Alterations in Thyroid Function Parameters Following Administration of Fatty Acids

ABSTRACT Thirty patients with newly diagnosed hyperthyroidism were examined with regard to a unified analysis of the relationship between the changes in lipid metabolism and the thyroid function. Before and after one week's treatment with thiamazol, determinations of the free fatty acids (FFA), glycerol, cholesterol, phospholipid, triglyceride and paper lipoprotein electrophoresis were made on venous blood, together with determinations of PBI, T4, T3 test and basal metabolic rate (BMR). The FFA and glycerol concentrations were increased, but not correlated in the untreated patients. During treatment the lipolysis decreased in step with the fall in thyroid function and BMR. The concentrations of cholesterol, phospholipid and triglyceride were well correlated in the untreated patients. During the treatment the serum cholesterol rose significantly, while the rise in phospholipid and triglyceride was less pronounced. The changes were related with the changes in the T3 test. The rise occurred more frequently in patients with goitre. The lipid changes could not be demonstrated by the technique of lipoprotein electrophoresis used. Thus FFA, glycerol and to a lesser extent cholesterol in the blood are sensitive indicators of the antithyroid treatment.

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Thyroid function in a hibernator, Spermophilus tridecemlineatus

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.230.5.1211 ◽

1976 ◽

Vol 230 (5) ◽

pp. 1211-1216 ◽

Cited By ~ 26

Author(s):

AJ Hulbert ◽

JW Hudson

Keyword(s):

Fatty Acids ◽

Oxygen Consumption ◽

Thyroid Hormone ◽

Thyroid Function ◽

Release Rate ◽

Hormone Secretion ◽

Body Temperatures ◽

Spermophilus Tridecemlineatus ◽

Hypophysectomized Rats ◽

Low Rate

Thyroid hormone secretion (assessed as thyroid 125I release rate) was monitored in Spermophilus tridecemlineatus from summer to winter (July-December) in 1973. The average release rate in July was 2.3% per day, but in August this rate decreased significantly and remained at an average 0.52% per day until December. This low rate (being similar to that of hypophysectomized rats), and the absence of any change in oxygen consumption following thyroidectomy, suggested hormone secretion was "turned off" during this period. During the period August-December, four S. tridecemlineatus showed normal thermoregulatory responses to anterior hypothalamic cooling but no thyroidal response whether restrained, unrestrained, or anesthetized. Thyroid 125I uptake (and presumably hormone manufacture) continued during the period August-December and 24-h uptake averaged 27.0% in December. Possible reasons for "turning off" thyroid hormone secretion are discussed, and it is concluded this is to allow the membrane fatty acids to revert to a less-saturated condition in preparation for low body temperatures during hibernation.

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Increased Epoxyeicosatrienoic Acids and Hydroxyeicosatetraenoic Acids After Treatment of Iodide Intake Adjustment and 1,25-Dihydroxy-Vitamin D3 Supplementation in High Iodide Intake–Induced Hypothyroid Offspring Rats

Frontiers in Physiology ◽

10.3389/fphys.2021.669652 ◽

2021 ◽

Vol 12 ◽

Author(s):

Qing Liu ◽

Yue Zhang ◽

Hailing Zhao ◽

Xiaomei Yao

Keyword(s):

Fatty Acids ◽

Thyroid Function ◽

Vitamin D3 ◽

Cardiac Dysfunction ◽

Density Lipoprotein ◽

Thyroid Peroxidase ◽

Thyroid Function Tests ◽

Free Triiodothyronine ◽

Pregnant Rats ◽

Hydroxyeicosatetraenoic Acids

Aim: This study aimed to investigate the potential role of fatty acids in high iodide intake–induced hypothyroidism and its complications and also in the intervention of iodide intake adjustment and 1,25-dihydroxy-vitamin D3 [1,25(OH)2D3] supplementation.Methods: Pregnant rats were allocated to two groups, namely, normal iodide (NI, 7.5 μg/day) intake and 100 times higher-than-normal iodide (100 HI, 750 μg/day) intake. The offspring were continuously administered potassium iodide from weaning [i.e., postnatal day 21 (PN21)] to PN90. After PN90, the offspring were either administered iodide intake adjustment (7.5 μg/day) or 1,25(OH)2D3 supplementation (5 μg·kg−1·day−1), or both, for 4 weeks. Thyroid function tests (free triiodothyronine, free thyroxine, thyrotropin, thyroid peroxidase antibody, and thyroglobulin antibody), blood lipids (triglyceride, total cholesterol, free fatty acid, and low-density lipoprotein cholesterol), and vitamin D3 (VD3) levels were detected by ELISA. Cardiac function was measured by echocardiography. Blood pressure was measured using a non-invasive tail-cuff system. The serum fatty acids profile was analyzed by liquid chromatography–mass spectrometry.Results: In the offspring rats with continued 100 HI administration, the levels of 8,9-dihydroxyeicosatrienoic acid (8,9-DHET) and thromboxane B2 (TXB2) were decreased, while those of prostaglandin J2 (PGJ2), prostaglandin B2 (PGB2), 4-hydroxydocosahexaenoic acid (4-HDoHE), 7-HDoHE, 8-HDoHE, and 20-HDoHE were increased. Significant correlations were found between PGB2, 8,9-DHET, 7-HDoHE levels and thyroid dysfunction, between PGJ2, 20-HDoHE, PGB2, 8,9-DHET levels and cardiac dysfunction, between PGJ2, 20-HDoHE levels and hypertension, between 4-HDoHE, 8-HDoHE, TXB2 levels and dyslipidemia, and between PGB2 and decreased VD3 level. After the treatment of iodide intake adjustment and 1,25(OH)2D3 supplementation, the levels of 16-hydroxyeicosatetraenoic acids (16-HETE), 18-HETE, 5,6-epoxyeicosatrienoic acid (5,6-EET), 8,9-EET, 11,12-EET, 14,15-EET, PGE2, 5-oxo-ETE, and 15-oxo-ETE were increased. The significant associations between PGE2, 16-HETE, 18-HETE and improved thyroid function and also between 5,6-EET, 11,12-EET, 14,15-EET, 16-HETE, 15-oxo-ETE and attenuated dyslipidemia were detected.Conclusion: Increased levels of prostaglandins (PGs) and HDoHEs and decreased levels of 8,9-DHET and TXB2 might occur in the progression of cardiac dysfunction, hypertension, and dyslipidemia in high iodide intake–induced hypothyroidism. The increased levels of EETs and HETEs might help to ameliorate these complications after iodide intake adjustment and 1,25(OH)2D3 supplementation.

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