Hi everyone,
It seems that long term pertubations of the pituitary-thyroid axis by various xenobiotics or physiologic alterations ( eg, iodine deficiency, partial thyroidectomy, PUFA, goitrogenic foods...) are more likely to predispose laboratory rodents than humans to a higher incidence of proliferative lesions in the thyroid.
" This appears to be particulary true in the male rat, which usually has higher circulating levels of TSH than the female rat.
The greater sensitivity of the rodent thyroid/metabolism to derangement by drugs, chemicals, herbs, foods and physiologic pertubations also is related to the shorter plasma half-life of T4 rodents than in humans due to considerable differences between species in the transport proteins for T4.
The plasma half-life of T4 in rats (12 -24 hours) is considerably shorter than in humans (5-9 days). This is related in part to differences between species in the transport proteins for T4 and T3. In humans and in monkeys, circulating T4 is bound primarily to thyroxine-binding globulin (TBG); however, this high-affinity binding protein for T4 is not present or is present in minute amounts in rodents, birds, amphibians, and fish. The binding affinity of TBG for T4 is about 1000 times higher than for T4-binding prealbumin or transthyretin. The percentage of unbound active T4 is lower in species with high levels of TBG than in animals in which T4 binding is limited to albumin and prealbumin.
T3 is transported bound to TBG and albumins in humans, monkeys, and dogs but only to albumin and transthyretin in mice, rats, and chickens." source: Werner and Ingbar's The Thyroid.
Keeping the statement made above in mind, I was wondering how relevant is to transpose studies (involving the thyroid, PUFA ect....) made on rodents to humans?
In most case, it seems that those studies probably reflect the worst scenario for humans.....and that our tolerance for any thyroid disturbing subtances are probably much higher than we think.
Any opinions?
It seems that long term pertubations of the pituitary-thyroid axis by various xenobiotics or physiologic alterations ( eg, iodine deficiency, partial thyroidectomy, PUFA, goitrogenic foods...) are more likely to predispose laboratory rodents than humans to a higher incidence of proliferative lesions in the thyroid.
" This appears to be particulary true in the male rat, which usually has higher circulating levels of TSH than the female rat.
The greater sensitivity of the rodent thyroid/metabolism to derangement by drugs, chemicals, herbs, foods and physiologic pertubations also is related to the shorter plasma half-life of T4 rodents than in humans due to considerable differences between species in the transport proteins for T4.
The plasma half-life of T4 in rats (12 -24 hours) is considerably shorter than in humans (5-9 days). This is related in part to differences between species in the transport proteins for T4 and T3. In humans and in monkeys, circulating T4 is bound primarily to thyroxine-binding globulin (TBG); however, this high-affinity binding protein for T4 is not present or is present in minute amounts in rodents, birds, amphibians, and fish. The binding affinity of TBG for T4 is about 1000 times higher than for T4-binding prealbumin or transthyretin. The percentage of unbound active T4 is lower in species with high levels of TBG than in animals in which T4 binding is limited to albumin and prealbumin.
T3 is transported bound to TBG and albumins in humans, monkeys, and dogs but only to albumin and transthyretin in mice, rats, and chickens." source: Werner and Ingbar's The Thyroid.
Keeping the statement made above in mind, I was wondering how relevant is to transpose studies (involving the thyroid, PUFA ect....) made on rodents to humans?
In most case, it seems that those studies probably reflect the worst scenario for humans.....and that our tolerance for any thyroid disturbing subtances are probably much higher than we think.
Any opinions?