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Research Article Free access | 10.1172/JCI105651
Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri
Department of Biochemistry, Washington University School of Medicine, St. Louis, Missouri
‡Teaching and Research Scholar of the American College of Physicians.
Address requests for reprints to Dr. Philip W. Majerus, Division of Hematology, Barnes and Wohl Hospitals, 4550 Scott Avenue, St. Louis, Mo. 63110.
*Received for publication 8 May 1967 and in revised form 29 June 1967.
This investigation was supported in part by grants from the United States Public Health Service, AM-10550, the National Science Foundation, GB-5056X, and the American Cancer Society, PRA-33.
Find articles by Majerus, P. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri
Department of Biochemistry, Washington University School of Medicine, St. Louis, Missouri
‡Teaching and Research Scholar of the American College of Physicians.
Address requests for reprints to Dr. Philip W. Majerus, Division of Hematology, Barnes and Wohl Hospitals, 4550 Scott Avenue, St. Louis, Mo. 63110.
*Received for publication 8 May 1967 and in revised form 29 June 1967.
This investigation was supported in part by grants from the United States Public Health Service, AM-10550, the National Science Foundation, GB-5056X, and the American Cancer Society, PRA-33.
Find articles by Lastra R., R. in: JCI | PubMed | Google Scholar
Published October 1, 1967 - More info
Extracts from human leukocytes have been examined for the enzymes of de novo fatty acid biosynthesis. These extracts do not catalyze the synthesis of long-chain fatty acids because they lack acetyl CoA carboxylase, the first enzyme unique to the fatty acid synthesis pathway.
Since these cells cannot form malonyl CoA, they are unable to synthesize long-chain fatty acids. This inability can be corrected by addition of either purified acetyl CoA carboxylase from rat liver or malonyl CoA to leukocyte extracts. The incorporation of acetate-1-14C into fatty acids by intact leukocytes is shown to represent chain elongation of preformed fatty acids rather than de novo synthesis by the fact that 60-100% of the label incorporated resides in the carboxyl carbon of the fatty acids formed.
Both mature leukocytes and erythrocytes are unable to synthesize fatty acids because of a lack of acetyl CoA carboxylase even though both contain the other enzymes of fatty acid synthesis. It is possible that a precursor hematopoietic cell may have the capacity to synthesize fatty acids de novo. This hypothesis is supported by the finding of acetyl CoA carboxylase activity in extracts from human leukemic blast cells.
The leukocyte fatty acid synthetase activity from malonyl CoA of a number of normal volunteers and of patients with a variety of hematologic diseases is reported.