Regulation of adipose tissue lipoprotein lipase gene expression by thyroid hormone in rats.

Lipoprotein lipase (LPL) is an important enzyme in lipid metabolism, and adipose LPL activity is increased in rats that are deficient in thyroid hormone. To examine the mechanism of thyroid hormone's effect on LPL, LPL gene expression was assessed in the epididymal fat pads of hypothyroid rats....

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Main Authors: B Saffari, JM Ong, PA Kern
Format: Article
Language:English
Published: Elsevier 1992-02-01
Series:Journal of Lipid Research
Online Access:http://www.sciencedirect.com/science/article/pii/S0022227520415445
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spelling doaj-9a99ad8889324dd4815ca1022af2a87b2021-04-26T05:52:54ZengElsevierJournal of Lipid Research0022-22751992-02-01332241249Regulation of adipose tissue lipoprotein lipase gene expression by thyroid hormone in rats.B Saffari0JM Ong1PA Kern2Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048.Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048.Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048.Lipoprotein lipase (LPL) is an important enzyme in lipid metabolism, and adipose LPL activity is increased in rats that are deficient in thyroid hormone. To examine the mechanism of thyroid hormone's effect on LPL, LPL gene expression was assessed in the epididymal fat pads of hypothyroid rats. When compared to control rats, LPL activity, mass, and synthetic rate in hypothyroid rats were increased; heparin-releasable LPL activity and mass were increased to 448% and 300% of control, respectively, and [35S]methionine incorporation into LPL was increased to 250% of control. The increases in LPL activity and mass were reversed by treatment of hypothyroid rats with triiodothyronine (T3). However, there was no change in the level of LPL mRNA when compared to the level of gamma-actin mRNA and no effect on LPL transcription using run-off assays. Isolated adipocytes were prepared from normal rats and exposed to 2 nM T3 in vitro for 24 h. The addition of T3 to cultures of adipocytes resulted in a decrease in LPL activity, mass, and [35S]methionine incorporation, but still no change in LPL mRNA level. To determine whether thyroid hormone regulated catecholamine responsiveness, adipocytes were prepared from hypothyroid and control rats, and the responses to epinephrine were compared. Although epinephrine inhibited [35S]methionine incorporation into LPL in control rat adipocytes, there was essentially no effect in hypothyroid rat cells. In addition, T3 treatment of the hypothyroid rats restored the responsiveness to epinephrine. Thus, thyroid hormone regulates LPL in rat adipose tissue posttranscriptionally, resulting in parallel changes in LPL synthetic rate, immunoreactive mass, and activity.(ABSTRACT TRUNCATED AT 250 WORDS)http://www.sciencedirect.com/science/article/pii/S0022227520415445
collection DOAJ
language English
format Article
sources DOAJ
author B Saffari
JM Ong
PA Kern
spellingShingle B Saffari
JM Ong
PA Kern
Regulation of adipose tissue lipoprotein lipase gene expression by thyroid hormone in rats.
Journal of Lipid Research
author_facet B Saffari
JM Ong
PA Kern
author_sort B Saffari
title Regulation of adipose tissue lipoprotein lipase gene expression by thyroid hormone in rats.
title_short Regulation of adipose tissue lipoprotein lipase gene expression by thyroid hormone in rats.
title_full Regulation of adipose tissue lipoprotein lipase gene expression by thyroid hormone in rats.
title_fullStr Regulation of adipose tissue lipoprotein lipase gene expression by thyroid hormone in rats.
title_full_unstemmed Regulation of adipose tissue lipoprotein lipase gene expression by thyroid hormone in rats.
title_sort regulation of adipose tissue lipoprotein lipase gene expression by thyroid hormone in rats.
publisher Elsevier
series Journal of Lipid Research
issn 0022-2275
publishDate 1992-02-01
description Lipoprotein lipase (LPL) is an important enzyme in lipid metabolism, and adipose LPL activity is increased in rats that are deficient in thyroid hormone. To examine the mechanism of thyroid hormone's effect on LPL, LPL gene expression was assessed in the epididymal fat pads of hypothyroid rats. When compared to control rats, LPL activity, mass, and synthetic rate in hypothyroid rats were increased; heparin-releasable LPL activity and mass were increased to 448% and 300% of control, respectively, and [35S]methionine incorporation into LPL was increased to 250% of control. The increases in LPL activity and mass were reversed by treatment of hypothyroid rats with triiodothyronine (T3). However, there was no change in the level of LPL mRNA when compared to the level of gamma-actin mRNA and no effect on LPL transcription using run-off assays. Isolated adipocytes were prepared from normal rats and exposed to 2 nM T3 in vitro for 24 h. The addition of T3 to cultures of adipocytes resulted in a decrease in LPL activity, mass, and [35S]methionine incorporation, but still no change in LPL mRNA level. To determine whether thyroid hormone regulated catecholamine responsiveness, adipocytes were prepared from hypothyroid and control rats, and the responses to epinephrine were compared. Although epinephrine inhibited [35S]methionine incorporation into LPL in control rat adipocytes, there was essentially no effect in hypothyroid rat cells. In addition, T3 treatment of the hypothyroid rats restored the responsiveness to epinephrine. Thus, thyroid hormone regulates LPL in rat adipose tissue posttranscriptionally, resulting in parallel changes in LPL synthetic rate, immunoreactive mass, and activity.(ABSTRACT TRUNCATED AT 250 WORDS)
url http://www.sciencedirect.com/science/article/pii/S0022227520415445
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