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Molecular and Cellular Biology, September 2002, p. 6142-6147, Vol. 22, No. 17
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.17.6142-6147.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Transketolase Haploinsufficiency Reduces Adipose Tissue and Female Fertility in Mice

Zheng-Ping Xu, Eric F. Wawrousek, and Joram Piatigorsky*

Laboratory of Molecular and Developmental Biology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892-2730

Received 21 March 2002/ Accepted 3 June 2002

Transketolase (TKT) is a ubiquitous enzyme used in multiple metabolic pathways. We show here by gene targeting that TKT-null mouse embryos are not viable and that disruption of one TKT allele can cause growth retardation ({approx}35%) and preferential reduction of adipose tissue ({approx}77%). Other TKT+/- tissues had moderate ({approx}33%; liver, gonads) or relatively little ({approx}7 to 18%; eye, kidney, heart, brain) reductions in mass. These mice expressed a normal level of growth hormone and reduced leptin levels. No phenotype was observed in the TKT+/- cornea, where TKT is especially abundant in wild-type mice. The small female TKT+/- mice mated infrequently and had few progeny (with a male/female ratio of 1.4:1) when pregnant. Thus, TKT in normal mice appears to be carefully balanced at a threshold level for well-being. Our data suggest that TKT deficiency may have clinical significance in humans and raise the possibility that obesity may be treated by partial inhibition of TKT in adipose tissue.

* Corresponding author. Mailing address: Laboratory of Molecular and Developmental Biology, National Eye Institute, NIH, 6 Center Dr., Building 6/Room 201, Bethesda, MD 20892-2730. Phone: (301) 496-9467. Fax: (301) 402-0781. E-mail: joramp{at}nei.nih.gov.

Molecular and Cellular Biology, September 2002, p. 6142-6147, Vol. 22, No. 17
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.17.6142-6147.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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