PMID:10428828

Citation	Heikkinen, S, Pietilä, M, Halmekytö, M, Suppola, S, Pirinen, E, Deeb, SS, Jänne, J and Laakso, M (1999) Hexokinase II-deficient mice. Prenatal death of homozygotes without disturbances in glucose tolerance in heterozygotes. J. Biol. Chem. 274:22517-23
Abstract	Type 2 diabetes is characterized by decreased rates of insulin-stimulated glucose uptake and utilization, reduced hexokinase II mRNA and enzyme production, and low basal levels of glucose 6-phosphate in insulin-sensitive skeletal muscle and adipose tissues. Hexokinase II is primarily expressed in muscle and adipose tissues where it catalyzes the phosphorylation of glucose to glucose 6-phosphate, a possible rate-limiting step for glucose disposal. To investigate the role of hexokinase II in insulin action and in glucose homeostasis as well as in mouse development, we generated a hexokinase II knock-out mouse. Mice homozygous for hexokinase II deficiency (HKII(-/-)) died at approximately 7.5 days post-fertilization, indicating that hexokinase II is vital for mouse embryogenesis after implantation and before organogenesis. HKII(+/-) mice were viable, fertile, and grew normally. Surprisingly, even though HKII(+/-) mice had significantly reduced (by 50%) hexokinase II mRNA and activity levels in skeletal muscle, heart, and adipose tissue, they did not exhibit impaired insulin action or glucose tolerance even when challenged with a high-fat diet.
Links	PubMed
Keywords	Adipose Tissue/enzymology; Animals; Chimera; Dietary Fats/pharmacology; Female; Fertility; Fetal Death; Genes, Lethal; Glucose/metabolism; Glucose Tolerance Test; Heterozygote; Hexokinase/deficiency; Hexokinase/genetics; Homozygote; Insulin/metabolism; Insulin Resistance; Male; Mice; Mice, Mutant Strains/embryology; Muscle, Skeletal/enzymology; Pregnancy; Stem Cells
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