{"id":4360,"date":"2017-03-28T21:52:02","date_gmt":"2017-03-28T21:52:02","guid":{"rendered":"https:\/\/courses.lumenlearning.com\/wm-biology2\/?post_type=chapter&#038;p=4360"},"modified":"2024-04-26T01:39:08","modified_gmt":"2024-04-26T01:39:08","slug":"blood-calcium-levels-and-growth","status":"publish","type":"chapter","link":"https:\/\/courses.lumenlearning.com\/wm-biology2\/chapter\/blood-calcium-levels-and-growth\/","title":{"raw":"Blood Calcium Levels and Growth","rendered":"Blood Calcium Levels and Growth"},"content":{"raw":"<div class=\"textbox learning-objectives\">\r\n<h3>Learning Outcomes<\/h3>\r\n<ul>\r\n \t<li>Explain the role of hormones in blood calcium levels<\/li>\r\n \t<li>Explain the role of hormones in growth<\/li>\r\n<\/ul>\r\n<\/div>\r\n<h2>Hormonal Control of Blood Calcium Levels<\/h2>\r\nRegulation of blood calcium concentrations is important for generation of muscle contractions and nerve impulses, which are electrically stimulated. If calcium levels get too high, membrane permeability to sodium decreases and membranes become less responsive. If calcium levels get too low, membrane permeability to sodium increases and convulsions or muscle spasms can result.\r\n\r\n[caption id=\"attachment_2741\" align=\"alignright\" width=\"400\"]<img class=\"wp-image-2741\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/1223\/2017\/02\/07230544\/Figure_37_03_06.jpeg\" alt=\"The parathyroid glands, which are located in the neck, release parathyroid hormone, or PTH. PTH causes the release of calcium from bone and triggers the reabsorption of calcium from the urine in the kidneys. PTH also triggers the formation of calcitriol from vitamin D. Calcitriol causes the intestines to absorb more calcium. The result is increased calcium in the blood.\" width=\"400\" height=\"473\" \/> Figure 1.\u00a0Parathyroid hormone (PTH) is released in response to low blood calcium levels. It increases blood calcium levels by targeting the skeleton, the kidneys, and the intestine. (credit: modification of work by Mikael H\u00e4ggstr\u00f6m)[\/caption]\r\n\r\nBlood calcium levels are regulated by <b>parathyroid hormone (PTH)<\/b>, which is produced by the parathyroid glands, as illustrated in\u00a0Figure\u00a01. PTH is released in response to low blood Ca<sup>2+<\/sup> levels. PTH increases Ca<sup>2+ <\/sup>levels by targeting the skeleton, the kidneys, and the intestine. In the skeleton, PTH stimulates osteoclasts, which causes bone to be reabsorbed, releasing Ca<sup>2+ <\/sup>from bone into the blood. PTH also inhibits osteoblasts, reducing Ca<sup>2+ <\/sup>deposition in bone. In the intestines, PTH increases dietary CA<sup>2+<\/sup> absorption, and in the kidneys, PTH stimulates reabsorption of the CA<sup>2+<\/sup>. While PTH acts directly on the kidneys to increase Ca<sup>2+<\/sup> reabsorption, its effects on the intestine are indirect. PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the intestines to increase absorption of dietary calcium. PTH release is inhibited by rising blood calcium levels.\r\n\r\nHyperparathyroidism results from an overproduction of parathyroid hormone. This results in excessive calcium being removed from bones and introduced into blood circulation, producing structural weakness of the bones, which can lead to deformation and fractures, plus nervous system impairment due to high blood calcium levels. Hypoparathyroidism, the underproduction of PTH, results in extremely low levels of blood calcium, which causes impaired muscle function and may result in tetany (severe sustained muscle contraction).\r\n\r\nThe hormone <b>calcitonin<\/b>, which is produced by the parafollicular or C cells of the thyroid, has the opposite effect on blood calcium levels as does PTH. Calcitonin decreases blood calcium levels by inhibiting osteoclasts, stimulating osteoblasts, and stimulating calcium excretion by the kidneys. This results in calcium being added to the bones to promote structural integrity. Calcitonin is most important in children (when it stimulates bone growth), during pregnancy (when it reduces maternal bone loss), and during prolonged starvation (because it reduces bone mass loss). In healthy nonpregnant, unstarved adults, the role of calcitonin is unclear.\r\n<h2>Hormonal Regulation of Growth<\/h2>\r\nHormonal regulation is required for the growth and replication of most cells in the body. <b>Growth hormone (GH)<\/b>, produced by the anterior portion of the pituitary gland, accelerates the rate of protein synthesis, particularly in skeletal muscle and bones. Growth hormone has direct and indirect mechanisms of action. The first direct action of GH is stimulation of triglyceride breakdown (lipolysis) and release into the blood by adipocytes. This results in a switch by most tissues from utilizing glucose as an energy source to utilizing fatty acids. This process is called a <b>glucose-sparing effect<\/b>. In another direct mechanism, GH stimulates glycogen breakdown in the liver; the glycogen is then released into the blood as glucose. Blood glucose levels increase as most tissues are utilizing fatty acids instead of glucose for their energy needs. The GH mediated increase in blood glucose levels is called a <b>diabetogenic effect<\/b> because it is similar to the high blood glucose levels seen in diabetes mellitus.\r\n\r\n[caption id=\"attachment_2742\" align=\"alignright\" width=\"400\"]<img class=\"wp-image-2742\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/1223\/2017\/02\/07230627\/Figure_37_03_07.png\" alt=\"Growth hormone, or GH released from the pituitary gland stimulates bone and muscle growth. It also stimulates fat breakdown by adipocytes and glucagon breakdown by the liver. The liver releases IGFs, which cause target cells to take up amino acids, promoting protein synthesis. GH-releasing hormone stimulates the release of GH, and GH-inhibiting hormone, inhibits the release of GH.\" width=\"400\" height=\"320\" \/> Figure\u00a02.\u00a0Growth hormone directly accelerates the rate of protein synthesis in skeletal muscle and bones. Insulin-like growth factor 1 (IGF-1) is activated by growth hormone and also allows formation of new proteins in muscle cells and bone. (credit: modification of work by Mikael H\u00e4ggstr\u00f6m)[\/caption]\r\n\r\nThe indirect mechanism of GH action is mediated by <b>insulin-like growth factors (IGFs)<\/b> or somatomedins, which are a family of growth-promoting proteins produced by the liver, which stimulates tissue growth. IGFs stimulate the uptake of amino acids from the blood, allowing the formation of new proteins, particularly in skeletal muscle cells, cartilage cells, and other target cells, as shown in\u00a0Figure\u00a02. This is especially important after a meal, when glucose and amino acid concentration levels are high in the blood. GH levels are regulated by two hormones produced by the hypothalamus. GH release is stimulated by <b>growth hormone-releasing hormone (GHRH)<\/b> and is inhibited by <b>growth hormone-inhibiting hormone (GHIH)<\/b>, also called somatostatin.\r\n\r\nA balanced production of growth hormone is critical for proper development. Underproduction of GH in adults does not appear to cause any abnormalities, but in children it can result in <b>pituitary dwarfism<\/b>, in which growth is reduced. Pituitary dwarfism is characterized by symmetric body formation. In some cases, individuals are under 30 inches in height. Oversecretion of growth hormone can lead to <b>gigantism<\/b> in children, causing excessive growth. In some documented cases, individuals can reach heights of over eight feet. In adults, excessive GH can lead to <b>acromegaly<\/b>, a condition in which there is enlargement of bones in the face, hands, and feet that are still capable of growth.\r\n<div class=\"textbox tryit\">\r\n<h3>Try It<\/h3>\r\nhttps:\/\/assess.lumenlearning.com\/practice\/72e9c6cb-2a8b-4eb5-b290-2193ad02bdce\r\nhttps:\/\/assess.lumenlearning.com\/practice\/99957153-c51e-4581-a3c6-2bd50cb6d8bd\r\n<\/div>","rendered":"<div class=\"textbox learning-objectives\">\n<h3>Learning Outcomes<\/h3>\n<ul>\n<li>Explain the role of hormones in blood calcium levels<\/li>\n<li>Explain the role of hormones in growth<\/li>\n<\/ul>\n<\/div>\n<h2>Hormonal Control of Blood Calcium Levels<\/h2>\n<p>Regulation of blood calcium concentrations is important for generation of muscle contractions and nerve impulses, which are electrically stimulated. If calcium levels get too high, membrane permeability to sodium decreases and membranes become less responsive. If calcium levels get too low, membrane permeability to sodium increases and convulsions or muscle spasms can result.<\/p>\n<div id=\"attachment_2741\" style=\"width: 410px\" class=\"wp-caption alignright\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-2741\" class=\"wp-image-2741\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/1223\/2017\/02\/07230544\/Figure_37_03_06.jpeg\" alt=\"The parathyroid glands, which are located in the neck, release parathyroid hormone, or PTH. PTH causes the release of calcium from bone and triggers the reabsorption of calcium from the urine in the kidneys. PTH also triggers the formation of calcitriol from vitamin D. Calcitriol causes the intestines to absorb more calcium. The result is increased calcium in the blood.\" width=\"400\" height=\"473\" \/><\/p>\n<p id=\"caption-attachment-2741\" class=\"wp-caption-text\">Figure 1.\u00a0Parathyroid hormone (PTH) is released in response to low blood calcium levels. It increases blood calcium levels by targeting the skeleton, the kidneys, and the intestine. (credit: modification of work by Mikael H\u00e4ggstr\u00f6m)<\/p>\n<\/div>\n<p>Blood calcium levels are regulated by <b>parathyroid hormone (PTH)<\/b>, which is produced by the parathyroid glands, as illustrated in\u00a0Figure\u00a01. PTH is released in response to low blood Ca<sup>2+<\/sup> levels. PTH increases Ca<sup>2+ <\/sup>levels by targeting the skeleton, the kidneys, and the intestine. In the skeleton, PTH stimulates osteoclasts, which causes bone to be reabsorbed, releasing Ca<sup>2+ <\/sup>from bone into the blood. PTH also inhibits osteoblasts, reducing Ca<sup>2+ <\/sup>deposition in bone. In the intestines, PTH increases dietary CA<sup>2+<\/sup> absorption, and in the kidneys, PTH stimulates reabsorption of the CA<sup>2+<\/sup>. While PTH acts directly on the kidneys to increase Ca<sup>2+<\/sup> reabsorption, its effects on the intestine are indirect. PTH triggers the formation of calcitriol, an active form of vitamin D, which acts on the intestines to increase absorption of dietary calcium. PTH release is inhibited by rising blood calcium levels.<\/p>\n<p>Hyperparathyroidism results from an overproduction of parathyroid hormone. This results in excessive calcium being removed from bones and introduced into blood circulation, producing structural weakness of the bones, which can lead to deformation and fractures, plus nervous system impairment due to high blood calcium levels. Hypoparathyroidism, the underproduction of PTH, results in extremely low levels of blood calcium, which causes impaired muscle function and may result in tetany (severe sustained muscle contraction).<\/p>\n<p>The hormone <b>calcitonin<\/b>, which is produced by the parafollicular or C cells of the thyroid, has the opposite effect on blood calcium levels as does PTH. Calcitonin decreases blood calcium levels by inhibiting osteoclasts, stimulating osteoblasts, and stimulating calcium excretion by the kidneys. This results in calcium being added to the bones to promote structural integrity. Calcitonin is most important in children (when it stimulates bone growth), during pregnancy (when it reduces maternal bone loss), and during prolonged starvation (because it reduces bone mass loss). In healthy nonpregnant, unstarved adults, the role of calcitonin is unclear.<\/p>\n<h2>Hormonal Regulation of Growth<\/h2>\n<p>Hormonal regulation is required for the growth and replication of most cells in the body. <b>Growth hormone (GH)<\/b>, produced by the anterior portion of the pituitary gland, accelerates the rate of protein synthesis, particularly in skeletal muscle and bones. Growth hormone has direct and indirect mechanisms of action. The first direct action of GH is stimulation of triglyceride breakdown (lipolysis) and release into the blood by adipocytes. This results in a switch by most tissues from utilizing glucose as an energy source to utilizing fatty acids. This process is called a <b>glucose-sparing effect<\/b>. In another direct mechanism, GH stimulates glycogen breakdown in the liver; the glycogen is then released into the blood as glucose. Blood glucose levels increase as most tissues are utilizing fatty acids instead of glucose for their energy needs. The GH mediated increase in blood glucose levels is called a <b>diabetogenic effect<\/b> because it is similar to the high blood glucose levels seen in diabetes mellitus.<\/p>\n<div id=\"attachment_2742\" style=\"width: 410px\" class=\"wp-caption alignright\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-2742\" class=\"wp-image-2742\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/1223\/2017\/02\/07230627\/Figure_37_03_07.png\" alt=\"Growth hormone, or GH released from the pituitary gland stimulates bone and muscle growth. It also stimulates fat breakdown by adipocytes and glucagon breakdown by the liver. The liver releases IGFs, which cause target cells to take up amino acids, promoting protein synthesis. GH-releasing hormone stimulates the release of GH, and GH-inhibiting hormone, inhibits the release of GH.\" width=\"400\" height=\"320\" \/><\/p>\n<p id=\"caption-attachment-2742\" class=\"wp-caption-text\">Figure\u00a02.\u00a0Growth hormone directly accelerates the rate of protein synthesis in skeletal muscle and bones. Insulin-like growth factor 1 (IGF-1) is activated by growth hormone and also allows formation of new proteins in muscle cells and bone. (credit: modification of work by Mikael H\u00e4ggstr\u00f6m)<\/p>\n<\/div>\n<p>The indirect mechanism of GH action is mediated by <b>insulin-like growth factors (IGFs)<\/b> or somatomedins, which are a family of growth-promoting proteins produced by the liver, which stimulates tissue growth. IGFs stimulate the uptake of amino acids from the blood, allowing the formation of new proteins, particularly in skeletal muscle cells, cartilage cells, and other target cells, as shown in\u00a0Figure\u00a02. This is especially important after a meal, when glucose and amino acid concentration levels are high in the blood. GH levels are regulated by two hormones produced by the hypothalamus. GH release is stimulated by <b>growth hormone-releasing hormone (GHRH)<\/b> and is inhibited by <b>growth hormone-inhibiting hormone (GHIH)<\/b>, also called somatostatin.<\/p>\n<p>A balanced production of growth hormone is critical for proper development. Underproduction of GH in adults does not appear to cause any abnormalities, but in children it can result in <b>pituitary dwarfism<\/b>, in which growth is reduced. Pituitary dwarfism is characterized by symmetric body formation. In some cases, individuals are under 30 inches in height. Oversecretion of growth hormone can lead to <b>gigantism<\/b> in children, causing excessive growth. In some documented cases, individuals can reach heights of over eight feet. In adults, excessive GH can lead to <b>acromegaly<\/b>, a condition in which there is enlargement of bones in the face, hands, and feet that are still capable of growth.<\/p>\n<div class=\"textbox tryit\">\n<h3>Try It<\/h3>\n<p>\t<iframe id=\"assessment_practice_72e9c6cb-2a8b-4eb5-b290-2193ad02bdce\" class=\"resizable\" src=\"https:\/\/assess.lumenlearning.com\/practice\/72e9c6cb-2a8b-4eb5-b290-2193ad02bdce?iframe_resize_id=assessment_practice_id_72e9c6cb-2a8b-4eb5-b290-2193ad02bdce\" frameborder=\"0\" style=\"border:none;width:100%;height:100%;min-height:300px;\"><br \/>\n\t<\/iframe><br \/>\n\t<iframe id=\"assessment_practice_99957153-c51e-4581-a3c6-2bd50cb6d8bd\" class=\"resizable\" src=\"https:\/\/assess.lumenlearning.com\/practice\/99957153-c51e-4581-a3c6-2bd50cb6d8bd?iframe_resize_id=assessment_practice_id_99957153-c51e-4581-a3c6-2bd50cb6d8bd\" frameborder=\"0\" style=\"border:none;width:100%;height:100%;min-height:300px;\"><br \/>\n\t<\/iframe>\n<\/div>\n\n\t\t\t <section class=\"citations-section\" role=\"contentinfo\">\n\t\t\t <h3>Candela Citations<\/h3>\n\t\t\t\t\t <div>\n\t\t\t\t\t\t <div id=\"citation-list-4360\">\n\t\t\t\t\t\t\t <div class=\"licensing\"><div class=\"license-attribution-dropdown-subheading\">CC licensed content, Shared previously<\/div><ul class=\"citation-list\"><li>Biology 2e. <strong>Provided by<\/strong>: OpenStax. <strong>Located at<\/strong>: <a target=\"_blank\" href=\"http:\/\/cnx.org\/contents\/185cbf87-c72e-48f5-b51e-f14f21b5eabd@10.8\">http:\/\/cnx.org\/contents\/185cbf87-c72e-48f5-b51e-f14f21b5eabd@10.8<\/a>. <strong>License<\/strong>: <em><a target=\"_blank\" rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY: Attribution<\/a><\/em>. <strong>License Terms<\/strong>: Access for free at https:\/\/openstax.org\/books\/biology-2e\/pages\/1-introduction<\/li><\/ul><\/div>\n\t\t\t\t\t\t <\/div>\n\t\t\t\t\t <\/div>\n\t\t\t <\/section>","protected":false},"author":17,"menu_order":15,"template":"","meta":{"_candela_citation":"[{\"type\":\"cc\",\"description\":\"Biology 2e\",\"author\":\"\",\"organization\":\"OpenStax\",\"url\":\"http:\/\/cnx.org\/contents\/185cbf87-c72e-48f5-b51e-f14f21b5eabd@10.8\",\"project\":\"\",\"license\":\"cc-by\",\"license_terms\":\"Access for free at https:\/\/openstax.org\/books\/biology-2e\/pages\/1-introduction\"}]","CANDELA_OUTCOMES_GUID":"e6b33b67-a26a-4196-90b0-6c3f632e9b75, c943593b-5070-4716-ad76-1372059b7729, aa49fb6b-b0ea-4b00-93cf-ed66f870348c","pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":[],"pb_section_license":""},"chapter-type":[],"contributor":[],"license":[],"class_list":["post-4360","chapter","type-chapter","status-publish","hentry"],"part":3800,"_links":{"self":[{"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/pressbooks\/v2\/chapters\/4360","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/wp\/v2\/users\/17"}],"version-history":[{"count":7,"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/pressbooks\/v2\/chapters\/4360\/revisions"}],"predecessor-version":[{"id":8539,"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/pressbooks\/v2\/chapters\/4360\/revisions\/8539"}],"part":[{"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/pressbooks\/v2\/parts\/3800"}],"metadata":[{"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/pressbooks\/v2\/chapters\/4360\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/wp\/v2\/media?parent=4360"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/pressbooks\/v2\/chapter-type?post=4360"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/wp\/v2\/contributor?post=4360"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/wm-biology2\/wp-json\/wp\/v2\/license?post=4360"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}