1Division of Cardiology, Department of Internal Medicine, Chung-Ang University College of Medicine, Seoul, Korea
2Division of Endocrinology and Metabolism, Department of Internal Medicine, Chung-Ang University College of Medicine, Seoul, Korea
Copyright © 2021 Korean Diabetes Association
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
CONFLICTS OF INTEREST
No potential conflict of interest relevant to this article was reported.
FUNDING
This study was supported by grants from the Basic Science Research Program through the National Research Foundation of Korea (2020R1A2C1009647 to Wang-Soo Lee and 2020R1A2C1010217 to Jaetaek Kim).
Model | Species | Intervention | Manipulation | Target | DM onset | Phenotypes | |
---|---|---|---|---|---|---|---|
Type 1 DM | |||||||
STZ [14] | Mice | Pharmacological | Injection | β-Cell | 2 day | Necrosis & loss of insulin production, hyperlipidemia | |
Alloxan [20] | Mice | Pharmacological | Injection | β-Cell | 5 day | Necrosis & loss of insulin production, high TG | |
OVE26 [21] | Mice | Transgenic | Overexpression | Calmodulin | 2–3 wk | β-cell damage, high TG | |
NOD [17] | Mice | Transgenic | Insulitis | β-Cell | 30 wk | β-cell failure, high TG | |
Akita [14,17] | Mice | Transgenic | Spontaneous missense mutation | Insulin-2 gene | 5–6 wk | Misfolding of insulin protein, facilitate ER stress, β-cell failure, high TG | |
Type 2 DM | |||||||
HFD/HSD [14,21] | Mice | Diet-induced | Feeding | 1 wk | Obesity, high TG | ||
HFD+low dose STZ [14,21] | Mice | Diet & Pharmacological | Feeding+injection | β-Cell | 2–10 wk | Obesity, IR | |
ob/ob [14,21] | Mice | Transgenic | Deficiency | Leptin | 8–15 wk | Obesity, IR, high TG, FFA | |
db/db [14,21] | Mice | Transgenic | Nonfunctioning | Leptin receptor | 4–8 wk | Obesity, IR, high TG, FFA | |
ZF/ZDF [14,21] | Rats | Transgenic | Nonfunctioning | Leptin receptor | 14 wk | Obesity, high TG | |
GK [18,20] | Rats | Transgenic | Overexpression | SREBP-1c | 3 wk | IR, high TG, FFA | |
OLETF [20,21] | Rats | Polygenic | Food-intake control defect | CCK-1R, Odb2 | 18 wk | Obesity, high TG | |
KK-Ay [17,20] | Mice | Polygenic | Spontaneous | Agouti gene | 8–16 wk | Obesity, high TG, IR | |
NZO/HiLt (male) [17,18] | Mice | Polygenic | Spontaneous | Ab to leptin transporter | 12–24 wk | Obesity, leptin resistance, IR | |
TallyHo/JngJ (male) [17,18] | Mice | Polygenic | Spontaneous | Tanidd1-3 | 10–16 wk | Obesity, hyperlipidemia, hyperinsulinemia | |
NONcNZO10/LtJ [18,20] | Mice | Polygenic | Spontaneous | Zinc homeostasis or glucose metabolism | 8–24 wk | Obesity, IR |
DM, diabetes mellitus; STZ, streptozotocin-induced mice; TG, triglyceride; OVE26, OVE26 diabetic mice; NOD, nonobese diabetic mice; Akita, a C57BL/6NSlc mouse with a spontaneous mutation in the insulin‑2 gene; ER, endoplasmic reticulum; HFD/HSD, high-fat/high-sucrose diet; IR, insulin resistance; ob/ob, leptin-deficient mice; FFA, free fatty acid; db/db, leptin receptor-deficient mice; ZF, Zucker fatty rats; ZDF, Zucker diabetic fatty rats; GK, Goto-Kakizaki rats; CCK-1R, cholecystokinnin-1 receptor; Odb2, diabetogenic gene located on chromosome 14; SREBP-1c, sterol regulatory element-binding protein-1c; OLETF, Otsuka Long-Evans Tokushima fatty rats; KK-Ay, yellow obese gene transgenic Kuo Kondo mice; NZO, New Zealand obese mice; Ab, antibody; Tanidd1, a mouse chromosome 19 quantitative trait loci associated with diabetes in TALLYHO mice; NONcNZO10/LtJ, a recombinant congenic strain comprising approximately 88% genome contribution from the NON/LtJ (nonobese and nondiabetic) strain and 12% from the New Zealand obese strain.
Strain | Model | Manipulation | Phenotypes | |
---|---|---|---|---|
Mice | ||||
ob/ob | Obesity [138,153] | Hypertrophy, diastolic dysfunction | ||
db/db | DM [138,154] | IR, hypertrophy, diastolic dysfunction | ||
SAMP8 | Aging [144] | Diastolic dysfunction | ||
C57BL/6 | Obesity+HTN [145] | HFD+L-NAME | Hypertrophy, diastolic dysfunction, pulmonary congestion | |
HTN [146] | TAC | Hypertrophy, fibrosis, diastolic dysfunction | ||
HTN [138,147] | Aldosterone, unilateral nephrectomy, 1% NaCl water-drinking | Hypertrophy, fibrosis, diastolic dysfunction | ||
HTN [145,148] | DOCA salt, unilateral nephrectomy, 1% NaCl water-drinking | Mild HTN, hypertrophy | ||
Rats | ||||
Wistar | HTN [149] | DOCA salt, unilateral nephrectomy, 1% NaCl water-drinking | Severe HTN, hypertrophy | |
DSS | HTN [138,148] | 4%–8% NaCl chow | Severe HTN, diastolic HF |
ob/ob, mice with leptin deficiency; db/db, mice with leptin receptor deficiency; DM, diabetes mellitus; IR, insulin resistance; SAMP8, mice with senescence-accelerated mouse prone 8; HTN, hypertension; HFD, high-fat diet; L-NAME, L-NG-nitroarginine methyl ester; TAC transverse aortic constriction; DOCA, deoxycorticosterone acetate; DSS, Dahl salt-sensitive rats; HF, heart failure.
Model | Species | Intervention | Manipulation | Target | DM onset | Phenotypes | |
---|---|---|---|---|---|---|---|
Type 1 DM | |||||||
STZ [14] | Mice | Pharmacological | Injection | β-Cell | 2 day | Necrosis & loss of insulin production, hyperlipidemia | |
Alloxan [20] | Mice | Pharmacological | Injection | β-Cell | 5 day | Necrosis & loss of insulin production, high TG | |
OVE26 [21] | Mice | Transgenic | Overexpression | Calmodulin | 2–3 wk | β-cell damage, high TG | |
NOD [17] | Mice | Transgenic | Insulitis | β-Cell | 30 wk | β-cell failure, high TG | |
Akita [14,17] | Mice | Transgenic | Spontaneous missense mutation | Insulin-2 gene | 5–6 wk | Misfolding of insulin protein, facilitate ER stress, β-cell failure, high TG | |
Type 2 DM | |||||||
HFD/HSD [14,21] | Mice | Diet-induced | Feeding | 1 wk | Obesity, high TG | ||
HFD+low dose STZ [14,21] | Mice | Diet & Pharmacological | Feeding+injection | β-Cell | 2–10 wk | Obesity, IR | |
ob/ob [14,21] | Mice | Transgenic | Deficiency | Leptin | 8–15 wk | Obesity, IR, high TG, FFA | |
db/db [14,21] | Mice | Transgenic | Nonfunctioning | Leptin receptor | 4–8 wk | Obesity, IR, high TG, FFA | |
ZF/ZDF [14,21] | Rats | Transgenic | Nonfunctioning | Leptin receptor | 14 wk | Obesity, high TG | |
GK [18,20] | Rats | Transgenic | Overexpression | SREBP-1c | 3 wk | IR, high TG, FFA | |
OLETF [20,21] | Rats | Polygenic | Food-intake control defect | CCK-1R, Odb2 | 18 wk | Obesity, high TG | |
KK-Ay [17,20] | Mice | Polygenic | Spontaneous | Agouti gene | 8–16 wk | Obesity, high TG, IR | |
NZO/HiLt (male) [17,18] | Mice | Polygenic | Spontaneous | Ab to leptin transporter | 12–24 wk | Obesity, leptin resistance, IR | |
TallyHo/JngJ (male) [17,18] | Mice | Polygenic | Spontaneous | Tanidd1-3 | 10–16 wk | Obesity, hyperlipidemia, hyperinsulinemia | |
NONcNZO10/LtJ [18,20] | Mice | Polygenic | Spontaneous | Zinc homeostasis or glucose metabolism | 8–24 wk | Obesity, IR |
Strain | Model | Manipulation | Phenotypes | |
---|---|---|---|---|
Mice | ||||
ob/ob | Obesity [138,153] | Hypertrophy, diastolic dysfunction | ||
db/db | DM [138,154] | IR, hypertrophy, diastolic dysfunction | ||
SAMP8 | Aging [144] | Diastolic dysfunction | ||
C57BL/6 | Obesity+HTN [145] | HFD+L-NAME | Hypertrophy, diastolic dysfunction, pulmonary congestion | |
HTN [146] | TAC | Hypertrophy, fibrosis, diastolic dysfunction | ||
HTN [138,147] | Aldosterone, unilateral nephrectomy, 1% NaCl water-drinking | Hypertrophy, fibrosis, diastolic dysfunction | ||
HTN [145,148] | DOCA salt, unilateral nephrectomy, 1% NaCl water-drinking | Mild HTN, hypertrophy | ||
Rats | ||||
Wistar | HTN [149] | DOCA salt, unilateral nephrectomy, 1% NaCl water-drinking | Severe HTN, hypertrophy | |
DSS | HTN [138,148] | 4%–8% NaCl chow | Severe HTN, diastolic HF |
DM, diabetes mellitus; STZ, streptozotocin-induced mice; TG, triglyceride; OVE26, OVE26 diabetic mice; NOD, nonobese diabetic mice; Akita, a C57BL/6NSlc mouse with a spontaneous mutation in the insulin‑2 gene; ER, endoplasmic reticulum; HFD/HSD, high-fat/high-sucrose diet; IR, insulin resistance;