Abstract
Young rats exposed to the cold (4°C) for 15–25 days exhibit remarkable modifications in their thyroid state and in the mitochondrial population of target organs such as liver.
The serum total and free T3 levels more or less doubled (from 77±7 to 130±7 ng/100 ml and from 350±25 to 530 ±25 pg/100 ml, respectively) after 2 h of exposure while the serum total T4 levels underwent a limited and transitory increase; mitochondrial α-glycerophosphate dehydrogenase activity increased. On re-exposure to room temperature the thyroid state returned to normal. Cold exposure diminished the cellular volumes of hepatic cells, while the successive warm re-exposure increased the number of liver cells. The number of mitochondria per nucleus increased after 5 days of cold exposure and doubled after 10 days (from 1,200±120 to 2,400±130), while the mean protein content per organelles exhibited an exactly contrary trend.
These results suggest that during cold acclimatation, the thyroid plays a role in inducing an augmentation of mitochondrial membrane surfaces per cell by stimulation of the mitochondrial protein synthesizing mechanism. At present, it is not possible to establish whether these effects are due to transcriptional modifications of the nuclear genoma only or, more likely, to a dual action at nuclear and mitochondrial level.
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Goglia, F., Liverini, G., De Leo, T. et al. Thyroid state and mitochondrial population during cold exposure. Pflugers Arch. 396, 49–53 (1983). https://doi.org/10.1007/BF00584697
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DOI: https://doi.org/10.1007/BF00584697