Journal of Diabetes Research

Review Article

Updating Experimental Models of Diabetic Cardiomyopathy

Table 1

Main experimental models of T1DM and T2DM and related plasma and cardiac characteristics.
 Type I diabetesType II diabetes
ToxicsGeneticsGenetics DIO
STZAlloxanOVE26AkitaNODBB ratob/obdb/dbZDFKK AyOLETFGKFatSweet
(Antibiotic toxicity)(Uric acid derivative toxicity)(Calmodulin overexpression)()(Nonobese diabetic mouse)(Nonobese
diabetic rat)		()()()(Polygenic obese + )(Polygenic obese)(Polygenic nonobese) (Diet-induced obesity
and diabetes)
Serum profile              
Hyperglycemia onset
(d: days; w: weeks)		2 d after
injection [123]		5 d after injection [123]2-3 w [79]5-6 w [71]30 w [51]12 w [124]8–15 w [125]4–8 w [125]14 w [126]16 w [127]18 w [128]3 w [129]1 w [130]1 w [14]
HyperlipidemiaTG, Ch [123] 
LDL, HDL [131]		TG, Ch [123]TG [79]TG [71]TG [132]
Ch, HDL [133]		FFA [124]TG, FFA [64]
LDL, HDL [134]		TG, LDL, HDL [135]TG, VLDL, LDL, HDL [136]TG [137]TG, Ch [11]TG, FFA, LDL, HDL [12]TG, FFA, Ch [138, 139]TG, Ch [14]
Cardiac abnormalities              
Functional               
Diastolic function↓[140]↓[141]↓[90]↓[24]↓[142]↓[143]↓[5]↓[144]↓[8–10] ↓[11]↓[12]↓[13, 144]↓[14]
Systolic function↓[140]↓[141]↓[90]↓[145]/ 
~[24, 71]		↓[146]↓[147]~[5]↓[142]/ 
~[148]		↓[8]/ 
~[9, 10]		 ~[11]~[12]↓[13, 144]↓[14]
Structural               
Hypertrophy↑[20] ↑[22, 23]~[24]  ↑[46, 149]↑[64]↑[26]/ 
~[27]		↑[10, 28]  ↑[12, 30]↑[13]↑[32]
Inflammation~[21]  ↑[22]↑[40]  ↑[150]↑[41]↑[42]   ↑[44]~[32]
Fibrosis↑[21] ↑[22, 23]~[24]  [25]↑[41]/ 
~[25]		↑[10, 29]↑[151]↑[11, 47]↑[12]↑[43]~[32]
Steatosis↑[21]  ↑[24]↑[51] ↑[5]↑[5]↑[8, 10]   ↑[144]↑[53]
Apoptosis↑[21] ↑[58]   ↑[52]↑[59]↑[10, 60]  ↑[12]↑[13, 65]~[32]
Metabolic alterations              
Glucose oxidation↓[70]  ↓[24, 71]  ↓[5, 64]↓[26]↓[10, 72]  ↓[31, 80]↓[74] 
FA oxidation↑[70] ↑[62]↑[24, 71]  ↑[5, 64]↑[63]↑[10, 86]  ↑[31]~[74]/↑[73]↑[53]
Mitoch. function↓[70] ↓[62]↓[71]  ↓[81]↓[152]↓[10]↓[151]↓[83]↓[84]↓[73] 
Oxidative stress↑[70, 76]↑[153]↑[78, 79]~[71]  ↑[92]↑[152]↑[10, 86] ↑[47, 83]↑[84, 85]↑[34]↑[53]
Ca2+ mobilization↓[70] ↓[90]↓[24] ↓[91]↓[25]↓[93]~[72]  ↓[94]↓[13, 95]↓[14]
T1DM was induced by toxins [streptozotocin (STZ) or alloxan] or genetic mutations (OVE26, calmodulin transgenic; Akita, insulin-2 deficient; NOD, nonobese diabetic or BB, BioBreeding diabetes-prone mice). T2DM models were produced by genetic alterations [ob/ob, leptin deficient mice; db/db, leptin receptor deficient mice; ZDF, Zucker Diabetic Fatty rats; KK Ay, yellow obese gene transgenic KK mice; OLEFT, Otsuka Long-Evans Tokushima fatty rats; GK, Goto-Kakizaki rats or DIO, diet-induced (fat, sweet) obesity].