The LPL activity assay kit was from Cell Biolabs, Inc. (San Diego, CA). Antibodies for PPARγ, fatty acid synthase (FASN), and β-actin proteins were from Cell Signaling Technology, Inc. (Danvers, MA). Anti-SIRT1, CCAAT/enhancer binding protein-α (C/EBPα), and SREBP1c antibodies were from Santa Cruz Biotechnology (Dallas, TX). FBS, penicillin-streptomycin, DMEM, and F-12K medium were from Invitrogen (Carlsbad, CA). HF diet (60 kcal% from fat, 20 kcal% from protein, 20 kcal% from carbohydrate, energy density 5.24 kcal/g; catalog number D12492) was from Research Diets, Inc. (New Brunswick, NJ). Regular chow (17 kcal% from fat, 25 kcal% from protein, 58 kcal% from carbohydrate, energy density 3.1 kcal/g; catalog number 7912) was from Harlan Laboratories (Madison, WI).

Qiao L., Guo Z., Bosco C., Guidotti S., Wang Y., Wang M., Parast M., Schaack J., Hay WW J.r., Moore T.R, & Shao J. (2015). Maternal High-Fat Feeding Increases Placental Lipoprotein Lipase Activity by Reducing SIRT1 Expression in Mice. Diabetes, 64(9), 3111-3120.

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Chemogenetic Modulation of Locomotion

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Mice were injected with VEH or CNO between 8–9AM once daily for five consecutive days in home cages while fed ad lib standard chow (Harlan Teklad 7913). Food, water, and body weight were weighed prior to the morning injection and again between 5–6pm. A cross-over study design was used, thus each animal received both VEH and CNO over the course of two separate experiments, with 24 hr between studies. On day 5, locomotor activity was assessed in CPP chambers described below. Animals were randomly assigned to one side of the chamber and were allowed to acclimate for 30 min. Following acclimation, they received VEH or CNO and locomotor activity was measured by laser beam breaks for 1 hr. HF-Diet Experiments: As above, mice were injected once daily with VEH or CNO between 8–9AM in home cages with ad lib access to high fat, high sugar diet (HF diet, D12451, Research Diets). Mice received 24 hr of access to HF diet prior to the study. On day 5, locomotor activity was assessed as described above, and injections were given for 10 consecutive days to allow time for weight gain. These experiments also used a cross-over design, with 2 wk between experiments during which mice only had access to standard chow.

Woodworth H.L., Beekly B.G., Batchelor H.M., Bugescu R., Perez-Bonilla P., Schroeder L.E, & Leinninger G.M. (2017). Lateral hypothalamic neurotensin neurons orchestrate dual weight loss behaviors via distinct mechanisms. Cell reports, 21(11), 3116-3128.

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Cilostazol Treatment in Type 2 Diabetes Mice

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Male BALB/c mice were obtained from the National Laboratory Animal Breeding and Research Center (Taipei, Taiwan). To induce type 2 diabetes mellitus, the mice were housed in laboratory cages and fed with a high-fat (HF) diet (40% fat, Research Diets, Inc., NJ, USA) [14 (link)] for 3 weeks. Subsequently, the mice received 75 mg/kg and 150 mg/kg of intravenous STZ, 5 days apart. Feed was not withheld from any of the animals at the time of STZ administration. After induction, blood glucose was measured daily by tail-vein sampling using a ACCUCHEK glucometer (Roche, Basel, Switzerland). Animals with a blood glucose level more than 11.1 mmol/L (200 mg/dL) were included in this study. Six mice were treated with cilostazol for 2 months, where cilostazol was diluted from 0.5% CMC (carboxymethyl cellulose sodium salt), which was used as a vehicle control. Another six mice were treated with 0.5% CMC for 2 months. Finally, the animals were sacrificed and blood and ascending aorta samples were taken. The Animal Ethics Board of National Defense Medical Center (Taipei, Taiwan) approved all animal experimental procedures.

Su S.C., Hung Y.J., Huang C.L., Shieh Y.S., Chien C.Y., Chiang C.F., Liu J.S., Lu C.H., Hsieh C.H., Lin C.M, & Lee C.H. (2019). Cilostazol inhibits hyperglucose-induced vascular smooth muscle cell dysfunction by modulating the RAGE/ERK/NF-κB signaling pathways. Journal of Biomedical Science, 26, 68.

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Adipocyte Differentiation Characterization

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Glucose, insulin, T3, collagenase and Dulbecco’s modified Eagle’s medium (DMEM) were from Sigma-Aldrich (St. Louis, MO). Antibody against estrogen receptor α (ERα) and PE-conjugated anti-Sca-1 or PDGFRα antibodies were from R&D System (Minneapolis, MN). The anti-UCP1 antibody, FITC-conjugated antibody against CD29 or CD34, and mouse estradiol ELISA kit were purchased from the Abcam (Cambridge, MA). Anti-GAPDH antibody was from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA). NuPAGE gels, SuperScript III reverse transcriptase and oligo(dT)_12–18 primers were from Invitrogen (Carlsbad, CA). The mouse diabetes multiplex assay kit was from Bio-Rad (Hercules, CA). HF diet (60 kCal% from fat, 20 kCal% from protein, 20 kCal% from carbohydrate, energy density: 5.24 kCal/g, catalog number D12492) was from Research Diets, Inc (New Brunswick, NJ). Regular chow (17 kCal% from fat, 25 kCal% from protein, 58 kCal% from carbohydrate, energy density: 3.1 kCal/g, catalog number 7912) was from Harlan Laboratories (Madison, WI).

Qiao L., Chu K., Wattez J.S., Lee S., Gao H., Feng G.S., Hay WW J.r, & Shao J. (2019). High-fat Feeding Reprograms Maternal Energy Metabolism and Induces Long-term Postpartum Obesity in Mice. International journal of obesity (2005), 43(9), 1747-1758.

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Adipocyte Differentiation Characterization

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Antibody-Based Protein Analysis for AKT Signaling

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Antibodies against AKT and phospho-AKT (Ser473) were from Cell Signaling (Danvers, MA). Anti-GAPDH and horseradish peroxidase–linked secondary antibodies were from Santa Cruz Biotechnology (Santa Cruz, CA). Glucose, Glucose oxidase, collagenase, and RPMI medium were from Sigma-Aldrich (St. Louis, MO). Free FA (FFA) and TG assay kits ware purchased from Wako Diagnostics (Richmond, VA). The LipidTOX green neutral lipid stain, NuPAGE gels, SuperScript III reverse transcriptase, and oligo(dT)_12–18 primer were from Invitrogen (Carlsbad, CA). The ultrasensitive mouse insulin ELISA kit was from ALPCO (Salem, NH). The anti-insulin and anti-glucagon antibodies were from Abcam (Cambridge, MA). HF diet (60 kcal% from fat; catalog number D12492) was from Research Diets (New Brunswick, NJ). The control diet (CD) (17 kcal% from fat, catalog number 7912) was from Harlan Laboratories (Madison, WI).

Qiao L., Wattez J.S., Lim L., Rozance P.J., Hay WW J.r, & Shao J. (2019). Prolonged Prepregnant Maternal High-Fat Feeding Reduces Fetal and Neonatal Blood Glucose Concentrations by Enhancing Fetal β-Cell Development in C57BL/6 Mice. Diabetes, 68(8), 1604-1613.

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