1. Главная
  2. Ресурсы
  3. Библиотечный поиск
Thyroid hormonereduces PCSK9 andstimulates bile acidsynthesis in humans Ylva BondeOlof BreuerDieter Lütjohann2014 год

Thyroid hormone reduces PCSK9 and stimulates bile acid synthesis in humans
статья из журнала

Полный текстСтраница публикацииПубликация в OpenAlex
Аннотация: Reduced plasma LDL-cholesterol is a hallmark of hyperthyroidism and is caused by transcriptional stimulation of LDL receptors in the liver. Here, we investigated whether thyroid hormone (TH) actions involve other mechanisms that may also account for the reduction in LDL-cholesterol, including effects on proprotein convertase subtilisin/kexin type 9 (PCSK9) and bile acid synthesis. Twenty hyperthyroid patients were studied before and after clinical normalization, and the responses to hyperthyroidism were compared with those in 14 healthy individuals after 14 days of treatment with the liver-selective TH analog eprotirome. Both hyperthyroidism and eprotirome treatment reduced circulating PCSK9, lipoprotein cholesterol, apoB and AI, and lipoprotein(a), while cholesterol synthesis was stable. Hyperthyroidism, but not eprotirome treatment, markedly increased bile acid synthesis and reduced fibroblast growth factor (FGF) 19 and dietary cholesterol absorption. Eprotirome treatment, but not hyperthyroidism, reduced plasma triglycerides. Neither hyperthyroidism nor eprotirome treatment altered insulin, glucose, or FGF21 levels. TH reduces circulating PSCK9, thereby likely contributing to lower plasma LDL-cholesterol in hyperthyroidism. TH also stimulates bile acid synthesis, although this response is not critical for its LDL-lowering effect.
Год издания: 2014
Авторы: Ylva Bonde, Olof Breuer, Dieter Lütjohann, Stefan Sjöberg, Bo Angelin, Mats Rudling
Издательство: Elsevier BV
Источник: Journal of Lipid Research
Ключевые слова: Thyroid Disorders and Treatments, Growth Hormone and Insulin-like Growth Factors, Neuroendocrine Tumor Research Advances
Другие ссылки: Journal of Lipid Research (PDF)
Journal of Lipid Research (HTML)
DOAJ (DOAJ: Directory of Open Access Journals) (HTML)
Europe PMC (PubMed Central) (PDF)
Europe PMC (PubMed Central) (HTML)
PubMed Central (HTML)
PubMed (HTML)