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Below is some information on Metabolism and some examples of a little research used to update the Take it Off and Thyroid Modules.
Anabolism (pronounced: uh-nah-buh-lih-zum), or constructive metabolism, is all about building and storing: It supports the growth of new cells, the maintenance of body tissues, and the storage of energy for use in the future. During anabolism, small molecules are changed into larger, more complex molecules of carbohydrate, protein, and fat.
Catabolism (pronounced: kuh-tah-buh-lih-zum), or destructive metabolism, is the process that produces the energy required for all activity in the cells. In this process, cells break down large molecules (mostly carbohydrates and fats) to release energy. This energy release provides fuel for anabolism, heats the body, and enables the muscles to contract and the body to move. As complex chemical units are broken down into more simple substances, the waste products released in the process of catabolism are removed from the body through the skin, kidneys, lungs, and intestines.
Several of the hormones of the endocrine system are involved in controlling the rate and direction of metabolism. Thyroxine (pronounced: thigh-rahk-sun), a hormone produced and released by the thyroid (pronounced: thigh-royd) gland, plays a key role in determining how fast or slow the chemical reactions of metabolism proceed in a person's body.
Another gland, the pancreas (pronounced: pan-kree-us) secretes hormones that help determine whether the body's main metabolic activity at a particular time will be anabolic or catabolic. For example, after eating a meal, usually more anabolic activity occurs because eating increases the level of glucose - the body's most important fuel - in the blood. The pancreas senses this increased level of glucose and releases the hormone insulin (pronounced: in-suh-lin), which signals cells to increase their anabolic activities.
Peripheral metabolism of thyroid hormones is a critical component of the impact these hormones have on intracellular function. Primary hypothyroidism, which manifests as elevated thyroid stimulating hormone (TSH) and low T4 levels, and secondary hypothyroidism, manifesting as a combination of low T4 levels and low TSH secondary to pituitary dysfunction, are both well defined.
However, perturbations in thyroid hormone levels secondary to alterations in peripheral metabolism have received far less clinical attention. Several syndromes, such as "euthyroid sick syndrome" (ESS) and "low T3 syndrome," have been classified within the medical literature. The common feature of these disorders is a low level of circulating T3, with generally normal to slightly elevated blood T4 levels, and either normal or slightly suppressed TSH levels.
This pattern of altered thyroid hormones is now generally agreed to be a result of impairment in extra-thyroidal peripheral metabolism.' The liver, and to a lesser degree the kidneys, play a dominant, although often under-discussed role in the metabolism of thyroid hormones. The majority of the most metabolically active thyroid hormone, 3,5,3'-triiodothyronine (T3) (Figure 1), is generated in peripheral tissue. Similarly, the preponderance of its competitive inhibitor, 3,3',5'-triiodothyronine (rT3; reverse T3) (Figure 1) is generated outside the thyroid gland. Further transformations to T2 and T1 isomers also occur almost exclusively in peripheral tissue. These transformations are all catalyzed by deiodination enzymes, which remove iodine atoms from the inner tyrosyl or outer phenolic benzene rings. This stepwise deiodination is the major route of thyroid hormone metabolism and results in both active and inactive metabolites.
Tissue-specific deiodination of thyroid hormones determines, to a large degree, the fate of these hormones. The majority of the activation of the prohormone T4 to the more metabolically active T3 occurs through non-thyroidal deiodination. The inactivation of T3 to T2 isomers, the inactivation of T4 to yield rT3, and the eventual degradation of rT3 to T2 isomers are also catalyzed by the deiodinase family of enzymes. This stepwise removal of iodine from the benzene ring of the inner tyrosyl and outer phenolic benzene ring is currently thought to be the major route of peripheral thyroid hormone metabolism.
The thyroid hormones, thyroxine (T4) and triiodothyronine (T3), are tyrosine-based hormones produced by the thyroid gland. An important component in the synthesis is iodine. The major form of thyroid hormone in the blood is thyroxine (T4). The ratio of T4 to T3 released in the blood is roughly 20 to 1. Thyroxine is converted to the active T3 (three to four times more potent than T4) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (T1a) and thyronamine (T0a).
Most of the thyroid hormone circulating in the blood is bound to transport proteins. Only a very small fraction of the circulating hormone is free (unbound) and biologically active, hence measuring concentrations of free thyroid hormones is of great diagnostic value.
When thyroid hormone is bound, it is not active, so the amount of free T3/T4 is what is important. For this reason, measuring total thyroxine in the blood can be misleading.
The thyronamines function via some unknown mechanism to inhibit neuronal activity; this plays an important role in the hibernation cycles of mammals and the moulting behaviour of birds. One effect of administering the thyronamines is a severe drop in body temperature.
Free T4 index: normal 5-11.
Total T3: normal 75-175 ng/dL. This measurement IS NOT indicated if hypothyroidism is suspected (will be normal in 20-30% of hypothyroid patients).
Free T3 index: normal 75-175.
Free T4 (by equilibrium dialysis): normal 0.7-2.2 ng/dL is most precise method since it measures free fraction directly
Free T3 (by dialysis): normal 210-440 pg/dL
The Design of Metabolism
Anabolism (pronounced: uh-nah-buh-lih-zum), or constructive metabolism, is all about building and storing: It supports the growth of new cells, the maintenance of body tissues, and the storage of energy for use in the future. During anabolism, small molecules are changed into larger, more complex molecules of carbohydrate, protein, and fat.
Catabolism (pronounced: kuh-tah-buh-lih-zum), or destructive metabolism, is the process that produces the energy required for all activity in the cells. In this process, cells break down large molecules (mostly carbohydrates and fats) to release energy. This energy release provides fuel for anabolism, heats the body, and enables the muscles to contract and the body to move. As complex chemical units are broken down into more simple substances, the waste products released in the process of catabolism are removed from the body through the skin, kidneys, lungs, and intestines.
Several of the hormones of the endocrine system are involved in controlling the rate and direction of metabolism. Thyroxine (pronounced: thigh-rahk-sun), a hormone produced and released by the thyroid (pronounced: thigh-royd) gland, plays a key role in determining how fast or slow the chemical reactions of metabolism proceed in a person's body.
Another gland, the pancreas (pronounced: pan-kree-us) secretes hormones that help determine whether the body's main metabolic activity at a particular time will be anabolic or catabolic. For example, after eating a meal, usually more anabolic activity occurs because eating increases the level of glucose - the body's most important fuel - in the blood. The pancreas senses this increased level of glucose and releases the hormone insulin (pronounced: in-suh-lin), which signals cells to increase their anabolic activities.
Peripheral metabolism of thyroid hormones is a critical component of the impact these hormones have on intracellular function. Primary hypothyroidism, which manifests as elevated thyroid stimulating hormone (TSH) and low T4 levels, and secondary hypothyroidism, manifesting as a combination of low T4 levels and low TSH secondary to pituitary dysfunction, are both well defined.
However, perturbations in thyroid hormone levels secondary to alterations in peripheral metabolism have received far less clinical attention. Several syndromes, such as "euthyroid sick syndrome" (ESS) and "low T3 syndrome," have been classified within the medical literature. The common feature of these disorders is a low level of circulating T3, with generally normal to slightly elevated blood T4 levels, and either normal or slightly suppressed TSH levels.
This pattern of altered thyroid hormones is now generally agreed to be a result of impairment in extra-thyroidal peripheral metabolism.' The liver, and to a lesser degree the kidneys, play a dominant, although often under-discussed role in the metabolism of thyroid hormones. The majority of the most metabolically active thyroid hormone, 3,5,3'-triiodothyronine (T3) (Figure 1), is generated in peripheral tissue. Similarly, the preponderance of its competitive inhibitor, 3,3',5'-triiodothyronine (rT3; reverse T3) (Figure 1) is generated outside the thyroid gland. Further transformations to T2 and T1 isomers also occur almost exclusively in peripheral tissue. These transformations are all catalyzed by deiodination enzymes, which remove iodine atoms from the inner tyrosyl or outer phenolic benzene rings. This stepwise deiodination is the major route of thyroid hormone metabolism and results in both active and inactive metabolites.
Tissue-specific deiodination of thyroid hormones determines, to a large degree, the fate of these hormones. The majority of the activation of the prohormone T4 to the more metabolically active T3 occurs through non-thyroidal deiodination. The inactivation of T3 to T2 isomers, the inactivation of T4 to yield rT3, and the eventual degradation of rT3 to T2 isomers are also catalyzed by the deiodinase family of enzymes. This stepwise removal of iodine from the benzene ring of the inner tyrosyl and outer phenolic benzene ring is currently thought to be the major route of peripheral thyroid hormone metabolism.
The thyroid hormones, thyroxine (T4) and triiodothyronine (T3), are tyrosine-based hormones produced by the thyroid gland. An important component in the synthesis is iodine. The major form of thyroid hormone in the blood is thyroxine (T4). The ratio of T4 to T3 released in the blood is roughly 20 to 1. Thyroxine is converted to the active T3 (three to four times more potent than T4) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (T1a) and thyronamine (T0a).
Most of the thyroid hormone circulating in the blood is bound to transport proteins. Only a very small fraction of the circulating hormone is free (unbound) and biologically active, hence measuring concentrations of free thyroid hormones is of great diagnostic value.
When thyroid hormone is bound, it is not active, so the amount of free T3/T4 is what is important. For this reason, measuring total thyroxine in the blood can be misleading.
The thyronamines function via some unknown mechanism to inhibit neuronal activity; this plays an important role in the hibernation cycles of mammals and the moulting behaviour of birds. One effect of administering the thyronamines is a severe drop in body temperature.
Free T4 index: normal 5-11.
Total T3: normal 75-175 ng/dL. This measurement IS NOT indicated if hypothyroidism is suspected (will be normal in 20-30% of hypothyroid patients).
Free T3 index: normal 75-175.
Free T4 (by equilibrium dialysis): normal 0.7-2.2 ng/dL is most precise method since it measures free fraction directly
Free T3 (by dialysis): normal 210-440 pg/dL
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