Thyroid hormone affects the hydrolysis of inositol phospholipids in the rat hypothalamus

Iriuchijima, Tokuji; Mizuma, Haruo; Michimata, Toshio; Ogiwara, Takayuki; Yamada, Masanobu; Murakami, Masami; Mori, Masataka

doi:10.1016/0304-3940(92)90534-e

Cited by 4 publications

(3 citation statements)

References 17 publications

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“…Similarly, decreased PS + PI might be related to turnover, in the sense that PS can be decarboxylated to yield (which we found to increase), and that PI hydrolysis is often a feature of stimulated phospholipid turnover [25]. In this connection, it should be mentioned that thyroid hormones have been reported to promote inositol phospholipid hydrolysis in rat hypothalamus [26]. These and other possible mechanisms for changes in PC and PE content exist, and remain to be explored.…”

Section: Discussionmentioning

confidence: 72%

Thyroid hormone treatment alters phospholipid composition and membrane fluidity of rat brain mitochondria

Bangur

Howland

Katyare

1995

Biochemical Journal

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We examined effects of graded doses of thyroid hormones 3,3', 5-tri-iodo-L-thyronine (T3) and L-thyroxine (T4) on the lipid composition of rat brain mitochondria. Neither hormone significantly affected the mitochondrial cholesterol or total phospholipid content, but did increase phosphatidylethanolamine (PE) at the expense of phosphatidylserine (PS), phosphatidylinositol (PI) and phosphatidylcholine (PC). The phosphatidic acid (PA) content was also elevated, suggesting enhanced phospholipid turnover. Changes in sphingomyelin (SPM) and diphosphatidylglycerol (DPG) were minimal. Mitochondrial membrane fluidity also increased after thyroid-hormone treatment, and the increase was closely correlated with PC/PE and SPM/PE molar ratios.

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Section: Discussionmentioning

confidence: 72%

Thyroid hormone treatment alters phospholipid composition and membrane fluidity of rat brain mitochondria

Bangur

Howland

Katyare

1995

Biochemical Journal

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“…The hypothyroidism enhanced the insuline-mediated phosphoinositides synthesis. The hypothyroidism caused a significant increase in both the basal and ouabain-stimulated accumulation of [ 3 H]inositol phosphate in the hypothalamic slices, whereas the thyroxine (L-T 4 ) completely restored the hypothalamic [ 3 H]inositol phosphate formation [18]. The results indicate that the negative feedback action of the thyroid hormone may occur at a post-receptor site in the hypothalamus.…”

Section: Introductionmentioning

confidence: 99%

Effects of thyroxine and 1-methyl, 2-mercaptoimidazol on phosphoinositides synthesis in rat liver

Babenko

Krasilnikova

2004

Lipids Health Dis

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BackgroundPhosphoinositides mediate one of the intracellular signal transduction pathways and produce a class of second messengers that are involved in the action of hormones and neurotransmitters on target cells. Thyroid hormones are well known regulators of lipid metabolism and modulators of signal transduction in cells. However, little is known about phosphoinositides cycle regulation by thyroid hormones. The present paper deals with phosphoinositides synthesis de novo and acylation in liver at different thyroid status of rats.ResultsThe experiments were performed in either the rat liver or hepatocytes of 90- and 720-day-old rats. Myo-[3H]inositol, [14C]CH3COONa, [14C]oleic and [3H]arachidonic acids were used to investigate the phosphatidylinositol (PtdIns), phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate (PtdInsP2) synthesis. 1-methyl, 2-mercaptoimidazol-induced hypothyroidism was associated with the decrease of myo-[3H]inositol and [3H]arachidonic acids incorporation into liver phosphoinositides and total phospholipids, respectively. The thyroxine (L-T4) injection to hypothyroid animals increased the hormones contents in blood serum and PtdInsP2 synthesis de novo as well as [3H]arachidonic acids incorporation into the PtdIns and PtdInsP2. Under the hormone action, the [14C]oleic acid incorporation into PtdIns reduced in the liver of hypothyroid animals. A single injection of L-T4 to the euthyroid [14C]CH3COONa-pre-treated animals or addition of the hormone to a culture medium of hepatocytes was accompanied by the rapid prominent increase in the levels of the newly synthesized PtdIns and PtdInsP2 and in the mass of phosphatidic acid in the liver or the cells.ConclusionsThe data obtained have demonstrated that thyroid hormones are of vital importance in the regulation of arachidonate-containing phosphoinositides metabolism in the liver. The drug-induced malfunction of thyroid gland noticeably changed the phosphoinositides synthesis de novo. The L-T4 injection to the animals was followed by the time-dependent increase of polyphosphoinositide synthesis in the liver. The both long-term and short-term hormone effects on the newly synthesized PtdInsP2 have been determined.

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“…In contrast, experimental hyperthyroidism caused a significant increase in inositol trisphosphate formation and PLC activation in the perfused hearts while hypothyroidism was associated with a decrease in this activity [ 12 ]. Hypothyroidism increased the basal PLC-linked inositol phospholipid hydrolysis in rat hypothalamus, whereas L-T 4 supplementation to hypothyroid rats resulted in a complete restoration of hypothalamic inositol phosphate formation to the value of euthyroid control [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Drug-induced and postnatal hypothyroidism impairs the accumulation of diacylglycerol in liver and liver cell plasma membranes

Krasilnikova¹,

Kavok²,

Babenko³

2002

BMC Physiol

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Background: Thyroid hormones are well known modulators of signal transduction. The effect of hyper-and hypo-thyroidism on diacylglycerol/protein kinase C (DAG/PKC) signaling in cardiomiocytes has been determined. Triiodothyronine (T 3 ) has been shown to prevent the α1-adrenoreceptor-mediated activation of PKC but does not alter the stimulation of enzyme and hepatic metabolism by phorbol ethers. It has been suggested that the elevation of endogenous DAG in senescent or hypothyroid cells changes the PKC-dependent response of cells to phorbol esters and hormones. In the present study, was examined the formation of DAG and activation of PKC in liver cells from rats of different thyroid status.

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Thyroid hormone affects the hydrolysis of inositol phospholipids in the rat hypothalamus

Cited by 4 publications

References 17 publications

Thyroid hormone treatment alters phospholipid composition and membrane fluidity of rat brain mitochondria

Thyroid hormone treatment alters phospholipid composition and membrane fluidity of rat brain mitochondria

Effects of thyroxine and 1-methyl, 2-mercaptoimidazol on phosphoinositides synthesis in rat liver

Drug-induced and postnatal hypothyroidism impairs the accumulation of diacylglycerol in liver and liver cell plasma membranes

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