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Db db mice

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Db/db mice are a type of genetically modified mouse model that exhibit symptoms of type 2 diabetes. These mice have a mutation in the leptin receptor gene, which leads to obesity, hyperglycemia, and other metabolic abnormalities associated with the disease.

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Lab products found in correlation

C57bl 6 mice, by Jackson ImmunoResearch (5 mentions) D12492, by Research Diets (4 mentions) Ob ob mice, by Jackson ImmunoResearch (4 mentions) C57bl 6, by Jackson ImmunoResearch (3 mentions) C57bl 6j wt mice, by Jackson ImmunoResearch (3 mentions) Fluoview fv1000 confocal microscope, by Olympus (2 mentions) Lna anti mir, by Qiagen (2 mentions) C57bl 6j mice, by Research Diets (2 mentions) C57bl 6j, by Jackson ImmunoResearch (2 mentions) S0130, by Merck Group (1 mentions) H21492, by Thermo Fisher Scientific (1 mentions) Dia 310, by Dianova (1 mentions) Tegaderm, by 3M (1 mentions) Bks cg dock7m leprdb j, by Jackson ImmunoResearch (1 mentions) D03012908, by Research Diets (1 mentions) Wild type mice, by Jackson ImmunoResearch (1 mentions) Streptozotocin (stz), by Merck Group (1 mentions) Cd31 microbeads kit, by Miltenyi Biotec (1 mentions) Paris kit, by Merck Group (1 mentions) Apoe mice, by Jackson ImmunoResearch (1 mentions)

Spelling variants of this product

C57BKS.Cg-m/Leprdb/J (Db) mice (4 citations) C57BLKS db/db mice (3 citations) T2DM db/db mice (3 citations) Control db/+ mice (3 citations) B6.Cg-m+/+Leprdb/J (db/db) mice (3 citations) C57BL/KsJ-db/db mice (3 citations) Male db/db and db/+ mice (2 citations) Homozygous db/db mice (2 citations) BKS-Cg-Dock7m +/+ Lepr db/J heterozygous (db/+) mice (2 citations) C57BKS.Cg-m+/+Leprdb/J mice (db/db), (2 citations)

60 protocols using db db mice

1

Diabetic Wound Healing Protocols

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All animal studies were carried out according to the protocol approved by the Animal and Care Committee at the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Db/db mice were purchased from Jackson Laboratory. Streptozotocin‐induced diabetic mice were generated as previously described (Sawaya et al, 2020 (link)). Both male and female mice were used in the wound healing studies. Treatments were performed at 7–9 weeks of age and all experiments were conducted using littermate controls.
Sawaya A.P., Stone R.C., Mehdizadeh S., Pastar I., Worrell S., Balukoff N.C., Kaplan M.J., Tomic‐Canic M, & Morasso M.I. (2022). FOXM1 network in association with TREM1 suppression regulates NET formation in diabetic foot ulcers. EMBO Reports, 23(8), e54558.
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2

Unilateral Nephrectomy and STZ-Induced Diabetes

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Wild-type male C57BL/6 mice were purchased from Shandong University Experimental Animal Center (Jinan, China). Tim-3 TALEN (Tim-3KO) mice were generated by SiDanSai Biotechnology Company (Shanghai, China) [26] (link), and db/db mice were obtained from the Jackson laboratory (Nevada, USA). During the experiments, all mice were housed in a controlled environment with unrestricted access to food and water in accordance with the Institutional Animal Care and Use Committee procedures of Shandong University.
Mice underwent unilateral nephrectomy (Unx) with intrarenal delivery with shTim-3-lv or ctrl-lv (2 × 106 IU/kidney) to the intact kidney [27] (link), [28] . The detailed procedure is presented in the Supplementary Materials and Methods. After one-week recovery from unilateral nephrectomy, mice rendered diabetic were induced by intraperitoneal (I.P) injection of STZ (S0130, Sigma, St. Louis, MO, USA) at a dose 50 mg per kg body weight in sodium citrate buffer as previously described [29] (link).
Yang H., Xie T., Li D., Du X., Wang T., Li C., Song X., Xu L., Yi F., Liang X., Gao L., Yang X, & Ma C. (2019). Tim-3 aggravates podocyte injury in diabetic nephropathy by promoting macrophage activation via the NF-κB/TNF-α pathway. Molecular Metabolism, 23, 24-36.
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3

Oxidative Stress in Diabetic Mice

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Protocols for animal care and experimentation were approved by the Institutional Animal Care and Use Committee of the University of Utah. UCP-DTA and littermate control mice (WT) were bred and maintained at the University of Utah until the ages of 13 or 24 weeks. UCP-DTA mice are on the FVB genetic background. Db/db mice and their WT controls were obtained from The Jackson Laboratory and maintained until 9 weeks of age. Db/db mice are on the C57BL/6J genetic background. All mice were kept in temperature-controlled animal facilities (21–23°C) on 12h light (6:00AM – 6:00PM) and 12h dark cycle and fed standard chow diet (#8656 Harlan Teklad, Madison, WI) ad libitum. MnTBAP [Mn (III) tetrakis (4-benzoic acid) porphyrin chloride solution in alkalized saline (VWR, PA) was administered intraperitoneally to UCP-DTA and wildtype littermate controls (WT) at 20mg/kg, 3 times/week for 4 weeks starting at the age of 9 or 20 weeks. For Db/db mice, MnTBAP was administered 3 times/week for 3–4 weeks starting at the age of 6 weeks.
Ilkun O., Wilde N., Tunei J., Pires K.M., Zhu Y., Bugger H., Soto J., Wayment B., Olsen C., Litwin S.E, & Abel E.D. (2015). Antioxidant treatment normalizes mitochondrial energetics and myocardial insulin sensitivity independently of changes in systemic metabolic homeostasis in a mouse model of the metabolic syndrome. Journal of molecular and cellular cardiology, 85, 104-116.
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4

Wound Healing in Diabetic Mice

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Animal protocols were approved by the Laboratory Animal Care at Harvard Medical School and Brigham and Women’s Hospital. For mouse dermal wound studies, male, 8–10 weeks old, db/db mice (Jackson Laboratories) were used for local intradermal injections of either scrambled control LNA-anti-miR or LNA-anti-miR-615–5p (Exiqon, Inc) at 0.63 mg/kg 48h and 24h prior to surgery. On day 0, dorsal full thickness skin wounds (1cm2) were generated and covered with semi-occlusive dressing (Tegaderm). Images of the wounds were immediately acquired after surgery (day 0) and on day 9 following the removal of the Tegaderm dressing. Mice were euthanized 9 days post-surgery and the 1×1 cm2 sections of skin surrounding the wound were excised down to fascia. Angiogenesis in wounds was analyzed by mouse CD31 staining (DIA-310; Dianova, Inc) and DAPI (H21492; Invitrogen, Inc) of the paraffin embedded wound sections. Granulation tissue thickness was measured on day 9 using H&E stained sections obtained from the center of the wound. Granulation tissue thickness is defined as the distance of intact tissue from the bottom of the epidermis to the top of the subcutaneous fat layer and was quantified using Image J. Maximal thickness of granulation tissue was quantified at a fixed distance 200 micrometers from the wound edge. Fluorescent images were acquired by Olympus Fluoview FV1000 confocal microscope.
Icli B., Wu W., Ozdemir D., Li H., Cheng H.S., Haemmig S., Liu X., Giatsidis G., Avci S.N., Lee N., Guimaraes R.B., Manica A., Marchini J.F., Rynning S.E., Risnes I., Hollan I., Croce K., Yang X., Orgill D.P, & Feinberg M.W. (2019). MicroRNA-615-5p regulates angiogenesis and tissue repair by targeting AKT/eNOS signaling in endothelial cells. Arteriosclerosis, thrombosis, and vascular biology, 39(7), 1458-1474.
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5

Dual Transgenic Mouse Model Study

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All experiments were conducted in accord with the National Institutes of Health (NIH) Guide for the Care and Use of Laboratory Animals and approved and monitored by the Georgia Regents University Institutional Animal Care and Use Committee (Augusta, GA). Two parental strains of male mice were used in these studies: leptin receptor mutant db/db mice bred on a C57/Bl6 background (#000697; The Jackson Laboratory, Bar Harbor, ME) and myostatin‐null mice bred on an Institute for Cancer Research background (gift of Dr Se‐Jin Lee). Because db/db mice are sterile, progeny were generated from dual heterozygotes (heterozygous for mutant leptin receptor and myostatin deletion). Mice heterozygous for each gene were used, and littermates served as controls to minimize any residual background effects from the founder strains.
Qiu S., Mintz J.D., Salet C.D., Han W., Giannis A., Chen F., Yu Y., Su Y., Fulton D.J, & Stepp D.W. (2014). Increasing Muscle Mass Improves Vascular Function in Obese (db/db) Mice. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 3(3), e000854.
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6

Sciatic Nerve Isolation from Mice

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Mice and rats were housed at the Animal unit at CIC bioGUNE (AAALAC-accredited facility). All procedures were approved by the institutional committee on animal use. Sciatic nerves were isolated from C57 BL6/J mice at newborn (NB), post-natal day 10 (P10) and P60 ages. Gnmt−/− mice were described previously(Martinez-Chantar et al., 2008 (link)) and nerves isolated at P90. Db/db mice, as described previously(Pande et al., 2011 (link)), were purchased from Jackson Laboratories and nerves extracted at P180. Nerves from mice of either sex were used. Immediately after isolation, nerves were desheathed and flash-frozen in liquid nitrogen.
Varela-Rey M., Iruarrizaga-Lejarreta M., Lozano J.J., Aransay A.M., Fernandez A.F., Lavin J.L., Mósen-Ansorena D., Berdasco M., Turmaine M., Luka Z., Wagner C., Lu S.C., Esteller M., Mirsky R., Jessen K.R., Fraga M.F., Martínez-Chantar M.L., Mato J.M, & Woodhoo A. (2014). S-adenosylmethionine levels regulate the Schwann cell DNA methylome. Neuron, 81(5), 1024-1039.
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7

High-Fat Diet Feeding in Mice

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All animal experiments were performed according to procedures approved by the Ulsan National Institute of Science and Technology’s Institutional Animal Care and Use Committee. Five-week-old male C57BL/6J mice (DBL, Chungbuk, Korea) were fed a high-fat diet (60% kcal fat, D12492, Research Diets Inc., New Brunswick, NJ, USA) for 8 weeks. The db/db mice used in this study were purchased from the Jackson Laboratory (Bar Harbor, ME, USA).
Khim K.W., Choi S.S., Jang H.J., Lee Y.H., Lee E., Hyun J.M., Eom H.J., Yoon S., Choi J.W., Park T.E., Nam D, & Choi J.H. (2020). PPM1A Controls Diabetic Gene Programming through Directly Dephosphorylating PPARγ at Ser273. Cells, 9(2), 343.
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8

Wound Healing in Diabetic Mice Using 3D Spheroids

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DB/DB mice (13 weeks old;
female; body weight, 43.1 ± 2.6 g)
were purchased from Jackson Laboratory. The animals were randomly
divided into three groups. The excisional wound-splinting model was
established as described previously.6 (link) First,
two 6 mm full-thickness excisional skin wounds were created on each
side of the midline of the dorsal skin after hair removal and anesthesia.
Each wound received 1.0 × 106 cells from the monolayer
or 3D spheroids encapsulated in 80 μL of the hydrogel. As the
control group, the equal numbers of single cells were dropped into
the wound bed directly without being embedded in the hydrogel. Then,
the donut-shaped silicone splint was placed and fixed on the skin
by the adhesive and interrupted sutures. Finally, Tegaderm (3M, London,
ON, Canada) was placed over the wound to avoid contamination. The
animals were housed individually and observed at week(s) 0, 1, 2,
and 3.
Yang M., He S., Su Z., Yang Z., Liang X, & Wu Y. (2020). Thermosensitive Injectable Chitosan/Collagen/β-Glycerophosphate Composite Hydrogels for Enhancing Wound Healing by Encapsulating Mesenchymal Stem Cell Spheroids. ACS Omega, 5(33), 21015-21023.
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9

Liver-Specific PTG Overexpression in Diabetic Mice

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All procedures were approved by the Barcelona Science Park’s Animal Experimentation Committee and were carried out following the European Community Council Directive and the National Institute of Health guidelines for the care and use of laboratory animals. Db/db mice (strain name BKS.Cg-Dock7m +/+ Leprdb/J) were purchased from the Jackson Lab. The Db/db mice were backcrossed to C57BL/6J for 8 generations and then mated with Cre-Albumin mice on the C57BL/6J background that overexpressed hepatic PTG. Mice overexpressing PTG specifically in the liver were generated as previously described (8 (link), 11 (link)). Heterozygous db/+ mice were used as controls. Since the PTG expression cassette was introduced into the Hprt locus in the X chromosome (8 (link)), and to avoid variability due to female X chromosome inactivation, all the studies were conducted in male animals. All the mice studied were littermates. Animals were sacrificed at 18 weeks of age under ad libitum-fed conditions between 8 and 10 a.m. by cervical dislocation, and tissues were collected and frozen in liquid nitrogen. Whole blood was collected from tails in EDTA-coated tubes and then centrifuged, and plasma was stored at –20°C for analysis.
López-Soldado I., Guinovart J.J, & Duran J. (2022). Hepatic overexpression of protein targeting to glycogen attenuates obesity and improves hyperglycemia in db/db mice. Frontiers in Endocrinology, 13, 969924.
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10

Investigating Diabetic Mouse Models

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All protocols concerning animal use (no. 2016N000182) were approved by the IACUC at Brigham and Women’s Hospital and Harvard Medical School and conducted in accordance with the Guide for the Care and Use of Laboratory Animals (National Academies Press, 2011). Animal studies were performed in male db/+ or db/db mice (The Jackson Laboratory). All patient samples (25 (link), 50 (link)) conform to the principles outlined in the Declaration of Helsinki and were approved by the IRB of Brigham and Women’s Hospital. All participants have given written consent to the inclusion in the study.
Cheng H.S., Pérez-Cremades D., Zhuang R., Jamaiyar A., Wu W., Chen J., Tzani A., Stone L., Plutzky J., Ryan T.E., Goodney P.P., Creager M.A., Sabatine M.S., Bonaca M.P, & Feinberg M.W. (2023). Impaired angiogenesis in diabetic critical limb ischemia is mediated by a miR-130b/INHBA signaling axis. JCI Insight, 8(10), e163041.
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