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Table 1 Progress on the effects of conventional metabolic therapies in experimental DCM

From: Targeting metabolic disturbance in the diabetic heart

 

Type 1 diabetes

Type 2 diabetes

 

STZ

OVE26

Akita

ob/ob

db/db

ZDF

GK

DIO †

Metformin

↑Glucose utilization ↑Cardiac function

↓Apoptosis ↑Cardiac function

 

↓Hypertrophy ~ Fibrosis ↑Cardiac function

 

~Hypertrophy ↑Fibrosis ↓Steatosis

↓/~Hypertrophy ↓Fibrosis ↓Apoptosis ~ Oxidative stress ↑Cardiac function

 

Sulfonylureas

↑Cardiac function

       

DPP-4 inhibitors

  

↑Hypertrophy ↑Cardiac function

 

~Hypertrophy ↓Fibrosis ↓Oxidative stress ~Cardiac function

 

↓Hypertrophy ↓Fibrosis ↓Apoptosis ↑Cardiac function

 

GLP-1R agonists

       

↑Glucose utilization ↓Hypertrophy ↓Apoptosis ↓Inflammation ↑Cardiac function

Statins

↓Fibrosis ↓Oxidative stress ↓Inflammation ↑Cardiac function

      

↓Hypertrophy ↓Fibrosis ↓Inflammation ↑Cardiac function

PPARα agonists

    

↑Glucose utilization ↓Steatosis ~ Cardiac function

~Hypertrophy ↓Fibrosis ↓Steatosis

 

↑Glucose utilization ↓ER stress ↓Inflammation ↑Cardiac function

PPARγ agonists

↓Hypertrophy ↓Apoptosis ↓Steatosis ↓Oxidative stress ↑Cardiac function

 

↑Hypertrophy

 

↑Glucose utilization ~ Cardiac function

↑Glucose utilization

  

Reference

[15,16,23,25-27]

[17]

[28,29]

[18]

[30-32]

[19,33]

[20,21]

[34-38]

  1. Conventional treatments against DCM have been assessed in different animal models of type-I [STZ, streptozotocin-treated mice/rats; OVE26, calmodulin transgenic mice; Akita, insulin-2 deficient mice] and type-II [ob/ob, leptin deficient mice; db/db, leptin receptor deficient mice; ZDF, Zucker Diabetic Fatty, heterozygous leptin receptor deficient rats; GK, Goto-Kakizaki rats; DIO, diet-induced obesity] diabetes. ↑, ↓ and ~ stand for increased, decreased or not modified effect, respectively. †For the sake of simplicity, evidence from low-dose STZ- plus diet-induced T2DM models are displayed in the DIO column. References: [34] and [37].