Abstract
IT has previously been reported that free fatty acid mobilization from the adipose tissue of hereditary obese–hyperglycæmie mice after incubation with epinephrine or fat-mobilizing substance1 or prolonged fast is far smaller than is seen with tissue from non-obese litter-mates2,3. It has also been shown that lipogenesis from acetate in adipose tissue from this animal proceeds at 10–15 times the normal rate4. The diminished free fatty release and the increased lipogenesis from acetate occurring in spite of a decrease in glucose uptake5 and utilization2,5 suggested to us that this syndrome might entail two abnormalities, possibly interrelated: an impaired lipolytic activity directly related to the epinephrine-sensitive lipolytic system in adipose tissue described by Rizack6; and an ability of this tissue to utilize ‘non-active’ glycerol in the esterification process possibly through a specific ‘glycero-kinase’.
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References
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LOCHAYA, S., HAMILTON, J. & MAYER, J. Lipase and Glycerokinose Activities in the Adipose Tissue of Obese-Hyperglycæmic Mice. Nature 197, 182–183 (1963). https://doi.org/10.1038/197182a0
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DOI: https://doi.org/10.1038/197182a0
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