Enhanced myocardial glucose use in patients with a deficiency in long-chain fatty acid transport (CD36 deficiency).
CD36 is a multifunctional, 88 kDa glycoprotein that is expressed on platelets and monocytes/macrophages. CD36 also has high homology with the long-chain fatty acid (LFA) transporter in the myocardium. Although platelet and monocyte CD36 levels can indicate a CD36 deficiency, they cannot predict specific clinical manifestations in the myocardium of a given person. We examined the hypothesis that a deficiency in LFA transport augments myocardial glucose uptake in patients with a type I CD36 deficiency. METHODS: Seven fasting patients with a type I CD36 deficiency and 9 controls were assessed by cardiac radionuclide imaging using beta-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) as a LFA tracer and by PET with 18F-fluorodeoxyglucose (FDG). RESULTS: None of the patients with a CD36 deficiency showed myocardial uptake of BMIPP. The percentage dose uptake of BMIPP in these subjects was significantly lower than that in normal controls (1.31+/-0.24 versus 2.90+/-0.2; P
Fukuchi, K; Nozaki, S; Yoshizumi, T; Hasegawa, S; Uehara, T; Nakagawa, T; Kobayashi, T; Tomiyama, Y; Yamashita, S; Matsuzawa, Y; Nishimura, T
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