Mcd-/- KO mice contain a neo cassette replacing exon 1 of the malonyl-CoA decarboxylase (Mlycd) gene, abolishing gene expression. Malonyl-CoA has been implicated in the regulating of feeding behavior, hepatocyte-mediated insulin resistance, energy expenditure and subsequent storage of fat in adipose tissue, pancreatic beta cell insulin secretion, skeletal muscle–mediated insulin resistance and type 2 diabetes, and cardiac ischemia/reperfusion injury. Expression of cardiac MCD protects the heart from ischemic damage by inhibiting fatty acid oxidation and stimulating glucose oxidation. MCD acts to regulate fatty acid oxidation by inhibiting carnitine palmitoyltransferase 1 (CPT1) which is the key enzyme involved in mitochondrial long-chain fatty acid uptake. Mice homozygous for this allele are viable and fertile. No protein from the targeted gene is detected by Western blot analysis of cardiac tissue. Mcd-/- KO mice exhibit no significant differences in rates of fatty acid oxidation, glucose oxidation, glycolysis, or in vivo and ex vivo cardiac function. They show an increase in the expression of genes regulating fatty acid utilization. They do have an increase in glucose oxidation and improved functional recovery of the heart after ischemia. These mice resist diet-induced glucose intolerance. When homozygotes are challenged with diet-induced obesity they display a more robust insulin-stimulated glucose oxidation and less incomplete fatty acid oxidation. Mcd-/- KO mice do not show pulmonary vasoconstriction during exposure to acute hypoxia and do not develop pulmonary arterial hypertension during chronic hypoxia.

Mcd-/- KO mice may be useful for studying the mechanisms of cardiac glucose oxidation and recovery from cardiac ischemic injury.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

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