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Glucose transporter isoform-3-null heterozygous mutation causes sexually dimorphic adiposity with insulin resistance

Division of Neonatology and Developmental Biology, Neonatal Research Center, Department of Pediatrics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California

Submitted 27 February 2008 ; accepted in final form 3 April 2008

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.

fetal programming; hepatic steatosis; transplacental glucose transport; type 2 diabetes mellitus

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