Serum concentrations of remnant‐like particles in hypothyroid patients before and after thyroxine replacement

M, Ito; Takamatsu, Junta; Matsuo, Takashi; Kameoka, Keiichi; Kubota, Sumihisa; Fukata, Shuji; Tamai, Hiroshi; Miyauchi, Akira; Kuma, Kanji; Hanafusa, Toshiaki

doi:10.1046/j.1365-2265.2003.01762.x

Cited by 35 publications

(25 citation statements)

References 32 publications

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“…These results may be explained in part by findings in previous studies. LPL and HTGL, which are essential for the degradation of chylomicrons or chylomicron remnants, were demonstrated to significantly increase after T 4 replacement [10,12]. Hepatocyte B-E receptors that are responsible for the uptake of LDL and chylomicrons were depressed in subjects with hypothyroidism, with an increase in expression in response to the administration of thyroid hormone [25,26].…”

Section: Discussionmentioning

confidence: 98%

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Effect of L-thyroxine replacement on apolipoprotein B-48 in overt and subclinical hypothyroid patients

Kitanaka

Arishima

et al. 2013

Endocr J

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Section: Discussionmentioning

confidence: 98%

“…With regard to the TG-rich lipoprotein in hypothyroidism, we previously reported the disturbed metabolism of remnant lipoprotein in overt hypothyroidism (OH) [12] and subclinical hypothyroidism (SH) [13].…”

Section: Resultsmentioning

confidence: 99%

Effect of L-thyroxine replacement on apolipoprotein B-48 in overt and subclinical hypothyroid patients

Kitanaka

Arishima

et al. 2013

Endocr J

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“…However, the rat and mouse, commonly used animals for T 3 and TR studies, differ from humans in their response to T 3 . Whereas LPL activity positively correlates with TH levels in humans (9,11), hypothyroidism in rats increases both adipose and heart LPL mass and activity via a translational mechanism involving its 3Ј-untranslated region (57), whereas T 3 reverses these effects (58). Accordingly, PTU-induced hypothyroidism in rats has been associated with reductions in plasma TG (49,50,59,60).…”

Section: Discussionmentioning

confidence: 99%

“…Such elevation in TG levels has been attributed to low lipoprotein lipase (LPL) (9) or low hepatic triglyceride lipase activities (6,10,11). In contrast, hyperthyroid patients exhibit elevated rates of clearance of VLDL and normal or decreased circulating TG levels (6), whereas treatment with thyroid hormones (TH) is associated with elevation in both LPL and hepatic triglyceride lipase activities (9,10,11) and concomitantly with a tendency to TG lowering (6,9,11). At present, the molecular mechanisms by which TH may regulate lipase activities and circulating TG levels in humans remain to be defined.…”

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confidence: 99%

Thyroid Hormone Regulates the Hypotriglyceridemic Gene APOA5

Prieur

Huby²,

Coste

et al. 2005

Journal of Biological Chemistry

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The apolipoprotein AV gene (APOA5) is a key determinant of plasma triglyceride levels, a major risk factor for coronary artery disease and a biomarker for the metabolic syndrome. Since thyroid hormones influence very low density lipoprotein triglyceride metabolism and clinical studies have demonstrated an inverse correlation between thyroid status and plasma triglyceride levels, we examined whether APOA5 is regulated by thyroid hormone. Here we report that 3,5,3-triiodo-Lthyronine (T 3 ) and a synthetic thyroid receptor ␤ (TR␤) ligand increase APOA5 mRNA and protein levels in hepatocytes. Our data revealed that T 3 -activated TR directly regulates APOA5 promoter through a functional direct repeat separated by four nucleotides (DR4). Interestingly, we show that upstream stimulatory factor 1, a transcription factor associated with familial combined hyperlipidemia and elevated triglyceride levels in humans, and upstream stimulatory factor 2 cooperate with TR, resulting in a synergistic activation of APOA5 promoter in a ligand-dependent manner via an adjacent E-box motif. In rats, we observed that apoAV levels declines with thyroid hormone depletion but returned to normal levels upon T 3 administration. In addition, treatments with a TR␤-selective agonist increased apoAV and diminished triglyceride levels. The identification of APOA5 as a T 3 target gene provides a new potential mechanism whereby thyroid hormones can influence triglyceride homeostasis. Additionally, these data suggest that TR␤ may be a potential pharmacological target for the treatment of hypertriglyceridemia.

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“…These data suggested that lower thyroid hormone was associated with the accumulation of apoB-48-containing lipoproteins (CM and CMR) because the activities of LPL and HTGL were impaired in patients with hypothyroidism. Moreover, since many studies reported that there were significant changes in LDL-C after L-T4 replacement in patients with OH 7,[38][39][40] , we investigated changes in serum apoB-48 after L-T4 ApoB-48 was measured before and after L-T4 treatment. After L-T4 replacement, serum apoB-48 decreased in 13 patients with OH (p＜0.05).…”

Section: Discussionmentioning

confidence: 99%

Thyroid Function Influences Serum Apolipoprotein B-48 Levels in Patients with Thyroid Disease

Mugii

Hanada

Okubo

et al. 2012

JAT

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Aim: Apolipoprotein B-48 (apoB-48) is a major apolipoprotein of intestine-derived chylomicrons (CM) and CM remnants (CMR).Clinically overt hypothyroidism (OH) has been associated with premature and accelerated coronary atherosclerosis. To clarify the clinical significance of apoB-48 measurement in patients with thyroid disease, we investigated the correlations between the serum apoB-48 level and thyroid hormones. Methods: From outpatients of Osaka University Hospital, patients with OH, subjects with subclinical hypothyroidism (SH) and subjects with normal thyroid function were collected and analyzed by measuring serum TSH, FT4 and FT3 levels. Serum apoB-48 levels were measured by a chemiluminescence enzyme immunoassay and the correlations with thyroid hormone levels or lipid profiles were assessed. These levels were compared among subjects with OH, SH and healthy controls. Results: Serum apoB-48 level was correlated with TSH, total cholesterol (TC) and triglycerides (TG), but negatively with FT4 and FT3 level. LDL-C and HDL-C levels were not correlated with serum apoB-48 levels. Serum apoB-48 in patients with OH (7.4±5.9 μg/mL) was significantly higher than in those with hyperthyroidism (5.1±3.5 μg/mL; p＜0.01) and normal subjects (4.7±3.7 μg/mL; p＜0.01), but decreased after levo-thyroxine replacement. ApoB-48, TG and TSH were significantly higher in SH subjects than normal subjects, suggesting that serum apoB-48 level depends on the thyroid function status, similar to TC, LDL-C and TG. Conclusion: Increased serum apoB-48 concentrations and CMR may contribute to the increased risk of atherosclerosis and premature coronary artery disease in the hypothyroid state.

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Serum concentrations of remnant‐like particles in hypothyroid patients before and after thyroxine replacement

Abstract: Hypothyroidism seems to be associated with a decrease in metabolism of serum RLPs. Such altered metabolism of RLPs may be related to the decreased activities of LPL and HTGL and can be corrected by T4 replacement therapy.

Cited by 35 publications

References 32 publications

Effect of L-thyroxine replacement on apolipoprotein B-48 in overt and subclinical hypothyroid patients

Effect of L-thyroxine replacement on apolipoprotein B-48 in overt and subclinical hypothyroid patients

Thyroid Hormone Regulates the Hypotriglyceridemic Gene APOA5

Thyroid Function Influences Serum Apolipoprotein B-48 Levels in Patients with Thyroid Disease

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