Post by Max on Jun 12, 2005 8:04:28 GMT -5
Levels of thyroxine and triiodothyronine were found to be lower after (Ro)accutane exposure in acne-subjects (p less than 0.05) [4]. Significant inhibition of thyroid receptor expression in various cell types has been observed in subjects treated with 5microM retinoic acid - plasma concentrations associated with the exposure to (Ro)accutane in acne-subjects. A decline that may be fortified with age.
In pituitary GH1 cells a maximal thyroid receptor beta-2 (TRbeta2) decrease of 50-70% in (Ro)accutane related doses in acne-subjects was observed [2]. TRbeta2 is found mainly in the pituitary gland and hypothalamus.
The amount of thyroid receptor (TR) mRNA, alpha as well as beta subtypes, was found to be significantly decreased in elderly, indicating an age-related sub-clinical hypothyroidism [1], and may mean that a worsening hypothyroidism with age in (Ro)accutane exposed subjects could be expected.
During and after a (Ro)accutane exposure a suppressive effect of the growth hormone stimulus is here suggested, by altered circulating GH/IGF-1 ratios, here suggested to be partially a result of inhibition of thyroid function [4] and inhibition of receptor TRbeta2 expression [2] (anterior pituitary cell-receptor inhibition and thyrotropes and somatropes increasingly undergoing apoptosis), 9-cis retinoic acid receptor-alpha (RXRalpha) interaction with IGFBP-3 [5]. The effects on GH/IGF-1 receptor expression during and after a (Ro)accutane exposure are not known.
A worsened effect of partial growth hormone deficiency is suggested to be worsened with age due to age-related further declining circulating GH-IGF levels, and with increasing age the GH/IGF-1 axis undergoes changes such as decreased GH and IGF-1 concentrations in the brain. This decline in hormone levels has been associated with changes of certain CNS functions such as age-related memory impairments [3].
Insulin-like growth factor-1 (IGF-1) and growth hormone (GH) have been suggested to promote memory and cognitive capabilities. Both GH and IGF-1 affect the size and morphology of the central nervous system (CNS) during development and alter differentiated cell functions like neural growth, myelination, and cognitive performance. [3]
In pituitary GH1 cells a maximal thyroid receptor beta-2 (TRbeta2) decrease of 50-70% in (Ro)accutane related doses in acne-subjects was observed [2]. TRbeta2 is found mainly in the pituitary gland and hypothalamus.
The amount of thyroid receptor (TR) mRNA, alpha as well as beta subtypes, was found to be significantly decreased in elderly, indicating an age-related sub-clinical hypothyroidism [1], and may mean that a worsening hypothyroidism with age in (Ro)accutane exposed subjects could be expected.
During and after a (Ro)accutane exposure a suppressive effect of the growth hormone stimulus is here suggested, by altered circulating GH/IGF-1 ratios, here suggested to be partially a result of inhibition of thyroid function [4] and inhibition of receptor TRbeta2 expression [2] (anterior pituitary cell-receptor inhibition and thyrotropes and somatropes increasingly undergoing apoptosis), 9-cis retinoic acid receptor-alpha (RXRalpha) interaction with IGFBP-3 [5]. The effects on GH/IGF-1 receptor expression during and after a (Ro)accutane exposure are not known.
A worsened effect of partial growth hormone deficiency is suggested to be worsened with age due to age-related further declining circulating GH-IGF levels, and with increasing age the GH/IGF-1 axis undergoes changes such as decreased GH and IGF-1 concentrations in the brain. This decline in hormone levels has been associated with changes of certain CNS functions such as age-related memory impairments [3].
Insulin-like growth factor-1 (IGF-1) and growth hormone (GH) have been suggested to promote memory and cognitive capabilities. Both GH and IGF-1 affect the size and morphology of the central nervous system (CNS) during development and alter differentiated cell functions like neural growth, myelination, and cognitive performance. [3]