| First Author | Ganguly A | Year | 2008 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 294 |
| Issue | 6 | Pages | E1144-51 |
| PubMed ID | 18445753 | Mgi Jnum | J:136657 |
| Mgi Id | MGI:3796756 | Doi | 10.1152/ajpendo.90251.2008 |
| Citation | Ganguly A, et al. (2008) Glucose transporter isoform-3-null heterozygous mutation causes sexually dimorphic adiposity with insulin resistance. Am J Physiol Endocrinol Metab 294(6):E1144-51 |
| abstractText | We examined male and female glucose transporter isoform-3 (GLUT3; placenta)-null heterozygous(+/-) mutation-carrying mice and compared them with age- and sex-matched wild-type(+/+) littermates. No difference in postnatal (1-2 days, 6-7 days, 12-13 days, 20-21 days), postsuckling (1-2 mo), and adult (3-6 mo) growth pattern was seen except for an increase in body weight of 9- to 11-mo-old male but not female GLUT3(+/-) mice. This change in male mutant mice was associated with increased total body fat mass, perirenal and epididymal white adipose tissue weight, and hepatic lipid infiltration. These minimally glucose-intolerant male mutant mice demonstrated no change in caloric intake but a decline in basal metabolic rate and insulin resistance. No perturbation in basal circulating glucose concentrations but an increase in insulin concentrations, triglycerides, and total cholesterol was observed in GLUT3(+/-) male mice. Tissue analysis in males and females demonstrated diminished GLUT3 protein in GLUT3(+/-) brain and skeletal muscle with no change in brain and adipose tissue GLUT1 protein concentrations. Furthermore, the male GLUT3(+/-) mice expressed decreased insulin-responsive GLUT4 in white adipose tissue and skeletal muscle sarcolemma. We conclude that the GLUT3(+/-) male mice develop adult-onset adiposity with insulin resistance. |
