The term short-feedback mechanism originates from endocrinology. It refers to a regulatory circuit in which a hormone can directly inhibit its own action.
What is the short-feedback mechanism?
Short-feedback mechanisms are independent, very small control circuits. One example is the short-feedback mechanism of thyroid-stimulating hormone (TSH). The short-feedback mechanism is one of the regulatory circuits. Regulatory circuits regulate many different body functions. The short-feedback mechanisms are mainly found in the field of hormones. Within this mechanism, a hormone can inhibit its own secretion. This process is usually based on an autocrine action. In the autocrine secretion mode, glandular cells release their hormone products directly into the surrounding interstitium. Thus, autocrine secretion is basically a special case of paracrine hormone secretion. Paracrine glands also release their secretion into the immediate environment, but they do not influence themselves by doing so. Examples of short-feedback mechanisms are the Brokken-Wiersinga-Prummel regulatory circuit or mechanisms in the secretion of LH and FSH. Insulin also has an autocrine effect, as do many cytokines and tissue hormones.
Function and role
Short-feedback mechanisms are independent, very small regulatory circuits. However, they usually complement larger regulatory circuits. An example of such a complementary control loop is the short-feedback mechanism of thyroid-stimulating hormone (TSH). TSH is a hormone produced in the pituitary gland. It travels through the bloodstream to the TSH receptors on the thyroid gland and binds there. TSH stimulates thyroid growth and the secretion of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). The pituitary gland constantly measures the levels of thyroid hormones in the blood and uses them to regulate its own hormone secretion. Therefore, when there are many thyroid hormones in the blood, it produces less FSH. If, on the other hand, the pituitary gland measures a deficiency of thyroid hormones, it produces more FSH to stimulate the thyroid gland to produce it. This control loop is also known as the thyrotropic control loop. Complementary to this, there is a long-feedback mechanism and a short-feedback mechanism. The latter is a short-feedback of the TSH level to its own release. For this purpose, TSH, which is produced in the pituitary gland, binds to so-called thyrotropin receptors. These are located directly in the anterior lobe of the pituitary gland, i.e. exactly at the site where TSH is also produced. When TSH binds to these folliculostellar cells, they presumably secrete thyrostimulin. This inhibits secretion from the thyrotropic cells of the pituitary gland. The short-feedback mechanism is thought to prevent the pituitary gland from excessive secretion of TSH. In addition, this short-feedback also allows for a pulse-like release of TSH. Other physiological short-feedback mechanisms are found in the secretion of LH and FSH. LH is the luteinizing hormone. Together with FSH, follicle-stimulating hormone, it is responsible for the production and maturation of female gametes. Both LH and FSH are produced in the pituitary gland. Other hormones of the hypothalamus, such as galanin and gonadotropin releasing hormone, are also regulated by short-feedback. In principle, any short-feedback mechanism in the body can be impaired. Frequently, this then leads to disturbances within the hormone balance.
Diseases and ailments
A well-known example of a disorder of the short-feedback mechanism is Graves’ disease. Graves’ disease is an autoimmune disease that predominantly affects the thyroid gland. Around two to three percent of all women in Germany suffer from Graves’ disease. Men are only very rarely affected. The maximum incidence of the disease is between the ages of 20 and 40. The causes of the disease are complex. On the one hand, a genetic defect has been identified in those affected. This presumably leads to a disorder of the immune system. However, various influences can increase the risk of the disease. These include smoking or viral infections. An outbreak of the disease is often observed after psychologically stressful events. The body forms antibodies against the tissue of the thyroid gland. The antibodies are called TSH receptor antibodies (TRAK).They are found in more than 90% of patients. These bind to the TSH receptors of the organ. Normally, TSH docks here and stimulates the thyroid gland to produce thyroid hormones. Now, however, the receptor is permanently occupied by antibodies. These have the same effect as TSH. Hyperthyroidism occurs. Normally, the short-feedback mechanism in the pituitary gland should protect against hyperthyroidism. But the thyroid is isolated from the regulatory loop by the attack of the antibodies. It produces hormones independently of the TSH level in the blood. As a result, the pituitary gland secretes almost no more TSH. Nevertheless, the short-feedback mechanism still plays a decisive role in Graves’ disease. Often, the TSH value alone is determined by the physician during follow-up examinations. However, this is often not sufficient, because the antibodies can bind not only to the thyroid receptors, but also to the TSH receptors located directly on the pituitary gland. There they inhibit the release of TSH. Thus, it could be that the thyroid gland is not in hyperthyroidism and yet the TSH level is low.
