Bio 11.2 part 2 Endocrine System PDF

A diagram of a blood glucose transfer Description automatically generated Chapter 11: Endocrine System 402 **Figure 11.28** Location of the thyroid gland. The **thyroid gland** is located in the neck, anterior to the trachea, as depicted in Figure 11.28. Two endocrine cell types compose the thyr...

A diagram of a blood glucose transfer Description automatically generated Chapter 11: Endocrine System 402 **Figure 11.28** Location of the thyroid gland. The **thyroid gland** is located in the neck, anterior to the trachea, as depicted in Figure 11.28. Two endocrine cell types compose the thyroid: follicular cells and C (parafollicular) cells The follicular cells of the thyroid produce **triiodothyronine (T3)** and the less potent **tetraiodothyronine (thyroxine, T4)**, collectively known as **thyroid hormones**. Both thyroid hormones are [tyrosine derivative](javascript:void(0)) [hormones](javascript:void(0)) that contain iodine atoms. Thyroid hormones are [lipophilic](javascript:void(0)) (ie, water-insoluble); therefore, these hormones travel in the bloodstream bound to plasma proteins. Most circulating thyroid hormone is T4, but target tissues increase circulating T3 levels by enzymatically converting T4 to T3. In adults, T3 and T4 influence the function of most cells in the body and help to set the basal rate of metabolism. Activation of nuclear thyroid hormone receptors has a general stimulatory effect on many processes and increases [cellular metabolism](javascript:void(0)) and body temperature via regulation of transcription in target cells. In children, thyroid hormones are necessary for proper development. Thyroid hormone production is regulated through the linked activities of the hypothalamus, pituitary, and thyroid gland (ie, the hypothalamic-pituitary-thyroid \[HPT\] axis), as discussed in Concept 11.2.03. The C cells of the thyroid gland produce **calcitonin**, a peptide hormone involved in calcium homeostasis. Calcitonin is secreted in response to increased plasma calcium concentration and is thought to reduce plasma calcium in several ways. First, calcitonin decreases [bone resorption](javascript:void(0)) by osteoclasts and promotes bone calcium storage. Calcitonin also increases renal excretion of calcium and decreases intestinal absorption of calcium. The effects of calcitonin are illustrated in Figure 11.29.  Chapter 11: Endocrine System 403 **Figure 11.29** Physiological effects of calcitonin. **Concept Check 11.1** Hypothyroidism is a condition in which thyroid hormones are secreted at lower levels than normal. Predict the effects of hypothyroidism on hypothalamic thyrotropin-releasing hormone (TRH) and anterior pituitary thyroid-stimulating hormone (TSH) secretion. In addition, predict some clinical features of patients with hypothyroidism. [**Solution**](javascript:void(0)) 11.2.08 Parathyroid Hormones The vast majority of the body\'s calcium is stored in the bone; however, free calcium ions play an integral role in processes throughout the body. Extracellular calcium concentrations are much higher than cytosolic calcium concentrations, and cytosolic calcium entry can affect the membrane potential of a cell. In addition, calcium entry into the cytosol from outside the cell or from intracellular compartments (eg, [sarcoplasmic reticulum](javascript:void(0))) can act as a signal to stimulate intracellular processes (eg, [muscle contraction](javascript:void(0))). The **parathyroid glands** are four small endocrine glands located in the neck on the posterior surface of the thyroid gland (Figure 11.30). Through the production of the peptide hormone **parathyroid hormone (PTH)**, the parathyroid glands are important in regulating calcium homeostasis in the body, and to a A diagram of human organs Description automatically generated  Chapter 11: Endocrine System 404 lesser extent, phosphate homeostasis. The actions of PTH are antagonistic to those of calcitonin produced by the thyroid gland (see Concept 11.2.07). **Figure 11.30** The parathyroid glands. PTH is released in response to decreased plasma calcium and acts in three primary ways to produce a net calcium increase. First, PTH stimulates bone resorption (ie, breakdown) through indirect actions on osteoclasts, the bone cells responsible for resorption. The majority of calcium in the body is stored as hydroxyapatite, a mineral found in the bone matrix that primarily contributes to bone strength and hardness (see Concept 18.1.03). When bone is resorbed through the actions of osteoclasts, calcium stored in the bone matrix is released into the blood, dissolving mineralized bone and increasing plasma calcium levels. However, osteoclasts do not possess PTH receptors. Therefore, the impact of PTH on osteoclasts is indirect and is achieved through PTH actions on osteoblasts, bone cells with PTH receptors. In response to increased PTH, osteoblasts are stimulated to [differentiate](javascript:void(0)) from osteoblast precursor cells. At the same time, PTH promotes the release of ligands by osteoblasts to promote differentiation of osteoclast precursor cells into osteoclasts. In this way, prolonged PTH exposure leads to increased osteoclast numbers and an increase in blood calcium levels, as shown in Figure 11.31. A diagram of the neck and back of a person Description automatically generated Chapter 11: Endocrine System 405 **Figure 11.31** Parathyroid hormone promotes bone resorption. The second way PTH increases blood calcium occurs in the kidneys. When PTH levels rise, the kidneys increase calcium reabsorption into peritubular capillaries, increasing blood calcium levels. As a result of increased calcium reabsorption, less calcium is excreted in the urine. PTH also inhibits phosphate reabsorption in the kidneys, increasing excretion of phosphate in the urine (Figure 11.32).  Chapter 11: Endocrine System 406 **Figure 11.32** Parathyroid hormone promotes calcium reabsorption and phosphate excretion in the kidney. The final way PTH affects blood calcium is through actions on intestinal cells. PTH increases the activity of the enzyme that catalyzes the final step in the conversion of inactive circulating vitamin D into its active form, **calcitriol**, in the kidneys. Calcitriol promotes absorption of calcium and phosphate in the intestinal lumen. However, because PTH also promotes phosphate excretion in the kidneys, the net effect of PTH on phosphate homeostasis is limited. In addition to promoting intestinal calcium absorption, calcitriol promotes reabsorption of calcium in the kidneys. Figure 11.33 summarizes the effects of PTH on calcium homeostasis. A diagram of the phosphoric release Description automatically generated Chapter 11: Endocrine System 407 **Figure 11.33** Effects of parathyroid hormone. When blood calcium levels are high, PTH release from the parathyroid glands is prevented via a negative feedback mechanism so that blood calcium levels remain in homeostasis. 11.2.09 Sex Hormones **Sex hormones** are steroid hormones with a role in sexual development and reproduction. The term **androgen** refers to the hormones involved in developing and maintaining masculine sexual characteristics, and the term **estrogen** refers to the hormones involved in developing and maintaining feminine sexual characteristics.  Chapter 11: Endocrine System 408 As discussed in Lessons 9.1 and 9.2, in an XY embryo, expression of the *SRY* gene on the Y chromosome promotes [sex determination](javascript:void(0)) and the development of the testes, the sex organs where most [testosterone](javascript:void(0)) (the primary androgen) is produced (note: the adrenal cortex secretes small amounts of testosterone, see Concept 11.2.04). The production of testosterone in a fetus typically promotes the development of male sex organs. Because an XX embryo does not express the *SRY* gene, XX fetuses are exposed to less testosterone, typically resulting in the development of female sex organs (Figure 11.34). **Figure 11.34** Differentiation of sex organs during development. The production of gametes (ie, sperm and egg cells) via [meiosis](javascript:void(0)) and the development of secondary sexual characteristics are under the control of various sex hormones. **Male Reproductive Hormones** Beginning at puberty, [spermatogenesis](javascript:void(0)) (ie, production of sperm) and development of secondary sexual characteristics are regulated by the **hypothalamic-pituitary-gonadal (HPG) axis**. Gonadotropin-releasing hormone (GnRH) from the hypothalamus stimulates the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary (see Concept 11.2.03). In the testes, LH promotes the secretion of testosterone by Leydig cells, and FSH promotes and maintains spermatogenesis by stimulating Sertoli (nurse) cells. A diagram of a female reproductive system Description automatically generated Chapter 11: Endocrine System 409 Two negative feedback systems operate to maintain appropriate sex hormone levels. First, high levels of testosterone inhibit both GnRH and LH, limiting excessive testosterone production. Second, Sertoli cells secrete a hormone known as **inhibin**, which functions to inhibit FSH, controlling the process of spermatogenesis. The effects of male reproductive hormones are summarized in Figure 11.35. **Figure 11.35** Summary of male reproductive hormones. **Female Reproductive Hormones** [Oogenesis](javascript:void(0)) (ie, production of ova) begins prior to birth, at the fetal stage, but the process is arrested during infancy and childhood due to low sex hormone levels. At puberty, hormonal stimulation from estrogens (eg, [estradiol](javascript:void(0))) and progesterone promotes the uterine (menstrual) cycle, the monthly resumption of oogenesis during the ovarian cycle, and the development of secondary sexual characteristics. The ovarian and uterine cycles [occur concurrently](javascript:void(0)), and the cycles last approximately 28 days. These cycles provide optimal conditions for fertilization and pregnancy. The HPG axis promotes the ovarian and uterine cycles through the production of FSH and LH. FSH promotes oogenesis by stimulating the release of estrogens from ovarian follicles, and a surge in LH secretion stimulates [ovulation](javascript:void(0)). Early in the ovarian cycle, low to moderate levels of estrogen released by ovarian follicles inhibit the release of GnRH, FSH, and LH in a negative feedback loop. However, later in the ovarian cycle (but prior to ovulation and high levels of progesterone), high levels of estrogen released from the dominant ovarian follicle promote GnRH, FSH, and LH release. **Progesterone**, released later in the ovarian cycle by the corpus luteum (ie, a structure that forms from the follicle after ovulation), promotes thickening of the endometrium to prepare an environment conducive to implantation. Progesterone also inhibits GnRH, FSH, and LH release. In yet another negative feedback loop, inhibin, produced by the dominant ovarian follicle, inhibits the release of FSH, which would otherwise cause additional follicles to mature during the same ovarian cycle. If [fertilization](javascript:void(0)) does not occur, estrogen and progesterone levels drop, and another ovarian cycle and menstrual cycle begin. However, if fertilization occurs, estrogen and progesterone levels [remain high](javascript:void(0)) to promote the proper uterine environment for embryonic and fetal development. A summary of female reproductive hormones is illustrated in Figure 11.36.  Chapter 11: Endocrine System 410 **Figure 11.36** Summary of female reproductive hormones. The complex actions and interactions of various sex hormones are discussed in further detail in Concepts 9.2.03 and 9.3.03. 11.2.10 Appetite Hormones Sufficient energy and essential nutrients must be taken in via the diet to supply the body\'s many energy- and nutrient-demanding processes. If dietary intake is chronically too low to meet metabolic demands, body mass is lost via the breakdown of endogenous molecules to compensate for deficient intake of energy and essential molecules, potentially leading to compromised function. Chronic excessive dietary intake can also compromise function by increasing metabolic costs and susceptibility to certain metabolic or body composition-related disorders (eg, insulin resistance, type 2 diabetes mellitus). The balance between intake and utilization of dietary nutrients is regulated by numerous factors, including hormones released from cells throughout the body. Some of these hormones promote desire for food intake (ie, increased appetite), whereas others promote a feeling of satiety (ie, fullness or dietary satisfaction). **Ghrelin** is a hormone released by cells in the stomach and transported via the bloodstream to the brain, where it acts on the hypothalamus to stimulate appetite prior to a meal. After a meal, the body is in an energy-rich state (ie, high concentrations of glucose and lipids) and the hormone **leptin** is released by adipose tissue. Leptin triggers feelings of satiety by communicating to the hypothalamus that the stomach is full, thereby suppressing appetite. In general, the greater the adipose tissue stores, the higher the leptin levels in the serum. In addition, delta cells of the pancreas produce **somatostatin**, a hormone that has a generalized inhibitory effect on digestive function (see Concept 11.2.06). Figure 11.37 summarizes the effects of hormones on appetite. A diagram of a structure Description automatically generated Chapter 11: Endocrine System 411 **Figure 11.37** Hormonal influences on appetite. Concept 15.3.01 explores endocrine control of digestion further. 11.2.11 Other Hormones There are several hormones that are important to know for the exam in addition to those covered in the previous concepts of this lesson. The amino acid--derived hormone **melatonin** is produced by the pineal gland, a brain structure. Melatonin is thought to influence circadian rhythms, promoting drowsiness and sleep. The pineal gland is stimulated to secrete melatonin when [retinal photoreceptors](javascript:void(0)) detect low light levels (Figure 11.38).  Chapter 11: Endocrine System 412 **Figure 11.38** Melatonin secretion influences circadian rhythms. The thymus, a lymphoid organ located anterior to the heart, releases the peptide hormone **thymosin**. Thymosin promotes [T cell development](javascript:void(0)) and differentiation, which are discussed in more detail in Concept 20.1.03. The thymus shrinks in size after puberty; accordingly, thymosin is most active in children. Atrial myocytes (ie, cardiac muscle cells of the atria) produce the peptide hormone **atrial natriuretic factor (ANF)** in response to excessive atrial stretch, a characteristic of high blood pressure. ANF targets the kidneys to increase [glomerular filtration rate](javascript:void(0)) via afferent arteriole vasodilation and efferent arteriole vasoconstriction. At the same time, ANF causes less sodium to be reabsorbed in the nephrons, allowing more water to remain in the filtrate to be excreted in the urine, thereby lowering blood volume. ANF also inhibits the secretion of renin, ultimately inhibiting aldosterone release. The actions of ANF are summarized in Figure 11.39. A diagram of a brain Description automatically generated Chapter 11: Endocrine System 413 **Figure 11.39** Actions of atrial natriuretic factor on the kidneys. Several peptide hormones are important in digestion, including gastrin, cholecystokinin (CCK), and secretin. **Gastrin** is released by the [G cells](javascript:void(0)) of the stomach wall in response to food ingestion and targets parietal cells of the stomach wall (see Concept 15.1.02). Secretion of gastrin promotes stomach motility and the release of hydrochloric acid (HCl) by parietal cells to promote digestion. **CCK** is produced by epithelial cells of the [duodenum](javascript:void(0)) (ie, small intestine) and promotes secretion of digestive enzymes from the pancreas and bile from the gallbladder to facilitate digestion. In addition, CCK decreases stomach motility and promotes the feeling of satiety (ie, fullness). **Secretin**, also produced by duodenal epithelial cells, promotes digestive enzyme and bicarbonate release from the pancreas into the duodenum to promote digestion. Secretin also inhibits HCl secretion by stomach parietal cells as chyme moves from the stomach to the small intestine. The actions of CCK and secretin are covered in further detail in Concept 15.1.03. Tables 11.3, 11.4, and 11.5 provide an overview of important hypothalamic and pituitary hormones, other hormones produced by endocrine glands, and hormones produced by organs and tissues outside the endocrine system, respectively.  Chapter 11: Endocrine System 414 **Table 11.3** Important hypothalamic and pituitary hormones. **Hormone name** **Hormone type** **Hormone source** **Hormone action** Antidiuretic hormone (ADH) Peptide Increases blood volume and pressure by increasing nephron water reabsorption Oxytocin Peptide Posterior pituitary (produced by hypothalamus) Stimulates uterine contractions and milk ejection from mammary glands Adrenocorticotropic hormone (ACTH) Peptide Promotes glucocorticoid synthesis and secretion in adrenal cortex Follicle-stimulating hormone (FSH) Peptide Stimulates ovarian follicle maturation and spermatogenesis Luteinizing hormone (LH) Peptide Stimulates estrogen production, triggers ovulation, promotes testosterone synthesis Thyroid-stimulating hormone (TSH) Peptide Promotes thyroid hormone synthesis and secretion in thyroid gland β-endorphins Peptide Decreases pain perception and causes feelings of euphoria Growth hormone (GH) Peptide Regulates growth by promoting protein synthesis and fat utilization Prolactin Peptide Anterior pituitary Promotes production and secretion of milk by mammary glands Corticotropin-releasing hormone (CRH) Peptide Stimulates ACTH production in the anterior pituitary Gonadotropin-releasing hormone (GnRH) Peptide Stimulates FSH and LH production in the anterior pituitary Thyrotropin-releasing hormone (TRH) Peptide Stimulates TSH production in the anterior pituitary Prolactin-inhibiting factor (PIF, dopamine) Amino acid--derived Hypothalamus Prevents prolactin production in the anterior pituitary Chapter 11: Endocrine System 415 **Table 11.4** Important hormones produced by endocrine glands. **Hormone name** **Hormone type** **Hormone source** **Hormone action** Glucocorticoids (cortisol, cortisone) Steroid Increase blood glucose during stress response Mineralocorticoids (aldosterone) Steroid Increase blood volume and pressure via increasing reabsorption of water and salt in the kidney Cortical sex hormones Steroid Adrenal cortex Stimulate sperm cell differentiation, development of male/female sexual traits Catecholamines (epinephrine, norepinephrine) Amino acid--derived Adrenal medulla Increase blood glucose levels, heart rate, blood flow to critical organs during stress response Glucagon Peptide Pancreas(alpha cells) Increases blood glucose levels Insulin Peptide Pancreas(beta cells) Decreases blood glucose levels Somatostatin Peptide Pancreas(delta cells), hypothalamus General inhibitory effect on digestion, inhibits GH secretion by anterior pituitary Thyroid hormone (T3, T4) Amino acid--derived Thyroid gland (follicular cells) Stimulatory effects, increases cellular metabolism, increases body temperature Calcitonin Peptide Thyroid gland(C \[parafollicular\] cells) Reduces blood calcium levels Parathyroid hormone (PTH) Peptide Parathyroid glands Increases blood calcium levels Testosterone Steroid Testes Promotes spermatogenesis and male sex trait development Estrogens Steroid Promotes oogenesis and female sex trait development Progesterone Steroid Ovaries and placenta Promotes thickening of endometrium Chapter 11: Endocrine System 416 Inhibin Peptide Testes and ovaries Inhibits FSH Melatonin Amino acid--derived Pineal gland Influences circadian rhythms, promotes drowsiness and sleep **T3** = triiodothyronine; **T4** = thyroxine. **Table 11.5** Important hormones produced by organs and tissues outside the endocrine system. **Hormone name** **Hormone type** **Hormone source** **Hormone action** Erythropoietin (EPO) Peptide Increases blood oxygen levels through promoting red blood cell production Calcitriol Steroid Kidney Promotes intestinal calcium absorption and nephron calcium reabsorption Ghrelin Peptide Acts on hypothalamus to stimulate appetite Gastrin Peptide Stomach Promotes stomach motility and HCl release in stomach parietal cells Leptin Peptide Adipose tissue Acts on hypothalamus to suppress appetite Thymosin Peptide Thymus Promotes T cell development and differentiation Atrial natriuretic factor (ANF) Peptide Heart Acts on kidneys to reduce blood volume and pressure Cholecystokinin (CCK) Peptide Promotes secretion of pancreatic enzymes and bile, decreases stomach motility Secretin Peptide Duodenum Promotes secretion of pancreatic enzymes and bicarbonate, inhibits stomach HCl secretion **HCl** = hydrochloric acid.