T2 articles

[Guest guest]

I actually researched this a bit a long time ago. Here is some of

it. Any links may be dead by now:

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Paper: Thyroid hormones and Mitochondria by goglia F, Silvestri E,

and Lanni A

Two iodothyronines have been identified as effectors of the actions

of thyroid hormones on energy metabolism: 3',3,5-triiodo-L-thyronine

(T3) and 3,5-diiodo-L-thyronine (T2). Both have significant effects

on BMR, but their mechanisms of action are not identical. T3 acts on

the nucleus to influence the expression of genes involved in the

regulation of cellular metabolism and mitochondria function; 3,5-T2,

on the other hand, acts by directly influencing the mitochondrial

energy-transduction apparatus. A molecular determinant of the

effects of T3 could be uncoupling protein-3 (UCP-3), while the

cytochrome-c oxidase complex is a possible target for 3,5-T2. In

conclusion, it is likely that iodothyronines regulate energy

metabolism by both short-term and long-term mechanisms, and that

they act in more than one way in affecting mitochondrial functions.

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Paper: Demonstration of in Vivo metabolic effects of 3,5

diiodothyronine by M cimmino, F Mion, F Goglia, Y Minaire and A

Geloen

" ...3,5-T(2) exerts metabolic effects on energy expenditure, on both

lipid beta-oxidation and leucine metabolism in hypothyroid rats. We

conclude that 3,5-T(2) is a metabolically active iodothronine. "

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Paper: Direct effects of 3,5,3' -triiodothyronine and 3,5-

diiodothyronine on mitochondrial metabolism in the goldfish

Carassius auratus byLeary sc, Barton kn, Ballantyne JS

" State 3 oxidation of pyruvite was significantly higher for liver

mitochondria treated with T2 and for red muscle mitochondria

incubated with T3 when compared to control mitochoondria. Rapid

elevation of state 3 rates of substrate oxidation by thyroid

hormones may be important in mediating diurnal changes in

mitochondrial metabolism. Significant increases in liver and red

muscle mitochondrial state 4 rates were also observed for pyruvite

in T2- and T3-treated mitochondrial and for glutamate in T3-treated

mitochondria. "

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Paper: 3,5-diiodothyronine and 3,5,3'-triiodothyronine both improve

cold tolerance of hypothyroid rats, but possibly via different

mechanisms by Lanni A, Moreno M, Lombardi A, Goglia F (The tittle

says it all.)

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Paper: 3,5,-diiodothyronine (T2) regulates glucose-6-phosphate

dehydrogenase activity in the rat by Lombardi A, Beneduce L, Moreno

M, Diano S, etc.

T2/100 g BW (grams per body weight) affects G6PD activity 3-5 times

more than the same dose of T3. These data provide the first evidence

that T2 is a factor capable of regulating G6PD activity.

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Paper: Action of thyroid hormones at the cellular level: the

mitochondrial target by Goglia F, Moreno M, Lanni A.

Not only triiodo-L-thyronine, but also diiothyronines are active in

regulating the energy metabolism. They influence resting metabolism

in rats with 3, 5-diiodo-L-thyronine seeming to show a clearer

effect.

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Paper: Calorigenic effect of diiodothyronines in the rat by Lanni A,

Moreno M, Lombardi A, Goglia F,

These results suggest that T8 isomers might be mediators of the

direct thyroid hormone regulation of energy metabolism.

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Bodybuilding article: T2 - The Fat Terminator? by M Berardi

(Article with citations.)

http://www.johnberardi.com/articles/supplementation/t2.htm

T2 may be benificial in rapid energy requiring situations like cold

exposure or overfeeding. (This may be important for energy under

stress, for which I was suffering a real lack of.)

In one human study, T2 significantly increased oxygen consumption in

blood cells in vitro.

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Paper: Effect of 3,5,3' -triiodothyroinine-induced hyperthyroidism

on iodothyronine metabolism in the rat: evidence for tissue

differences in metabolis responses by Chopra IJ, Huang TS, Hurd RE,

Solomon DH

The mondeiodination of 3,5-T2 to 3-T1 increased significantly only

in the cebral cortex and liver and not in any other tissue. (This

information along with other sources indicate that T1 is needed by

the brain. The brain has enzyme pathways that seem specificly there

for production of T1. An article listed later also talks about the

function of T1 in the brain)

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Paper: Di-iodothyronine as part of the oestradiol and catechol

oestrogen receptor—the role of iodine, thyroid hormones and

melatonin in the aetiology of breast cancer. by Clur A.

The present author proposes that the tyrosyl residue in the

hydrophobic oestrogen binding site of the oestrogen receptor is post

translationally modified to monoiodotyrosine and hence 3,3' di-

iodothyronine monoamine (T2) by peroxidase activity. He has

previously proposed that various monoamine receptors are also T2

based. The densities of these receptors are increased in

hypothyroidism and they exert control over release of prolactin and

other hormones, including melatonin at multiple sites in the

hypothalamic—pituitary axis. Melatonin is a metabolite of serotonin

and hence melatonin receptors may be T2 or rT3 based as well. These

factors could be significant in the aetiology of breast cancer as

high prolactin and melatonin levels may be protective. Oestrogen

receptor density may be increased in hypothyroidism as is certain

monoamine receptor density. This would amplify the effect of high

circulation oestrogen levels in hypothyroidism and may help explain

why hypothyroidism and low iodine intake are risk factors for

breast, uterine and ovarian cancer. (This paper indicates that

estrogen receptor and melatonin status are influenced by thyroid

hormones other than T3. Other studies have found that T2 production

and RT3 production increase in hypothyroidism and there is a

resultant increase in cellular sensitivity to estrogen. Therefore,

T3 only therapy may have unintended hormonal consequences such as

low estrogen symptoms and sleep disturbances.)

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Well dodumented article: The Thyroid Handbook by Cy Willson (Article

with citations)

http://www.t-mag.com/nation_articles/152thy.html

T3 increases aerobic mitochondria function or respiration, but

another thyroid hormone, T2 may actually be responsible for this

action.

This increase in beta-3 number (from T2) means that it can increase

the effectiveness of norephedrine and ephedrine. (Several articles

demonstrate that without adequate amounts of the other thyroid

hormones as would likely happen with T3 and T4 only therapy, more

work is required from the adrenals. This would not be a benificial

thing for the adrenally fatigued and I now suspect that those on T3

therapy recover from adrenal fatigue at a slower rate compared to

those who are able to use Armour.)

The authors of the study discovered that out of T4 and T3, only T2

was active in stimulating rapid hepatic oxygen consumption. They

concluded that it acts rapidly and directly through activation of

the mitochondria.

In another study, T3 and T2 were compared in terms of Resting

Metabolism (RM) and on the oxidative capacity of tissues that are

metabolically active (liver, muscle tissue, brown adipose tissue or

BAT, and heart). What they found was that T2 had a dose-dependent

effect which increased RM and oxidative capacity. They found the

greatest response to T2 was in liver and in BAT, which is exactly

what you'd want, if fighting fat was a main concern. The effects

again occurred rapidly and independent of protein synthesis. They

stated that their results suggested isomers like T2 could be direct

mediators of thyroid hormone regulation on energy metabolism.

Yet another study also found increased hepatic oxidative capacity

and thought that it was due to a direct action upon the mitochondria

by T2.(16) Other studies had similar findings. And yet another study

showed the same thing: increased oxidative capacity and energy

expenditure, causing them to deduce that T2 and T3 displayed similar

effects.(19) T2 was also shown to have a similar effect to that of

T3 on lipid metabolism with T2 actually doing a little better in

some tissue.

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Papaer: Peripheral Metabolism of Thyroid Hormones: A Review by Greg

, ND (This is an excellent paper with much information that I

highly recommend reading. I did not copy sections out of it as there

were so many things worth noting and it would take up a lot of

space.)

http://www.thorne.com/altmedrev/.fulltext/5/4/306.html

This paper discusses the function of T2 and discusses the various

enzyme pathways for thyroid hormone conversions in the body. From

this paper, I understood that by replacing with only T3, and

consequently impairing some enzyme pathways, depleting RT3, and

lowering levels of other thryoid hormones, I was depriving various

tissues of things they needed. I learned that T2 declines

significantly with age and thus may be a player in age related

physical slowing. The degradation of RT3 to T2 and then to T1 may be

improtant and neccessary body response to hypothyroid and stress

states as well as needed to be fully healthy and right. Certain

levels of RT3 may in fact be neccessary to the body. The enzymes

depleted by T3 only therapy would affect the brain and it's ability

to get adequate T1. The paper also covers how toxic metals disturb

these enzyme pathways and may be responsible for why some people

need such high levels of T3 to feel well.

[Guest guest]

>>Therefore,

T3 only therapy may have unintended hormonal consequences such as

low estrogen symptoms and sleep disturbances.) <<

HMMM This really makes me rethink all the added T3 I take. Maybe I should back

up and just try more Armour with lowered Cytomel. I am having problems with

sleep in that I wake up every morning at close to 4 AM. I have already discerned

it is not adrenal related. I have wondered if it might be when my thyroid (from

medication)runs out.

*Artistic Grooming * Hurricane, WV

Fat cat? Diabetes? Listowner for overweight or hypothyroid cats

http://groups.yahoo.com/group/hypokitties/

[Guest guest]

>>Therefore,

T3 only therapy may have unintended hormonal consequences such as

low estrogen symptoms and sleep disturbances.) <<

HMMM This really makes me rethink all the added T3 I take. Maybe I should back

up and just try more Armour with lowered Cytomel. I am having problems with

sleep in that I wake up every morning at close to 4 AM. I have already discerned

it is not adrenal related. I have wondered if it might be when my thyroid (from

medication)runs out.

*Artistic Grooming * Hurricane, WV

Fat cat? Diabetes? Listowner for overweight or hypothyroid cats

http://groups.yahoo.com/group/hypokitties/

[Guest guest]

>>Therefore,

T3 only therapy may have unintended hormonal consequences such as

low estrogen symptoms and sleep disturbances.) <<

HMMM This really makes me rethink all the added T3 I take. Maybe I should back

up and just try more Armour with lowered Cytomel. I am having problems with

sleep in that I wake up every morning at close to 4 AM. I have already discerned

it is not adrenal related. I have wondered if it might be when my thyroid (from

medication)runs out.

*Artistic Grooming * Hurricane, WV

Fat cat? Diabetes? Listowner for overweight or hypothyroid cats

http://groups.yahoo.com/group/hypokitties/