Table 1 Overview of pharmacological interventions in the experimental setting

Fatty acid metabolism inhibitors

Etomoxir

T2DM, infarction [89–91]

Stimulation glucose oxidation [99]

-

Perhexiline

T2DM, infarction [92]

Stimulation glucose oxidation

-

Oxfenicine

T2DM, infarction [92, 93]

Stimulation glucose oxidation

-

Trimetazidine

T2DM, infarction [94, 95]

Stimulation glucose oxidation

-

Ranolazine

T2DM, infarction [96, 97]

Stimulation glucose oxidation [96]

-

Dichloroacetate

T2DM, infarction [98]

Stimulation glucose oxidation [98]

-

Insulin

Glucose-insulin-potassium

Infarction [103]

Stimulation glucose oxidation

Hypoglycaemia

Insulin

T2DM

Reduction glucose levels

Hypoglycaemia

Infarction [108, 109]

Stimulation glucose oxidation

Hypoglycaemia

PPAR agonists

Fibrates (PPARα)

T2DM [47]

Reduction lipids

Myopathy

Infarction [115–117]

Reduction lipids

Myopathy

Thiozolidinediones (PPARγ)

T2DM [121, 122]

Insulin sensitizer

Increased risk heart attacks

Infarction [44, 48, 115, 119, 120]

Insulin sensitizer

Increased risk heart attacks

Biguanide

Metformin

T2DM, infarction [125–128]

Stimulation glucose oxidation

Lactic acidosis

GLP1

GLP1

T2DM, infarction [130]

Reduction glucose

Short half-life

Exendin-4

T2DM, infarction [131]

Reduction glucose

Hypoglycaemia

Exenatide

T2DM, infarction [132]

Reduction glucose

Hypoglycaemia

Liraglutide

T2DM, infarction [133, 134]

Reduction glucose

Hypoglycaemia