Body processes

Ultrashort Feedback Mechanism – Function, Task & Diseases

Ultrashort feedback mechanism

The ultrashort feedback mechanism is a regulatory circuit of endocrine secretion in autocrine and paracrine glands. A hormone inhibits its own release in this control loop without intermediate steps or other hormones. Malregulations in the ultra-feedback mechanism can be caused by diseases such as Graves ‘ disease .

What is the ultrashort feedback mechanism?

Glands and glandular cells produce secretions. They are either endocrine or exocrine in nature. Endocrine glands produce hormones or hormone-like substances that are secreted into the body through various modes of secretion .

In order to keep the household in balance, the secretion of glandular cells in the human organism is regulated by various control circuits. One of these control loops is the so-called ultra-short feedback mechanism, which plays a role in endocrine secretion in particular. In this control loop, a hormone inhibits its own release.

In addition to the autocrine secretion modes , the control circuit is also decisive for the paracrine secretion mode. Autocrine hormones inhibit or stimulate the secreting gland cell. In paracrine hormone secretion, the hormone binds to the receptors of tissues in the immediate vicinity. With the ultrashort feedback mechanism, regulation takes place without the intermediate step of a further hormone. This distinguishes the control circuit from other control mechanisms.

Other physiological feedback loops are short feedback , long feedback , or ultra-long feedback .

function & task

Control circuits create an equilibrium in physiological milieus. This balance is particularly important in the hormone system , because individual hormone secretions influence each other. The dysregulation of a single hormone can throw the entire hormone balance out of balance and cause numerous complaints that can even have life-threatening consequences.

In addition to the hormonal balance, the control loop of the ultrashort feedback mechanism regulates immunological processes and individual processes at synapses of excitable cells . In the hormonal area, for example, LH and FSH secretion is based on an ultra-short feedback mechanism. The mechanism is also responsible for the autoregulatory properties in the incretion (internal secretion) of the hypothalamic hormones GnRH and galanin. A less typical ultrashort feedback is the regulatory circuitry of CRH secretion in the hypothalamus . Here the ultra-short loop shows itself as a positive feedback and allows CRH to inhibit its own distribution in the event of stress .

One of the best-known and most typical examples of the ultrashort feedback mechanism is the Brokken-Wiersinga-Prummel control loop , which results in auto-inhibition of the TSH hormone. The regulation mechanism is also known as the Prummel-Wiersinga control loop. Pituitary TSH binds to thyrotropin receptors located on the folliculostellar cells in the tissue of the anterior pituitary in this ultrashort-feedback mechanism. Presumably, the secretion of TSH in all thyrotropic cells is inhibited via thyrostimulin. This feedback loop corresponds to a section of the thyrotropic feedback loop and not only prevents excessive TSH secretion, but also gives the TSH level pulsatility (heart beat likeness).

Every ultra-short mechanism in the human body can theoretically fail or be dysregulated by disease processes and thus mess up the hormonal balance. A failed ultra-short feedback can thus be symptomatic in the context of various diseases. Graves’ disease is one of the most well-known examples of a condition affecting ultrashort feedback.

Diseases & Ailments

Like all hormonal imbalances, Graves’ disease manifests itself in a variety of symptoms and affects various processes in the patient’s body. The disease is an autoimmune thyroid disease associated with HLA-DR3 and other autoimmune diseases . The cardinal symptom of Graves’ disease is excessive antibody production on the follicular cells of the thyroid gland . These antibodies correspond to the IgG type and mimic the action of TSH. The TSH receptors of the thyroid gland are thus strongly and permanently stimulated.

The ultra-short feedback mechanism is thus no longer able to auto-regulate hormone production. The constant stimulation of the TSH receptors leads to a chronic growth stimulus that promotes goiter . This is a pathological enlargement of the thyroid gland, which is associated with an overactive function of the organ . From then on, the glandular cells secrete excessive amounts of T3 and T4 . With this secretion they cause thyrotoxicosis.

External binding of the antibodies produced also causes endocrine orbitopathies or pretibial myxedema to develop outside the thyroid gland . Due to the dysregulation in the TSH control circuit, the secretion of the TSH hormone is also suppressed by antibodies suppressing individual TSH receptors in the pituitary gland . In addition to weight loss despite increased appetite , diarrhea , hyperhidrosis , polydipsia and heat intolerance, symptoms such as tremor , reduced performance or restlessness can occur.

Since the thyroid hormone also has an effect on the cardiovascular system, cardiac arrhythmias often occur . The hair can fall out and the muscles hurt.

Knowledge of the ultra-short feedback mechanism for the autoregulation of TSH is of importance for the physician in the context of Graves’ disease, above all for the interpretation of the TSH level. Patients with Graves’ disease have lower TSH levels because their TSH receptor autoantibodies bind to the TSH receptors and act directly in the pituitary gland. They thus inhibit the release of TSH through euthyroidism in the sense of an immunogenic TSH suppression. Thus, although TSH levels would be expected to be significantly higher given the low levels of FT4 in the blood of patients, their levels remain reduced.

The treatment of hyperthyroidism in the context of Graves’ disease thus proves to be a tightrope walk and the TSH level can no longer be used as the sole assessment criterion for assessing the current metabolic situation. The attending physician must respond to this in order to follow an appropriate path of therapy and to correctly assess the success of the therapy.

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Hello! I am Lisa Newlon, and I am a medical writer and researcher with over 10 years of experience in the healthcare industry. I have a Master’s degree in Medicine, and my deep understanding of medical terminology, practices, and procedures has made me a trusted source of information in the medical world.