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A novel function in the control of thyroid hormone release

T1 - Hormonal regulation of protein degradation and synthesis in skeletal muscle

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Cellular Action of Thyroid Hormone - Thyroid Disease Manager

Transcriptome profiling reveals that regulates expression of various genes implicated in molting including, cuticle collagens (), hedgehog-related genes ( genes), patch-related genes (), and molting genes () (). Similar to also affects expression of a number of genes functionally implicated in molting, including and (; ). Curiously, several genes involved in DA biosynthesis, including and also appear to be regulated, perhaps relevant to a role in the dauer molt (; ).

Here we discuss the basic circuitry which governs release of thyroid hormone by the thyroid gland.

AB - A variety of factors have been shown to influence rates of protein breakdown in rat skeletal muscles. Muscles isolated from hypophysectomized rats show lower rates of protein synthesis and breakdown than those from normal controls. The lack of growth hormone is primarily responsible for the lower rates of protein synthesis, but this hormone does not affect overal protein catabolism. The lack of thyroid hormones is responsible for reduced protein breakdown in muscle after hypophysectomy or thyroidectomy. Treatment with triiodothyronine or thyroxine stimulates protein breakdown as well as synthesis in muscle after a lag time of 2 days. This acceleration of protein catabolism accounts for the decrease in weight of muscle and liver in hyperthyroidism. Thyroid hormones also increase the content of lysosomal proteases and other hydrolases in muscle and liver, and this effect may be responsible for the concomitant increase in protein breakdown in these tissues. In fasting, proteolysis in muscle rises and protein synthesis falls to provide the organism with amino acid precursors for gluconeogenesis and protein synthesis. However, in muscles of adrenalectomized rats, protein breakdown does not increase and may even decrease on fasting. Consequently these muscles show no net loss of protein content. Treatment of these animals with glucocorticoids leads to an increase in protein breakdown and increased release of amino acids. This effect is evident in muscles of fasted but not fed animals. The ability of glucocorticoids to promote protein catabolism in muscle during fasting complements their actions in stimulating hepatic gluconeogenesis.

Synthesis and Release of Thyroid Hormones

The thyroid is an endocrine gland responsible for the production of thyroid hormones T3 and T4.

The thyroid gland: The thyroid gland is located in the anterior part of the neck, just in front of the trachea below the larynx. It helps regulate the body’s metabolism (how the body gets energy from food) and blood-calcium levels by secreting three hormones:

Four small parathyroid glands are located on the thyroid gland. They secrete parathyroid hormone, which raises calcium levels in the blood. They work together with the thyroid gland to keep blood calcium at just the right level.

Regulation of Thyroid Hormone Synthesis Flashcards | …

The drug levothyroxine, a synthetic form of the natural thyroid hormone, is widely prescribed.

A variety of factors have been shown to influence rates of protein breakdown in rat skeletal muscles. Muscles isolated from hypophysectomized rats show lower rates of protein synthesis and breakdown than those from normal controls. The lack of growth hormone is primarily responsible for the lower rates of protein synthesis, but this hormone does not affect overal protein catabolism. The lack of thyroid hormones is responsible for reduced protein breakdown in muscle after hypophysectomy or thyroidectomy. Treatment with triiodothyronine or thyroxine stimulates protein breakdown as well as synthesis in muscle after a lag time of 2 days. This acceleration of protein catabolism accounts for the decrease in weight of muscle and liver in hyperthyroidism. Thyroid hormones also increase the content of lysosomal proteases and other hydrolases in muscle and liver, and this effect may be responsible for the concomitant increase in protein breakdown in these tissues. In fasting, proteolysis in muscle rises and protein synthesis falls to provide the organism with amino acid precursors for gluconeogenesis and protein synthesis. However, in muscles of adrenalectomized rats, protein breakdown does not increase and may even decrease on fasting. Consequently these muscles show no net loss of protein content. Treatment of these animals with glucocorticoids leads to an increase in protein breakdown and increased release of amino acids. This effect is evident in muscles of fasted but not fed animals. The ability of glucocorticoids to promote protein catabolism in muscle during fasting complements their actions in stimulating hepatic gluconeogenesis.

Secretion of TSH is, in turn, inhibited by the negative feedback of thyroid hormones and stimulated or inhibited by stimuli from higher brain centers in response to environmental changes.
2.

Thyroid hormones remain stored as part of thyroglobulin for up to three months.
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  • Functions of Thyroid Hormones | SpringerLink

    Calcitonin lowers blood calcium and phosphate levels and is a direct antagonist of parathyroid hormone.C. Parathyroid

  • LATS) Leads to excessive thyroid hormone synthesis …

    For normal individuals, this regulation results in a fairly stable day-to-day level of circulating thyroid hormones.

  • Hormonal control of thyroid hormone release: ..

    Transported in the blood, TSH acts upon the thyroid gland promoting the synthesis and release of thyroid hormone.

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Regulation of thyroid hormone …

At the level of the hypothalamus, thyrotropin-releasing hormone or TRH, a tripeptide, is secreted into the portal capillaries relaying secreted TRH to the anterior pituitary.

the synthesis, secretion and regulation of thyroid hormones ..

by hypophysectomy in experimental animals) thyroid function is depressed and the thyroid gland atrophies; administration of TSH stimulates the thyroid gland and increases circulating levels of thyroid hormones.

an excess of thyroid hormone in the blood ..

N2 - A variety of factors have been shown to influence rates of protein breakdown in rat skeletal muscles. Muscles isolated from hypophysectomized rats show lower rates of protein synthesis and breakdown than those from normal controls. The lack of growth hormone is primarily responsible for the lower rates of protein synthesis, but this hormone does not affect overal protein catabolism. The lack of thyroid hormones is responsible for reduced protein breakdown in muscle after hypophysectomy or thyroidectomy. Treatment with triiodothyronine or thyroxine stimulates protein breakdown as well as synthesis in muscle after a lag time of 2 days. This acceleration of protein catabolism accounts for the decrease in weight of muscle and liver in hyperthyroidism. Thyroid hormones also increase the content of lysosomal proteases and other hydrolases in muscle and liver, and this effect may be responsible for the concomitant increase in protein breakdown in these tissues. In fasting, proteolysis in muscle rises and protein synthesis falls to provide the organism with amino acid precursors for gluconeogenesis and protein synthesis. However, in muscles of adrenalectomized rats, protein breakdown does not increase and may even decrease on fasting. Consequently these muscles show no net loss of protein content. Treatment of these animals with glucocorticoids leads to an increase in protein breakdown and increased release of amino acids. This effect is evident in muscles of fasted but not fed animals. The ability of glucocorticoids to promote protein catabolism in muscle during fasting complements their actions in stimulating hepatic gluconeogenesis.

Regulation of Thyroid Hormones.• ..

At the thyroid level, thyroid hormones, thyroxine, T4, triiodothyronine, T3, and to a much lesser extent, reverse T3, rT3, are iodothyronines, iodine-containing derivatives of the amino acid tyrosine.

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