Influence of thyroid status on hepatic α₁-adrenoreceptor responsiveness

Abstract

The present work aimed to elucidate the influence of thyroid functional status on the α1-adrenoreceptor-induced activation of hepatic metabolic functions. The experiments were performed in either a nonrecirculating liver perfusion system featuring continuous monitoring of portal pressure,[Formula: see text], pCa, and pH, or isolated hepatocytes from euthyroid, hyperthyroid, and hypothyroid rats. Hypothyroidism decreased the α1-adrenergic stimulation of respiration, glycogen breakdown, and gluconeogenesis. These effects were accompanied by a decreased intracellular Ca2+ mobilization corroborating that those processes are regulated by the Ca2+-dependent branch of the α1-adrenoreceptor signaling pathway. Moreover, in hyperthyroid rats the α1-adrenergic-induced increase in cytosolic Ca2+ was enhanced, and glucose synthesis or mobilization was not altered. The thyroid status influenced neither the α1-adrenergic stimulation of vascular smooth muscle contraction nor the α1-agonist-induced intracellular alkalinization and protein kinase C (PKC) activation. Thus the distinct impairment of the Ca2+-dependent branch of the α1-adrenoreceptor signaling pathway by thyroid status provides a useful tool to investigate the role played by each signaling pathway, Ca2+ or PKC, in controlling hepatic functions.

Anti-apoptotic effects of 3,5,3′-tri-iodothyronine in mouse hepatocytes

“…Our observations are consistent with previous reports regarding enhanced intracellular cAMP content in different cells after THs application (Yen 2001, Shih et al 2004. THs modulated the activity of phosphodiesterase (Morgan et al 1982) and mimicked the effects of cAMP-inducing hormones (Muller & Seitz 1983, Daza et al 1997. Furthermore, cAMPinduced PKA activation has been shown to mediate THs effects (Lin et al 1999), such as potentiation of growth hormone receptor signaling in cancer cells (Shih et al 2004).…”

“…The status of THs modulated the steady-state levels of specific G-proteins induced by b-adrenergic agonists (Daza et al 1997). It has also been shown that THs positively regulated epidermal growth factor receptor signaling pathway (Lin et al 1999, Di Fulvio et al 2000, Shih et al 2004) -established survival regulator of Fas-induced apoptosis (Gibson et al 1999).…”

Acute Effect of Leptin on Hepatic Glycogenolysis and Gluconeogenesis in Perfused Rat Liver

“…Epinephrine (50 nmol/L)-stimulated glucose release during control experiments (28.3 Ϯ 2.8 µmol/g liver within 30 minutes) was similar to that of 1,000 nmol/L phenylephrine in hepatocytes from fed rats (ϳ27 µmol/g liver within 30 minutes) 34 and even higher than in other liver perfusion systems (ϳ16 µmol/g liver within 30 minutes). 35 Insulin and leptin reduced, but did not completely block, epinephrinestimulated glycogenolysis. 36,37 However, simultaneous infusion of insulin and leptin did not additively inhibit epinephrine-induced hepatic glycogenolysis (Fig.…”

Effect of Thyroid Hormones on Distension-Induced Gastric Acid and Pepsin Secretions in Rats

“…In some organs like the heart, thyroid hormones increase beta-adrenergic receptors, 2 while in the liver and smooth muscle cells of vessel walls, alpha-adrenergic receptors are increased by thyroid hormones. 1,7 It is probable that thyroid hormones increase cholinergic, histaminic and gastrin receptors in chief cells and parietal cells of stomach. Kayode et al have observed that thyroxin increases mitotic activity of crypt cells of digestive tract in rats.…”

“…Thyroid hormones affect the function of some body organs including cardiovascular [1][2][3] and nervous systems, [4][5][6] liver, 7 development and reproductive systems and growth process. [8][9] There is evidence that they also affect gastric acid and pepsin secretions.…”