*Adipose tissue-specific GLUT4 knockout mice*

Adipose tissue selective GLUT4 inactivation, unlike the conventional GLUT4 disruption, does not affect growth, adipose mass or size. Cardiac hypertrophy is not seen in those animals. Fat specific GLUT4 null mice are insulin resistant and glucose intolerant and a subset of animals develop diabetes, which is also observed in muscle specific GLUT4 deficient mice. Muscle and liver are insulin-resistant in those animals. Surprisingly, insulin resistance in muscle was only observed in vivo but not ex vivo indicating a systemic impact of adipose tissue on insulin sensitivity.

## *Cardiac tissue specific GLUT4 knockout mice*

GLUT4 knockout mice specifically muscle and cardiac tissue specific GLUT4 deficient mice all develop cardiac hypertrophy. While homo-and heterozygous GLUT4 null mice show cardiac dysfunction under normal conditions, cardiac specific GLUT4 knockouts have normal contractile function under basal conditions but decreased recovery after hypoxia. Metabol‐ ically, heart specific GLUT4 knockout mice are normal and have a normal lifespan.

## **4.6. GLUT14** *(SLC2A14)*

Searching the human genome for additional genes coding for glucose transporters, a putative gene was identified and cloned showing 95% identity to GLUT3 on the nucleotide level. The *SLC2A14* gene maps to chromosome 12p13.3 with a 10Mb distance to GLUT3 and appears to be a consequence of a gene duplication of GLUT3. GLUT14 was shown to be specifically expressed in the testes. Two alternatively spliced forms of GLUT14 were identified. Interest‐ ingly, GLUT14 has no orthologue in mice, a finding that has also been made for GLUT11.
