Thyroid control over biomembranes: VI. Lipids in liver mitochondria and microsomes of hypothyroid rats |
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Authors: | F L Hoch C Subramanian G A Dhopeshwarkar J F Mead |
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Affiliation: | (1) Departments of Internal Medicine and Biological Chemistry, University of Michigan Medical School, 7696 Kresge Building, 48109 Ann Arbor, MI;(2) Department of Biological Chemistry and School of Public Health, University of California at Los Angeles, Los Angeles, USA;(3) Laboratory of Nuclear Medicine and Radiation Biology, University of California at Los Angeles, Los Angeles, USA;(4) Division of Environmental and Nutritional Sciences, School of Public Health, University of California at Los Angeles, Los Angeles, USA |
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Abstract: | The lipids of liver mitochondria prepared from normal rats and from rats made hypothyroid by thyroidectomy and injection with131INa contained similar amounts, per mg protein, of total lipids, phospholipids, neutral lipids and lipid phosphorus. Hypothyroidism
caused a doubling of the relative amounts of mitochondrial cardiolipins (CL; to 20.5% of the phospholipid P) and an accompanying
trend (although statistically not significant) toward decreased amounts of both phosphatidylcholines (PC) and phosphatidylserines
(PS), with phosphatidylethanolamines (PE) remaining unchanged. The pattern of elevated 18∶2 fatty acyl content and depleted
20∶4 acyl groups of the mitochondrial phospholipids of hypothyroid preparations was reflected to varying degrees in the resolved
phospholipids, with PC showing greater degrees of abnormality than PE, and CL showing none. Hypothyroidism produced the same
abnormal pattern of fatty acyl distributions in liver microsomal total lipids as was found in the mitochondria. Hypothyroid
rats, when killed 6 hr after injection of 1-14C] labeled linoleate, showed the following abnormalities: the liver incorporated less label into lipids, and converted 18∶2
not exclusively to 20∶4 (as normals do) but instead incorporated the label mainly into saturated fatty acids. These data,
together with the known decrease in β-oxidation, suggest that hypothyroidism involves possible defective step(s) in the conversion
of 18∶2 to 20∶4.
These studies were initiated during a leave at the University of California, Los Angeles. |
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