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K Fiedorowicz

Publications and source records attributed to K Fiedorowicz.

8 recordsLinked to original sources
PubMed1987

Decrease of rat-liver-T4-5'-deiodinase activity during chronical isoprenaline beta-action in vivo.

Pure adrenergic beta-action, brought about by long-term adrenaline + regitine application in rats, was able to increase liver T4-5'-deiodinase activity for 8 h (Nauman et al. 1984a). Long-term isoprenaline application without alpha-blocking yielded contrary results. One of the compensatory mechanism to be probably blamed could have been the very high endogenous adrenaline-levels (Porta et al. 1985). Simultaneous treatment with isoprenaline and alpha-methyltyrosinemethylester did not settle the problem since even then deiodinase activity was still drastically decreased. Two more components have been found which could very well be the reason for that "paradox beta-action" in vivo, namely very low glucose and insulin levels, both of which are known to influence deiodinase activity. In vivo--contrary to in vitro--it is seemingly not possible that catecholaminergic beta-action could increase the peripheral production of T3 unless general alpha-blocking took place.

Animals↗
PubMed1984

The effect of adrenaline pretreatment on the in vitro generation of 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine (reverse T3) in rat liver preparation.

The effects of adrenaline (A) on liver T3 and rT3 neogenesis from T4 were studied in Wistar rats. The animals were implanted subcutaneously either with A or placebo (P) especially coated tablets which linearly released the hormone. The serum A values 6 hrs after implantation of 7.5, 15.0 and 45.0 mg tablets were 6.5 +/- 1.31, 6.8 +/- 1.8 and 16.4 +/- 1.9 ng/ml, respectively vs 4.4 +/- 2.5 ng/ml seen in P pretreated group. The output rates of A were 0.11 (7.5 mg), 0.18 (15 mg) and 0.52 microgram/ml (45 mg). The pretreatment with A led to hyperglycemia and the "low T3 syndrome". Neogenesis of T3 from T4 in medium containing liver microsomes of P pretreated rats was 5.49 +/- 0.25 pmol of T3/mg protein/min and decreased in A pretreated rats to 3.82 +/- 0.17, 3.12 +/- 0.27 and 3.06 +/- 0.11 pmol of T3/mg of protein/min. Neogenesis of rT3 from T4 in microsomes from P group was 1.52 +/- 0.09 pmol rT3/mg protein/min and increased after A to 2.71 +/- 0.11, 2.60 +/- 0.21 and 2.21 +/- 0.34 pmol of rT3/mg protein/min thus showing no dose dependency. Enrichment of microsomes medium with cytosol either from P or A pretreated rats had no effect on T3 generation thus excluding effect of A on cytosolic cofactor. Although cytosol further increased rT3 neogenesis this was seen regardless of whether cytosol was obtained from A or P implanted rats. It is concluded that A decreases the activity of T4-5'-deiodinase in liver, and possibly increases the activity of T4-5-deiodinase.

Animals↗
PubMedDate not supplied

[Regulation of triiodothyronine levels in fatty tissue in obese patients].

Specific activity of T4-5'-deiodinase, the enzyme which catalyze peripheral production of triiodothyronine (T3) from thyroxine (T4) has been evaluated in the subcutaneous adipose tissue of obese patients. In lean healthy women (BMI less than 21) mean activity of T4-5'-D was found to be 122 +/- 29.4 fmol T3/mg of protein/min and was higher then respective activity of the enzyme in adipocytes of patients with mild obesity (22 less than BMI less than 30) where the mean was 92.14 +/- 18.05 fmol T3/mg/min. The activity of T4-5'-D was significantly decreased in patients with severe obesity (BMI less than 30) when compared with respective activity of the enzyme found in controls (47.36 +/- 18.4 fmol T3/mg/min vs 122.4 +/- 29.4 fmol T3/mg/min; p less than 0.01). As T4-5'-D in human adipose tissue has been previously characterized as type II of the enzyme, diminished activity found in obese subjects means that thyroid metabolic activity of adipocyte is decreased. Such a state would lead to antilipolytic action of catecholamines in obesity.

Adipose Tissue↗