Table 2.

The Phenotypes of Mouse Models with Genetically Modified GLUTs

Isoform	Overexpression or knockout	Tissue specific	General phenotype	Cardiac phenotype	Reference
GLUT1	Overexpression	Skeletal muscle	Increase basal glucose uptake	n.d.	(73)
GLUT1	Overexpression	Cardiac	Increase glucose uptake, glycolysis, and glycogen storage	Protect from pressure overload and ischemia induced heart failure; promote cardiac dysfunction in high fat diet induced obesity model	(125,135,259)
GLUT1	Inducible overexpression	Cardiac	n.d.	Preserve mitochondria function; exacerbates hypertrophic phenotype	(173)
GLUT4	Overexpression	Systematic*	Increased glucose uptake, glycolysis and glycogen in skeletal and cardiac muscle reduced fasting plasma glucose levels; improved glucose tolerance in high fat diet and db/db diabetic model	n.d.	(14,66,77,86)
GLUT4	Overexpression	Skeletal and cardiac muscle	Improve insulin action; reduce basal blood glucose levels in streptozotocin-induced diabetic mice	n.d.	(121)
GLUT1	Knock out	Systematic	Homozygous: lethal Heterozygous: growth retardation; severe brain dysfunction	n.d.	(80,248)
GLUT4	Knock out	Systematic*	Homozygous: growth-retarded, shorter life span with normal blood glucose level Heterozygous: reduce muscle glucose uptake; develop hyperglycemia and hyperinsulinemia	Homozygous: severe cardiac hypertrophy and dysfunction	(101,220)
GLUT4	Knockout	Cardiac	Normal systematic glucose metabolism with normal life span	Normal cardiac function with moderate hypertrophy at baseline. Impair glycolysis and exacerbate ischemia reperfusion injury	(1,232)

Note. n.d. not determined. Systematic *refers to overexpression or knock out of GLUT4 at the sites where endogenous GLUT4 is expressed.