18.3 Regulation of Body Processes - Concepts of Biology - 1st Canadian Edition (2023)

Some athletes try to increase their performance by using artificial hormones that increase muscle performance. Anabolic steroids, a form of the male sex hormone testosterone, are among the best-known performance-enhancing drugs. Steroids are used to help build muscle mass. Other hormones used to increase athletic performance include erythropoietin, which triggers red blood cell production, and human growth hormone, which can help build muscle mass. Most performance-enhancing drugs are illegal for non-medical purposes. They are also banned by national and international governing bodies, including the International Olympic Committee, the U.S. Olympic Committee, the National Collegiate Athletic Association, Major League Baseball and the National Football League.

The side effects of synthetic hormones are often significant and irreversible, and in some cases fatal. Androgens lead to several complications such as liver dysfunction and liver tumors, enlargement of the prostate, difficulty urinating, premature closure of the epiphyseal cartilage, testicular atrophy, infertility and depression of the immune system. The physiological burden caused by these substances is often greater than what the body can handle, resulting in unpredictable and dangerous effects and their use has been linked to heart attacks, strokes and impaired cardiac function.

Regulation of the female reproductive system

In addition to producing FSH and LH, the front part of the pituitary gland also produces the hormone Prolactin (PRL)in females. Prolactin stimulates milk production from the mammary glands after birth. Prolactin levels are regulated by hormones in the hypothalamus Prolactin-Releasing-Hormone (PRH)and Prolactin-hemmendes hormone (PIH), which is now known as dopamine. PRH stimulates the release of prolactin and PIH inhibits it.

Hormonal regulation of metabolism

concept in action

When blood sugar levels fall below normal levels, for example between meals or when glucose is used up quickly during exercise, the hormone becomes Glucagonis released from the alpha cells of the pancreas. Glucagon increases blood sugar levels and triggers what is known as a hyperglycemic effect by stimulating the breakdown of glycogen into glucose in skeletal muscle cells and liver cells in a process called Glycogenolysis. Glucose can then be used as energy by muscle cells and released into the circulatory system by liver cells. Glucagon also stimulates the uptake of amino acids from the blood by the liver, which then converts them into glucose. This process of glucose synthesis is called Glukoneogenese. Glucagon also stimulates fat cells to release fatty acids into the blood. These glucagon-mediated effects cause blood glucose levels to rise to normal homeostatic levels. Rising blood glucose levels inhibit further glucagon release by the pancreas via a negative feedback mechanism. In this way, insulin and glucagon work together to maintain homeostatic glucose levels, as shown in Figure 18.11.

The basal metabolic rate, i.e. the amount of calories that the body needs at rest, is determined by two hormones produced by the thyroid gland: thyroxine, also known as tetraiodothyronine or T₄, and Trijodthyronin, also known as T₃. These hormones affect almost every cell in the body except for the adult brain, uterus, testicles, blood cells, and spleen. They are transported across the plasma membrane of target cells and bind to receptors on the mitochondria, resulting in increased ATP production. At its core, T₃and t₄Activate genes involved in energy production and glucose oxidation. This results in increased metabolic rate and body heat production, which is known as the hormone's caloric effect.

T₃and t₄Release from the thyroid is stimulated by Thyroid Stimulating Hormone (TSH), which is produced by the anterior pituitary gland. TSH binding to the thyroid follicle receptors triggers the production of T₃and t₄from a glycoprotein called thyroglobulin. Thyroglobulin is present in the follicles of the thyroid gland and is converted into thyroid hormones with the addition of iodine. Iodine is formed from iodide ions that are actively transported from the bloodstream to the thyroid follicle. A peroxidase enzyme then binds the iodine to the tyrosine amino acid found in thyroglobulin. T₃has three bound iodine ions, while T₄bound four iodine ions. T₃and t₄are then released into the bloodstream, where T₄released in much larger quantities than T₃. Als T₃is more active than T₄and is responsible for most of the effects of thyroid hormones, tissues of the body convert T₄to T₃by removing an iodine ion. Most of the published T₃and t₄binds to transport proteins in the bloodstream and is unable to cross the plasma membrane of cells. These protein-bound molecules are only released when blood levels of the unbound hormone begin to fall. In this way, the reserve hormone is kept in the blood for a week. Increased T₃and t₄-Levels in the blood inhibit the release of TSH, resulting in lower TSH₃and t₄Release from the thyroid.

The follicular cells of the thyroid gland need iodide (iodine anions) to produce T₃and t₄. Iodides obtained from food are actively transported into the follicle cells, resulting in a concentration about 30 times higher than in the blood. The typical diet in North America provides more iodine than required due to the addition of iodide to table salt. Inadequate iodine intake, which occurs in many developing countries, results in an inability to absorb T₃and t₄hormones. The thyroid gland enlarges in what is called a condition goiter, which is caused by an overproduction of TSH without the formation of thyroid hormones. Thyroglobulin is contained in a liquid called colloid, and TSH stimulation causes higher accumulation of colloid in the thyroid. In the absence of iodine, it is not converted into thyroid hormone, and colloid begins to build up more and more in the thyroid, resulting in goiter.

Disorders can arise from both underproduction and overproduction of thyroid hormones. hypothyroidism, an underproduction of thyroid hormones, can cause a low metabolic rate, which leads to weight gain, sensitivity to cold and reduced mental activity, among other things. In children, hypothyroidism can cause cretinism, which can lead to mental retardation and stunted growth. hyperthyroidism, the overproduction of thyroid hormones, can lead to increased metabolic rate and its effects: weight loss, excessive heat production, sweating and an increased heart rate. Graves' disease is an example of an overactive thyroid.

The regulation of the calcium concentration in the blood is important for the generation of muscle contractions and nerve impulses that are electrically stimulated. When calcium levels get too high, membrane permeability to sodium decreases and membranes become less reactive. When calcium levels get too low, membrane permeability to sodium increases and cramps or muscle spasms may occur.

The level of calcium in the blood is regulated by Parathormon (PTH), which is produced by the parathyroid glands, as shown in Figure 18.12. PTH is released in response to low levels of Ca in the blood²⁺levels. PTH increased Approx²⁺levels by targeting the skeleton, kidneys, and intestines. In the skeleton, PTH stimulates osteoclasts, causing bone to be resorbed and Ca to be released²⁺from bone to blood. PTH also inhibits osteoblasts and reduces Ca²⁺deposits in the bone. In the gut, PTH increases dietary Ca²⁺absorption and in the kidneys, PTH stimulates reabsorption of CA²⁺. While PTH acts directly on the kidneys to increase Ca²⁺Reabsorption, its effects on the gut are indirect. PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the gut to increase the absorption of dietary calcium. The release of PTH is inhibited by rising calcium levels in the blood.

The long-term stress response differs from the short-term stress response. The body cannot long sustain the energy surges mediated by epinephrine and norepinephrine. Instead, other hormones come into play. In a long-term stress response, the hypothalamus triggers the release of ACTH from the anterior pituitary gland. ACTH stimulates the adrenal cortex to release so-called steroid hormones Corticosteroids. Corticosteroids turn on the transcription of certain genes in the nuclei of target cells. They change the enzyme concentrations in the cytoplasm and influence cell metabolism. There are two main corticosteroids: Glucocorticoids such as Cortisoland mineral corticoids such as aldosterone. These hormones target the breakdown of fat into fatty acids in adipose tissue. The fatty acids are released into the bloodstream for other tissues to use in ATP production. That Glucocorticoidmainly affect glucose metabolism by stimulating glucose synthesis. Glucocorticoids also have anti-inflammatory properties by inhibiting the immune system. For example, cortisone is used as an anti-inflammatory drug; however, it cannot be used permanently, as it increases susceptibility to disease due to its immunosuppressive effects.

Mineralocorticoids regulate the body's ion and water balance. The hormone aldosterone stimulates the reabsorption of water and sodium ions in the kidneys, leading to an increase in blood pressure and volume.

Hypersecretion of glucocorticoids can cause a condition known as Morbus Cushing, characterized by a shift in fat storage areas of the body. This can lead to accumulation of fatty tissue in the face and neck and excess glucose in the blood. Hyposecretion of the corticosteroids can lead to this Addison's disease, which can cause tanning of the skin, hypoglycemia, and low levels of electrolytes in the blood.

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