Sterol regulatory element-binding proteins are regulators of the NIS gene in thyroid cells.

The uptake of iodide into the thyroid, an essential step in thyroid hormone synthesis, is an active process mediated by the sodium-iodide symporter (NIS). Despite its strong dependence on TSH, the master regulator of the thyroid, the NIS gene was also reported to be regulated by non-TSH signaling pathways. In the present study we provide evidence that the rat NIS gene is subject to regulation by sterol regulatory element-binding proteins (SREBPs), which were initially identified as master transcriptional regulators of lipid biosynthesis and uptake.

Fasting and caloric restriction increases mRNA concentrations of novel organic cation transporter-2 and carnitine concentrations in rat tissues.

Background: Recently, we have shown that activation of peroxisome proliferator-activated receptor (PPAR)-alpha by clofibrate leads to an upregulation of novel organic cation transporter (OCTN)-2, a carnitine transporter, and in turn increases the carnitine concentration in the liver of rats. In this study, we tested the hypothesis that fasting and caloric restriction, conditions under which PPARalpha activation also occurs, cause similar effects.

Methods: Three groups of rats received the diet either ad libitum (control rats) or 10.

Clofibrate treatment up-regulates novel organic cation transporter (OCTN)-2 in tissues of pigs as a model of non-proliferating species.

Recent studies have shown that treatment of rodents with agonists of peroxisome proliferator-activated receptor (PPAR)-alpha causes an up-regulation of novel organic cation transporter (OCTN)-2, a carnitine transporter, and increases carnitine concentration in the liver. This study was performed to investigate whether such effects occur also in pigs which like humans have a lower expression of PPAR alpha and are less responsive to treatment with PPAR alpha agonists than rodents. An experiment with 18 pigs was performed which were fed a control diet or the same diet supplemented with 5 g clofibrate/kg for 28 days.

Research paper effects of 13-HPODE on expression of genes involved in thyroid hormone synthesis, iodide uptake and formation of hydrogen peroxide in porcine thyrocytes.

It has been shown that dietary oxidized fats influence thyroid function in rats and pigs. Mechanism underlying this phenomenon are unknown. This study was performed to investigate whether 13-hydroperoxy-9,11 -octadecadienic acid (13-HPODE), a primary oxidation product of linoleic acid, affects expression of gene involved in thyroid hormone synthesis and formation of hydrogen peroxide in primary porcine thyrocytes.

Dietary oxidised fat up regulates the expression of organic cation transporters in liver and small intestine and alters carnitine concentrations in liver, muscle and plasma of rats.

It has been shown that treatment of rats with clofibrate, a synthetic agonist of PPARalpha, increases mRNA concentration of organic cation transporters (OCTN)-1 and -2 and concentration of carnitine in the liver. Since oxidised fats have been demonstrated in rats to activate hepatic PPARalpha, we tested the hypothesis that they also up regulate OCTN. Eighteen rats were orally administered either sunflower-seed oil (control group) or an oxidised fat prepared by heating sunflower-seed oil, for 6 d.

Clofibrate treatment in pigs: effects on parameters critical with respect to peroxisome proliferator-induced hepatocarcinogenesis in rodents.

Background: In rodents treatment with fibrates causes hepatocarcinogenesis, probably as a result of oxidative stress and an impaired balance between apoptosis and cell proliferation in the liver. There is some debate whether fibrates could also induce liver cancer in species not responsive to peroxisome proliferation. In this study the effect of clofibrate treatment on peroxisome proliferation, production of oxidative stress, gene expression of pro- and anti-apoptotic genes and proto-oncogenes was investigated in the liver of pigs, a non-proliferating species.

Feeding of a deep-fried fat causes PPARalpha activation in the liver of pigs as a non-proliferating species.

Recent studies have shown that dietary oxidised fats influence the lipid metabolism in rats by activation of PPARalpha. In this study, we investigated whether a mildly oxidised fat causes activation of PPARalpha in pigs which are non-proliferators like man. Eighteen pigs were assigned to two groups and received either a diet containing 90 g/kg of a fresh fat or the same diet with 90 g/kg of an oxidised fat prepared by heating for 24 h at 180 degrees C in a deep fryer.

Clofibrate causes an upregulation of PPAR-{alpha} target genes but does not alter expression of SREBP target genes in liver and adipose tissue of pigs.

This study investigated the effect of clofibrate treatment on expression of target genes of peroxisome proliferator-activated receptor (PPAR)-alpha and various genes of the lipid metabolism in liver and adipose tissue of pigs. An experiment with 18 pigs was performed in which pigs were fed either a control diet or the same diet supplemented with 5 g clofibrate/kg for 28 days. Pigs treated with clofibrate had heavier livers, moderately increased mRNA concentrations of various PPAR-alpha target genes in liver and adipose tissue, a higher concentration of 3-hydroxybutyrate, and markedly lower concentrations of triglycerides and cholesterol in plasma and lipoproteins than control pigs (P < 0.

PPARalpha agonists up-regulate organic cation transporters in rat liver cells.

It has been shown that clofibrate treatment increases the carnitine concentration in the liver of rats. However, the molecular mechanism is still unknown. In this study, we observed for the first time that treatment of rats with the peroxisome proliferator activated receptor (PPAR)-alpha agonist clofibrate increases hepatic mRNA concentrations of organic cation transporters (OCTNs)-1 and -2 which act as transporters of carnitine into the cell.

Clofibrate increases hepatic triiodothyronine (T3)- and thyroxine (T4)-glucuronosyltransferase activities and lowers plasma T3 and T4 concentrations in pigs.

In rats, clofibrate acts as a microsomal enzyme inducer and disrupts the metabolism of thyroid hormones by increasing hepatic glucuronidation of thyroxine. Whether similar effects occur in the pig has not yet been investigated. This study was performed to investigate the effect of clofibrate treatment on metabolism of thyroid hormones in pigs.