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F3666

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The F3666 is a laboratory equipment product manufactured by Bio-Serv. It is designed to perform a core function within the laboratory setting, but a detailed description cannot be provided while maintaining an unbiased and factual approach without extrapolation.

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Lab products found in correlation

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30 protocols using f3666

1

Early Weaning and Ketogenic Diets in Animal Models

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Experimental rd10 and WT animals were early weaned at PD14/15 and provided either standard chow, a ketogenic diet, or a ketogenic & low-protein diet. To control for early weaning, additional rd10 and WT animals were weaned at the standard PD21 timepoint and provided standard chow. All groups are listed in Table 1. Table 2 lists fat, protein, and carbohydrate percentages (by weight) for each diet. Both ketogenic diets had high fat content (>65% by weight) and low carbohydrate content (<3.5%), but varied in protein content. We chose one diet that meets minimum protein requirements for mice (∼15%),23 which will be referred to as the ketogenic diet, and one diet with a low protein content (∼8%), which will be referred to as a ketogenic & low-protein diet. Table 3 lists fatty acid composition for the two different ketogenic diets. Standard chow, PicoLab Laboratory Rodent Diet 5L0D (LabDiet, St. Louis, MO, USA), was provided by the OHSU Department of Comparative Medicine. The ketogenic diet was purchased from ENVIGO (TD.96355; Madison, WI, USA). The ketogenic & low-protein diet was purchased from BioServ (F3666; Flemington, NJ, USA). In addition to the low protein content, the BioServ F3666 diet is reported to have low choline and methionine levels.24 (link) All diets were administered daily, so animals could eat ad libitum. Water was also available ad libitum.
Ryals R.C., Huang S.J., Wafai D., Bernert C., Steele W., Six M., Bonthala S., Titus H., Yang P., Gillingham M, & Pennesi M.E. (2020). A Ketogenic & Low-Protein Diet Slows Retinal Degeneration in rd10 Mice. Translational Vision Science & Technology, 9(11), 18.
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2

Creb3l3 Knockout Mice Experiments

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C57BL/6 mice were obtained from the Jackson Laboratory. Creb3l3−/− mice have been previously described (24 , 27 (link)). Mice were fed a standard chow diet containing 13.2% fat, 24.6% protein and 62.1% carbohydrate (kcal/100 kcal) (#5053, LabDiet), a ketogenic diet (F-3666, Bio-Serv) or a methionine and choline deficient diet (#960439, ICN Biomedicals). All animal experiments were approved by the Weill Cornell Medical College Institutional Animal Care and Use Committee.
Xu X., Park J.G., So J.S, & Lee A.H. (2015). Transcriptional activation of Fsp27 by the liver-enriched transcription factor CREBH promotes lipid droplet growth and hepatic steatosis. Hepatology (Baltimore, Md.), 61(3), 857-869.
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3

Animal Models of Neurological Disorders

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All animal procedures were conducted in accordance with protocols approved by the Legacy Institutional Animal Care and Use Committee (IACUC) and the principles outlined in the NIH Guide for the Care and Use of Laboratory Animals. All studies were performed in adult male CD-1 mice or Wistar rats (Charles River Laboratories, Wilmington, MA, USA). Pentylenetetrazole, pilocarpine, scopolamine, and valproic acid (all from Sigma Aldrich, St. Louis, MO, USA) were dissolved in 0.9% w/v saline to achieve the desired dosages via the intraperitoneal (i.p.) or subcutaneous (s.c.) routes. Ketogenic diet (KD: 8.6% protein w/w, 75.1% fat w/w, 3.2% carbohydrates w/w) for rodents was obtained from Bio-Serv (#F3666, Bio-Serv, Frenchtown, NJ, USA) and supplied ad libitum. Caloric composition of the KD is: 93.4% fat, 4.7% protein, and 1.8% carbohydrates. Standard chow (control diet, CD) with a caloric composition of 13.5% fat, 28.5% protein, and 58.0% carbohydrates was used in control animals or after diet reversal.
Lusardi T.A., Akula K.K., Coffman S.Q., Ruskin D., Masino S.A, & Boison D. (2015). Ketogenic Diet Prevents Epileptogenesis and Disease Progression in Adult Mice and Rats. Neuropharmacology, 99, 500-509.
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4

Ketogenic Diet Effects on BTBR Mice

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BTBR mice were obtained from the Jackson Laboratory (Bar Harbor, ME, USA) and a breeding colony has been maintained at the Health Sciences Animal Resource Center at University of Calgary. Detail animal protocol is presented in the schematic diagram (Figure 1A). The mice were born and reared in a quiet, temperature-controlled room and entrained to a 12-hour light-dark cycle. After weaning at postnatal day 21 (PD21), the mice were placed on either standard diet (SD) or ketogenic diet (KD; 6.3:1 ratio by weight of fat to carbohydrate plus protein; Bio-Serv F3666, Frenchtown, NJ, USA) for 10-14 days [73 (link),74 (link)] based on our previous experiments [38 (link),45 (link)]. F3666 is a ketogenic chow composed of lard, butter, corn oil, casein, cellulose, mineral mix, vitamin mix, and dextrose. This particular fomulation is rich in saturated fats [75 (link)]. Body weight was measured weekly the KD treatment (Figure 1). After dietary intervention, whole blood was analyzed for glucose and circulating ketone bodies (β-hydroxybutyrate) with Precision Xtra meters (Abbott Laboratories, Chicago, IL, USA) before animals were sacrificed. All experiments were performed around PD35. Only male mice were used. All procedures were carried out in accordance with the Canadian Animal Care Committee and approved by the University of Calgary Animal Care Committee under the protocol AC17-0217.
Ahn Y., Sabouny R., Villa B.R., Yee N.C., Mychasiuk R., Uddin G.M., Rho J.M, & Shutt T.E. (2020). Aberrant Mitochondrial Morphology and Function in the BTBR Mouse Model of Autism Is Improved by Two Weeks of Ketogenic Diet. International Journal of Molecular Sciences, 21(9), 3266.
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5

Ketogenic Diet Effects on Seizure Threshold

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On P21, 110 male mice were randomly assigned to one of three experimental groups. Group 1 mice were randomly weaned onto either a standard diet (SD) or one of three KD diets with ratios of 1:1, 3:1 or 6.3:1 (fat to carbohydrates plus proteins see Table 1 for nutritional content; Bio-Serv F3666, Frenchtown, NJ, U.S.A.) for 13-18 days. Group 2 mice were weaned onto an SD for 13-29 days. On the experimental day, four hours prior to flurothyl-exposure, Group 2 mice were intraperitoneal-injected (i.p.) with vehicle (1% carboxymethylcellulose in saline) or vehicle-pioglitazone (0.1, 1, 10, 80 mg/kg)7 (link). Group 3 mice were randomly weaned onto either SD or a 1:1 KD for 12-16 days. On the experimental day, four hours prior to flurothyl-exposure, Group 3 mice were injected i.p. with vehicle (1% carboxymethylcellulose in saline) or pioglitazone (0.1, 1, 10, 80 mg/kg in 1% carboxymethylcellulose in saline).
Simeone T.A., Matthews S.A, & Simeone K.A. (2017). Synergistic protection against acute flurothyl–induced seizures by adjuvant treatment of the ketogenic diet with the Type II Diabetes drug pioglitazone. Epilepsia, 58(8), 1440-1450.
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6

Dietary Impacts on Mouse Neurodevelopment

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All experimental protocols were in compliance with the ethical standards approved by the University of Calgary Animal Care and Use Committee. Juvenile male C57BL/6 (B6) and BTBRT + tf/j mice (n = 21 and 25, respectively) were age-matched to 5 weeks of age before being randomly selected for implementation of a standard chow (CH, 13 % kcal fat) or ketogenic diet (KD, 75 % kcal fat; Bio-Serv F3666, Frenchtown, USA) for 10–14 days. The time point of 7 weeks of age for both B6 and BTBR mice was established to ensure both cohorts were post-pubertal in development [11 ]. Prior to sacrifice, the animals were housed in a humidity-controlled room with a 12-h light/dark zeitgeber cycle and were fed ad libitum. Following 10–14 days of dietary intervention, the mice were sacrificed by cervical dislocation. At the time of sacrifice, the animals were 7 weeks of age.
Newell C., Bomhof M.R., Reimer R.A., Hittel D.S., Rho J.M, & Shearer J. (2016). Ketogenic diet modifies the gut microbiota in a murine model of autism spectrum disorder. Molecular Autism, 7(1), 37.
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7

Dietary Manipulation in C3HeB/FeJ Mice

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C3HeB/FeJ KO mice and WT mice were reared in a quiet room on a 12-hr light/dark cycle (lights on at Zeitgeber time (ZT) 00:00 hr) in Creighton University's animal resource facility and provided food and water ad libitum. Genotype was determined from tail clips by Transnetyx, Inc (Cordova, TN, USA). KO mice and their wild-type (WT) littermates were weaned onto either a standard diet (SD) or a KD (6.3:1, fat to carbohydrates plus proteins; Bio-Serv F3666, Frenchtown, NJ, U.S.A.) at P21. Experiments were conducted in accordance with the guidelines of the National Institutes of Health and approved by the Institutional Animal Care and Use Committee.
Iyer S.H., Matthews S.A., Simeone T.A., Maganti R, & Simeone K.A. (2017). Accumulation of rest deficiency precedes sudden death of epileptic Kv1.1 knockout mice, a model of SUDEP. Epilepsia, 59(1), 92-105.
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8

Xenograft Tumor Modeling and Diet Impact

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Subcutaneous xenograft tumors were generated for A375R1 and UCSD354 cell lines with 3 × 106 cells/animal in the right flank of NOD scid gamma (NSG) mice. The mice were separated into two diet cohorts—regular diet (caloric profile of 62.1% carbohydrate, 24.7% protein, 13.2% fat) (PicoLab #5053), and high-fat ketogenic diet (caloric profile of 1.8% carbohydrate, 4.7% protein, 93% fat) (Bio-Serv #F3666). Inhibitor treatments were performed by oral gavage daily once for the indicated number of days. Tumor volumes and mice weight were recorded every 3 days. Animals were excluded if they showed overt toxicity or lost > 15% body weight over the treatment course. For molecular analysis of inhibitor effects, tumor-bearing mice were treated with the inhibitors as above, and tumors were harvested 3 h after drug administration on the second day of treatment. All animal experiments were approved by the Institutional Animal Care and Use Committee.
de Groot E., Varghese S., Tan L., Knighton B., Sobieski M., Nguyen N., Park Y.S., Powell R., Lorenzi P.L., Zheng B., Stephan C, & Gopal Y.N. (2022). Combined inhibition of HMGCoA reductase and mitochondrial complex I induces tumor regression of BRAF inhibitor-resistant melanomas. Cancer & Metabolism, 10, 6.
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9

Ketogenic Diet Effects on Wild-Type Mice

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All animal experiments were approved by the Institutional Animal Care and Use Committee (IACUC) at Pennington Biomedical Research Center. Male C57BL/6J wild-type mice 8-12 weeks of age were fed a KD (Bio-Serv; F3666; 3% carbohydrate, 5% protein, 92% fat) ad lib for either 7 days (7d-KD) or 21 days (21d-KD). Littermate controls (7d-Chow; 21d-Chow) were fed Purina 5001 Rodent Laboratory Chow (58% carbohydrate, 29% protein, 13% fat).
Morrison C.D., Hill C.M., DuVall M.A., Coulter C.E., Gosey J.L., Herrera M.J., Maisano L.E., Sikaffy H.X, & McDougal D.H. (2020). Consuming a ketogenic diet leads to altered hypoglycemic counter-regulation in mice.. Journal of diabetes and its complications, 34(5), 107557.
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10

Ketogenic Diet in Epileptic Mice

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Spontaneously epileptic KO mice were generated using heterozygous breeding pairs in the animal facility at the Barrow Neurological Institute (BNI). Pups were genotyped by PCR analysis of tail genomic DNA. After weaning at postnatal day (PD) 18–21, mice were fed either a ketogenic (KD) Bio-Serv F3666 diet (Flemington, New Jersey, USA; 6.3:1 ratio of fats to carbohydrate plus protein by gross weight) or normal standard diet [SD, % of calories: 17 (fat), 18 (protein), 63 (Carbohydrate)]. It should be noted that the macronutrient composition of the SD compared to Western diet [30–35% fat] is somewhat different. All animal handling protocol was approved by the Institutional Animal Care and Use Committee at the BNI and St. Joseph’s Hospital & Medical Center.
Chun K.C., Ma S.C., Oh H., Rho J.M, & Kim D.Y. (2017). Ketogenic diet-induced extension of longevity in epileptic Kcna1-null mice is influenced by gender and age at treatment onset. Epilepsy research, 140, 53-55.
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