Thyroid control over biomembranes: VI. Lipids in liver mitochondria and microsomes of hypothyroid rats.

The lipids of liver mitochondria prepared from normal rats and from rats made hypothyroid by thyroidectomy and injection with 131 INa 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 beta-oxidation, suggest that hypothyroidism involves possible defective step(s) in the conversion of 18:2 to 20:4.