Chapter 18: The Endocrine System

Chapter 18: The Endocrine System
Copyright 2009, John Wiley & Sons, Inc.

Nervous and Endocrine Systems
Act together to coordinate functions of all body systems Nervous system Nerve impulses/ Neurotransmitters Faster responses, briefer effects, acts on specific target Endocrine system Hormone – mediator molecule released in 1 part of the body but regulates activity of cells in other parts Slower responses, effects last longer, broader influence Copyright 2009, John Wiley & Sons, Inc.

Copyright 2009, John Wiley & Sons, Inc.
Endocrine Glands 2 kinds of glands Exocrine – ducted Endocrine – ductless Secrete products into interstitial fluid, diffuse into blood Endocrine glands include Pituitary, thyroid, parathyroid, adrenal and pineal glands Hypothalamus, thymus, pancreas, ovaries, testes, kidneys, stomach, liver, small intestine, skin, heart, adipose tissue, and placenta not exclusively endocrine glands Copyright 2009, John Wiley & Sons, Inc.

Hormone Activity Hormones affect only specific target tissues with specific receptors Receptors constantly synthesized and broken down Down-regulation Up-regulation Copyright 2009, John Wiley & Sons, Inc.

Hormone types Circulating – circulate in blood throughout body Local hormones – act locally Paracrine – act on neighboring cells Autocrine – act on the same cell that secreted them Copyright 2009, John Wiley & Sons, Inc.

Chemical classes of hormones
Lipid-soluble – use transport proteins Steroid Thyroid Nitric oxide (NO) Water-soluble – circulate in “free” form Amine Peptide/ protein Eicosanoid Copyright 2009, John Wiley & Sons, Inc.

Mechanisms of Hormone Action
Response depends on both hormone and target cell Lipid-soluble hormones bind to receptors inside target cells Water-soluble hormones bind to receptors on the plasma membrane Activates second messenger system Amplification of original small signal Responsiveness of target cell depends on Hormone’s concentration Abundance of target cell receptors Influence exerted by other hormones Permissive, synergistic and antagonistic effects Copyright 2009, John Wiley & Sons, Inc.

Lipid-soluble and Water-soluble Hormones

Lipid-soluble hormone diffuses into cell Blood capillary Activated
1 Lipid-soluble hormone diffuses into cell Blood capillary Activated receptor-hormone complex alters gene expression Nucleus Receptor mRNA Newly formed mRNA directs synthesis of specific proteins on ribosomes DNA Cytosol Target cell New proteins alter cell's activity Transport protein Free hormone Ribosome New 2 3 4 1 Lipid-soluble hormone diffuses into cell Blood capillary Activated receptor-hormone complex alters gene expression Nucleus Receptor mRNA Newly formed mRNA directs synthesis of specific proteins on ribosomes DNA Cytosol Target cell Transport protein Free hormone Ribosome 2 3 1 Lipid-soluble hormone diffuses into cell Blood capillary Activated receptor-hormone complex alters gene expression Nucleus Receptor mRNA DNA Cytosol Target cell Transport protein Free hormone 2 1 Lipid-soluble hormone diffuses into cell Blood capillary Target cell Transport protein Free hormone

1 2 4 3 5 1 2 6 4 3 5 1 2 4 3 1 2 3 1 2 1 Water-soluble hormone
Receptor cAMP serves as a second messenger to activate protein kinases G protein Protein kinases cAMP Activated protein Protein— Second messenger Activated adenylate cyclase converts ATP to cAMP Activated protein phosphorylate cellular proteins Millions of phosphorylated proteins cause reactions that produce physiological responses Blood capillary Binding of hormone (first messenger) to its receptor activates G protein, which activates adenylate cyclase Adenylate cyclase Target cell P ADP Protein ATP 1 2 4 3 5 Water-soluble hormone Receptor cAMP serves as a second messenger to activate protein kinases G protein Protein kinases cAMP Activated protein Protein— Second messenger Phosphodiesterase inactivates cAMP Activated adenylate cyclase converts ATP to cAMP Activated protein phosphorylate cellular proteins Millions of phosphorylated proteins cause reactions that produce physiological responses Blood capillary Binding of hormone (first messenger) to its receptor activates G protein, which activates adenylate cyclase Adenylate cyclase Target cell P ADP Protein ATP 1 2 6 4 3 5 Water-soluble hormone Receptor cAMP serves as a second messenger to activate protein kinases G protein Protein kinases cAMP Activated protein Second messenger Activated adenylate cyclase converts ATP to cAMP Activated protein phosphorylate cellular proteins Blood capillary Binding of hormone (first messenger) to its receptor activates G protein, which activates adenylate cyclase Adenylate cyclase Target cell ATP 1 2 4 3 Protein— P ADP Protein Water-soluble hormone Receptor cAMP serves as a second messenger to activate protein kinases G protein Protein kinases cAMP Second messenger Activated adenylate cyclase converts ATP to cAMP Blood capillary Binding of hormone (first messenger) to its receptor activates G protein, which activates adenylate cyclase Adenylate cyclase Target cell ATP 1 2 3 Activated protein Water-soluble hormone Receptor G protein cAMP Second messenger Activated adenylate cyclase converts ATP to cAMP Blood capillary Binding of hormone (first messenger) to its receptor activates G protein, which activates adenylate cyclase Adenylate cyclase Target cell ATP 1 2 Water-soluble hormone Receptor G protein Blood capillary Binding of hormone (first messenger) to its receptor activates G protein, which activates adenylate cyclase Adenylate cyclase Target cell 1

Control of Hormone Secretion
Regulated by Signals from nervous system Chemical changes in the blood Other hormones Most hormonal regulation by negative feedback Few examples of positive feedback Copyright 2009, John Wiley & Sons, Inc.

Hypothalamus and Pituitary Gland
Hypothalamus is a major link between nervous and endocrine system Pituitary attached to hypothalamus by infundibulum Anterior pituitary or adenohypophysis Posterior pituitary or neurohypophysis Copyright 2009, John Wiley & Sons, Inc.

Hypothalamus and Pituitary Gland

Anterior pituitary Release of hormones stimulated by releasing and inhibiting hormones from the hypothalamus Also regulated by negative feedback Hypothalamic hormones made by neurosecretory cells transported by hypophyseal portal system Anterior pituitary hormones that act on other endocrine systems called tropic hormones Copyright 2009, John Wiley & Sons, Inc.

Hormones of the Anterior Pituitary
Human growth hormone (hGH) or somatostatin Stimulates secretion of insulin-like growth factors (IGFs) that promote growth, protein synthesis Thyroid-stimulating hormone (TSH) or thyrotropin Stimulates synthesis and secretion of thyroid hormones by thyroid Follicle-stimulating hormone (FSH) Ovaries initiates development of oocytes, testes stimulates testosterone production Luteinizing hormone (LH) Ovaries stimulates ovulation, testes stimulates testosterone production Copyright 2009, John Wiley & Sons, Inc.

Hormones of the Anterior Pituitary
Prolactin (PRL) Promotes milk secretion by mammary glands Adrenocorticotropic hormone (ACTH) or corticotropin Stimulates glucocorticoid secretion by adrenal cortex Melanocyte-stimulating Hormone (MSH) Unknown role in humans Copyright 2009, John Wiley & Sons, Inc.

Negative Feedback Regulation

GHIH inhibits secretion of hGH by somatotrophs Low blood glucose (hypoglycemia) stimulates release of High blood glucose (hyperglycemia) hGH GHRH stimulates secretion of hGH by GHIH GHRH hGH and IGFs speed up breakdown of liver glycogen into glucose, which enters the blood more rapidly Blood glucose level rises to normal (about 90 mg/100 mL) If blood glucose continues to increase, hyperglycemia inhibits release of GHRH 1 6 7 3 4 5 2 GHIH inhibits secretion of hGH by somatotrophs Low blood glucose (hypoglycemia) stimulates release of High blood glucose (hyperglycemia) Anterior pituitary hGH GHRH stimulates secretion of hGH by GHIH GHRH A low level of hGH and IGFs decreases the rate of glycogen breakdown in the liver and glucose enters the blood more slowly hGH and IGFs speed up breakdown of liver glycogen into glucose, which enters the blood more rapidly Blood glucose level rises to normal (about 90 mg/100 mL) If blood glucose continues to increase, hyperglycemia inhibits release of GHRH 1 6 7 8 3 4 5 2 GHIH inhibits secretion of hGH by somatotrophs Low blood glucose (hypoglycemia) stimulates release of High blood glucose (hyperglycemia) Anterior pituitary hGH GHRH stimulates secretion of hGH by GHIH GHRH A low level of hGH and IGFs decreases the rate of glycogen breakdown in the liver and glucose enters the blood more slowly Blood glucose level falls to normal (about 90 mg/100 mL) hGH and IGFs speed up breakdown of liver glycogen into glucose, which enters the blood more rapidly rises to normal If blood glucose continues to increase, hyperglycemia inhibits release of GHRH 1 6 7 8 9 3 4 5 2 GHIH inhibits secretion of hGH by somatotrophs Low blood glucose (hypoglycemia) stimulates release of High blood glucose (hyperglycemia) Anterior pituitary hGH GHRH stimulates secretion of hGH by GHIH GHRH A low level of hGH and IGFs decreases the rate of glycogen breakdown in the liver and glucose enters the blood more slowly Blood glucose level falls to normal (about 90 mg/100 mL) hGH and IGFs speed up breakdown of liver glycogen into glucose, which enters the blood more rapidly rises to normal If blood glucose continues to increase, hyperglycemia inhibits release of GHRH continues to decrease, hypoglycemia inhibits release of GHIH 1 6 7 8 9 10 3 4 5 2 Low blood glucose (hypoglycemia) stimulates release of High blood glucose (hyperglycemia) hGH GHRH stimulates secretion of hGH by somatotrophs GHIH GHRH hGH and IGFs speed up breakdown of liver glycogen into glucose, which enters the blood more rapidly Blood glucose level rises to normal (about 90 mg/100 mL) If blood glucose continues to increase, hyperglycemia inhibits release of GHRH 1 6 3 4 5 2 Anterior pituitary Low blood glucose (hypoglycemia) stimulates release of hGH GHRH stimulates secretion of hGH by somatotrophs GHRH hGH and IGFs speed up breakdown of liver glycogen into glucose, which enters the blood more rapidly Blood glucose level rises to normal (about 90 mg/100 mL) If blood glucose continues to increase, hyperglycemia inhibits release of GHRH 1 3 4 5 2 Anterior pituitary Low blood glucose (hypoglycemia) stimulates release of hGH GHRH stimulates secretion of hGH by somatotrophs GHRH 1 2 Low blood glucose (hypoglycemia) stimulates release of hGH GHRH stimulates secretion of hGH by somatotrophs GHRH hGH and IGFs speed up breakdown of liver glycogen into glucose, which enters the blood more rapidly 1 3 2 Low blood glucose (hypoglycemia) stimulates release of hGH GHRH stimulates secretion of hGH by somatotrophs GHRH hGH and IGFs speed up breakdown of liver glycogen into glucose, which enters the blood more rapidly Blood glucose level rises to normal (about 90 mg/100 mL) 1 3 4 2 Low blood glucose (hypoglycemia) stimulates release of GHRH 1

Posterior pituitary Does not synthesize hormones Stores and releases hormones made by the hypothalamus Transported along hypothalamohypophyseal tract Oxytocin (OT) Antidiuretic hormone (ADH) or vasopressin Copyright 2009, John Wiley & Sons, Inc.

Hypothalamohypophyseal tract

Oxytocin (OT) During and after delivery of baby affects uterus and breasts Enhances smooth muscle contraction in wall of uterus Stimulates milk ejection from mammary glands Copyright 2009, John Wiley & Sons, Inc.

Antidiuretic Hormone (ADH)
Decreases urine production by causing the kindeys to return more water to the blood Also decreases water lost through sweating and constriction of arterioles which increases blood pressure (vasopressin) Copyright 2009, John Wiley & Sons, Inc.

Osmoreceptors High blood osmotic pressure stimulates hypothalamic osmoreceptors Low blood osmotic pressure inhibits Nerve impulses liberate ADH from axon terminals in the posterior pituitary into the bloodstream activate the neurosecretory cells that synthesize and release ADH Hypothalamus Sudoriferous (sweat) glands decrease water loss by perspiration from the skin Arterioles constrict, which increases blood pressure Kidneys retain more water, which decreases urine output ADH Target tissues 1 2 3 4 5 Osmoreceptors High blood osmotic pressure stimulates hypothalamic osmoreceptors Low blood osmotic pressure inhibits Nerve impulses liberate ADH from axon terminals in the posterior pituitary into the bloodstream activate the neurosecretory cells that synthesize and release ADH Hypothalamus Inhibition of osmoreceptors reduces or stops ADH secretion Sudoriferous (sweat) glands decrease water loss by perspiration from the skin Arterioles constrict, which increases blood pressure Kidneys retain more water, which decreases urine output ADH Target tissues 1 2 3 4 5 6 Osmoreceptors High blood osmotic pressure stimulates hypothalamic osmoreceptors Nerve impulses liberate ADH from axon terminals in the posterior pituitary into the bloodstream activate the neurosecretory cells that synthesize and release ADH Hypothalamus Sudoriferous (sweat) glands decrease water loss by perspiration from the skin Arterioles constrict, which increases blood pressure Kidneys retain more water, which decreases urine output ADH Target tissues 1 2 3 4 Osmoreceptors High blood osmotic pressure stimulates hypothalamic osmoreceptors Nerve impulses liberate ADH from axon terminals in the posterior pituitary into the bloodstream activate the neurosecretory cells that synthesize and release ADH Hypothalamus ADH 1 2 3 Osmoreceptors High blood osmotic pressure stimulates hypothalamic osmoreceptors activate the neurosecretory cells that synthesize and release ADH Hypothalamus 1 2 Osmoreceptors High blood osmotic pressure stimulates hypothalamic osmoreceptors 1

Thyroid Gland Located inferior to larynx 2 lobes connected by isthmus Thyroid follicles produce thyroid hormones Thyroxine or tetraiodothyronine (T4) Triiodothyronine (T3) Both increase BMR, stimulate protein synthesis, increase use of glucose and fatty acids for ATP production Parafollicular cells or C cells produce calcitonin Lowers blood Ca2+ by inhibiting bone resorption Copyright 2009, John Wiley & Sons, Inc.

Control of thyroid hormone secretion
Thyrotropin-releasing hormone (TRH) from hypothalamus Thyroid-stimulating hormone (TSH) from anterior pituitary Situations that increase ATP demand also increase secretion of thyroid hormones Copyright 2009, John Wiley & Sons, Inc.

Low blood levels of T3 and T3 or low metabolic rate stimulate release of Hypothalamus TRH Actions of Thyroid Hormones: Increase basal metabolic rate Stimulate synthesis of Na+/K+ ATPase Increase body temperature (calorigenic effect) Stimulate protein synthesis Increase the use of glucose and fatty acids for ATP production Stimulate lipolysis Enhance some actions of catecholamines Regulate development and growth of nervous tissue and bones 1 Anterior pituitary TRH, carried by hypophyseal portal veins to anterior pituitary, stimulates release of TSH by thyrotrophs Low blood levels of T3 and T3 or low metabolic rate stimulate release of Hypothalamus TSH TRH Actions of Thyroid Hormones: Increase basal metabolic rate Stimulate synthesis of Na+/K+ ATPase Increase body temperature (calorigenic effect) Stimulate protein synthesis Increase the use of glucose and fatty acids for ATP production Stimulate lipolysis Enhance some actions of catecholamines Regulate development and growth of nervous tissue and bones 1 2 Anterior pituitary TRH, carried by hypophyseal portal veins to anterior pituitary, stimulates release of TSH by thyrotrophs TSH released into blood stimulates thyroid follicular cells Thyroid follicle Low blood levels of T3 and T3 or low metabolic rate stimulate release of Hypothalamus Anterior pituitary TSH TRH Actions of Thyroid Hormones: Increase basal metabolic rate Stimulate synthesis of Na+/K+ ATPase Increase body temperature (calorigenic effect) Stimulate protein synthesis Increase the use of glucose and fatty acids for ATP production Stimulate lipolysis Enhance some actions of catecholamines Regulate development and growth of nervous tissue and bones 1 2 3 T3 and T4 released into blood by follicular cells TRH, carried by hypophyseal portal veins to anterior pituitary, stimulates release of TSH by thyrotrophs TSH released into blood stimulates thyroid follicular cells Thyroid follicle Low blood levels of T3 and T3 or low metabolic rate stimulate release of Hypothalamus Anterior pituitary TSH TRH Actions of Thyroid Hormones: Increase basal metabolic rate Stimulate synthesis of Na+/K+ ATPase Increase body temperature (calorigenic effect) Stimulate protein synthesis Increase the use of glucose and fatty acids for ATP production Stimulate lipolysis Enhance some actions of catecholamines Regulate development and growth of nervous tissue and bones 1 2 3 4 T3 and T4 released into blood by follicular cells Elevated T3inhibits release of TRH and TSH (negative feedback) TRH, carried by hypophyseal portal veins to anterior pituitary, stimulates release of TSH by thyrotrophs TSH released into blood stimulates thyroid follicular cells Thyroid follicle Low blood levels of T3 and T3 or low metabolic rate stimulate release of Hypothalamus Anterior pituitary TRH Actions of Thyroid Hormones: Increase basal metabolic rate Stimulate synthesis of Na+/K+ ATPase Increase body temperature (calorigenic effect) Stimulate protein synthesis Increase the use of glucose and fatty acids for ATP production Stimulate lipolysis Enhance some actions of catecholamines Regulate development and growth of nervous tissue and bones 1 2 3 5 4

Parathyroid Glands Embedded in lobes of thyroid gland Usually 4 Parathyroid hormone (PTH) or parathormone Major regulator of calcium, magnesium, and phosphate ions in the blood Increases number and activity of osteoclasts Elevates bone resorption Blood calcium level directly controls secretion of both calcitonin and PTH via negative feedback Copyright 2009, John Wiley & Sons, Inc.

1 High level of Ca2+ in blood stimulates thyroid gland parafollicular cells to release more CT. Low level of Ca2+ in blood stimulates parathyroid gland chief cells to release more PTH. CALCITONIN inhibits osteoclasts, thus decreasing blood Ca2+ level. PARATHYROID HORMONE (PTH) promotes release of Ca2+ from bone extracellular matrix into blood and slows loss of Ca2+ in urine, thus increasing blood Ca2+ level. 3 4 2 1 High level of Ca2+ in blood stimulates thyroid gland parafollicular cells to release more CT. 1 High level of Ca2+ in blood stimulates thyroid gland parafollicular cells to release more CT. Low level of Ca2+ in blood stimulates parathyroid gland chief cells to release more PTH. CALCITONIN inhibits osteoclasts, thus decreasing blood Ca2+ level. 3 2 1 CALCITRIOL stimulates increased absorption of Ca2+ from foods, which increases blood Ca2+ level. PTH also stimulates the kidneys to release CALCITRIOL. High level of Ca2+ in blood stimulates thyroid gland parafollicular cells to release more CT. Low level of Ca2+ in blood stimulates parathyroid gland chief cells to release more PTH. CALCITONIN inhibits osteoclasts, thus decreasing blood Ca2+ level. PARATHYROID HORMONE (PTH) promotes release of Ca2+ from bone extracellular matrix into blood and slows loss of Ca2+ in urine, thus increasing blood Ca2+ level. 3 4 2 5 6 1 PTH also stimulates the kidneys to release CALCITRIOL. High level of Ca2+ in blood stimulates thyroid gland parafollicular cells to release more CT. Low level of Ca2+ in blood stimulates parathyroid gland chief cells to release more PTH. CALCITONIN inhibits osteoclasts, thus decreasing blood Ca2+ level. PARATHYROID HORMONE (PTH) promotes release of Ca2+ from bone extracellular matrix into blood and slows loss of Ca2+ in urine, thus increasing blood Ca2+ level. 3 4 2 5 1 High level of Ca2+ in blood stimulates thyroid gland parafollicular cells to release more CT. CALCITONIN inhibits osteoclasts, thus decreasing blood Ca2+ level. 2

Adrenal Glands 2 structurally and functionally distinct regions Adrenal cortex Mineralocorticoids affect mineral homeostasis Glucocorticoids affect glucose homeostasis cortisol Androgens have masculinzing effects Dehydroepiandrosterone (DHEA) only important in females Adrenal medulla Modified sympathetic ganglion of autonomic nervous system Intensifies sympathetic responses Epinephrine and norepinephrine Copyright 2009, John Wiley & Sons, Inc.

Pancreatic Islets Both exocrine and endocrine gland Roughly 99% of cells produce digestive enzymes Pancreatic islets or islets of Langerhans Alpha or A cells secrete glucagon – raises blood sugar Beta or B cells secrete insulin – lowers blood sugar Delta or D cells secrete somatostatin – inhibits both insulin and glucagon F cells secrete pancreatic polypeptide – inhibits somatostatin, gallbladder contraction, and secretion of pancreatic digestive enzymes Copyright 2009, John Wiley & Sons, Inc.

Negative Feedback Regulation of Glucagon and Insulin

Insulin acts on various
body cells to: • accelerate facilitated diffusion of glucose into cells • speed conversion of glucose into glycogen (glycogenesis) • increase uptake of amino acids and increase protein synthesis • speed synthesis of fatty acids (lipogenesis) • slow glycogenolysis • slow gluconeogenesis Glucagon acts on hepatocytes (liver cells) to: • convert glycogen into glucose (glycogenolysis) • form glucose from lactic acid and certain amino acids (gluconeogenesis) Glucose released by hepatocytes raises blood glucose level to normal If blood glucose continues to rise, hyperglycemia inhibits release of glucagon Low blood glucose (hypoglycemia) stimulates alpha cells to secrete High blood glucose (hyperglycemia) stimulates beta cells to secrete INSULIN GLUCAGON 1 5 2 3 4 6 Insulin acts on various body cells to: • accelerate facilitated diffusion of glucose into cells • speed conversion of glucose into glycogen (glycogenesis) • increase uptake of amino acids and increase protein synthesis • speed synthesis of fatty acids (lipogenesis) • slow glycogenolysis • slow gluconeogenesis Blood glucose level falls Glucagon acts on hepatocytes (liver cells) to: • convert glycogen into glucose (glycogenolysis) • form glucose from lactic acid and certain amino acids (gluconeogenesis) Glucose released by hepatocytes raises blood glucose level to normal If blood glucose continues to rise, hyperglycemia inhibits release of glucagon Low blood glucose (hypoglycemia) stimulates alpha cells to secrete High blood glucose (hyperglycemia) stimulates beta cells to secrete INSULIN GLUCAGON 1 5 2 3 4 6 7 Insulin acts on various body cells to: • accelerate facilitated diffusion of glucose into cells • speed conversion of glucose into glycogen (glycogenesis) • increase uptake of amino acids and increase protein synthesis • speed synthesis of fatty acids (lipogenesis) • slow glycogenolysis • slow gluconeogenesis If blood glucose continues to fall, hypoglycemia inhibits release of insulin Blood glucose level falls Glucagon acts on hepatocytes (liver cells) to: • convert glycogen into glucose (glycogenolysis) • form glucose from lactic acid and certain amino acids (gluconeogenesis) Glucose released by hepatocytes raises blood glucose level to normal If blood glucose continues to rise, hyperglycemia inhibits release of glucagon Low blood glucose (hypoglycemia) stimulates alpha cells to secrete High blood glucose (hyperglycemia) stimulates beta cells to secrete INSULIN GLUCAGON 1 5 2 3 4 6 7 8 Glucagon acts on hepatocytes (liver cells) to: • convert glycogen into glucose (glycogenolysis) • form glucose from lactic acid and certain amino acids (gluconeogenesis) Glucose released by hepatocytes raises blood glucose level to normal If blood glucose continues to rise, hyperglycemia inhibits release of glucagon Low blood glucose (hypoglycemia) stimulates alpha cells to secrete High blood glucose (hyperglycemia) stimulates beta cells to secrete GLUCAGON 1 5 2 3 4 INSULIN Glucagon acts on hepatocytes (liver cells) to: • convert glycogen into glucose (glycogenolysis) • form glucose from lactic acid and certain amino acids (gluconeogenesis) Glucose released by hepatocytes raises blood glucose level to normal If blood glucose continues to rise, hyperglycemia inhibits release of glucagon Low blood glucose (hypoglycemia) stimulates alpha cells to secrete GLUCAGON 1 2 3 4 Glucagon acts on hepatocytes (liver cells) to: • convert glycogen into glucose (glycogenolysis) • form glucose from lactic acid and certain amino acids (gluconeogenesis) Low blood glucose (hypoglycemia) stimulates alpha cells to secrete GLUCAGON 1 2 Glucagon acts on hepatocytes (liver cells) to: • convert glycogen into glucose (glycogenolysis) • form glucose from lactic acid and certain amino acids (gluconeogenesis) Glucose released by hepatocytes raises blood glucose level to normal Low blood glucose (hypoglycemia) stimulates alpha cells to secrete GLUCAGON 1 2 3 Low blood glucose (hypoglycemia) stimulates alpha cells to secrete 1 GLUCAGON

Ovaries and Testes Gonads – produce gametes and hormones Ovaries produce 2 estrogens (estradiol and estrone) and progesterone With FSH and LH regulate menstrual cycle, maintain pregnancy, prepare mammary glands for lactation, maintain female secondary sex characteristics Inhibin inhibits FSH Relaxin produced during pregnancy Testes produce testosterone – regulates sperm production and maintains male secondary sex characteristics Copyright 2009, John Wiley & Sons, Inc.

Pineal Gland Attached to roof of 3rd ventricle of brain at midline Masses of neuroglia and pinealocytes Melatonin – amine hormone derived from serotonin Appears to contribute to setting biological clock More melatonin liberated during darkness than light Copyright 2009, John Wiley & Sons, Inc.

Thymus and Other Endocrine Tissues
Located behind sternum between the lungs Produces thymosin, thymic humoral factor (THF), thymic factor (TF), and thymopoietin All involved in T cell maturation Copyright 2009, John Wiley & Sons, Inc.

The Stress Response Eustress in helpful stress / Distress is harmful Body’s homeostatic mechanisms attempt to counteract stress Stressful conditions can result in stress response or general adaptation syndrome (GAS) 3 stages – initial flight-or-fight, slower resistance reaction, eventually exhaustion Prolonged exposure to cortisol can result in wasting of muscles, suppression of immune system, ulceration of GI tract, and failure of pancreatic beta cells Copyright 2009, John Wiley & Sons, Inc.

End of Chapter 18 Copyright 2009 John Wiley & Sons, Inc. All rights reserved. Reproduction or translation of this work beyond that permitted in section 117 of the 1976 United States Copyright Act without express permission of the copyright owner is unlawful. Request for further information should be addressed to the Permission Department, John Wiley & Sons, Inc. The purchaser may make back-up copies for his/her own use only and not for distribution or resale. The Publishers assumes no responsibility for errors, omissions, or damages caused by the use of theses programs or from the use of the information herein. Copyright 2009, John Wiley & Sons, Inc.

Chapter 18: The Endocrine System

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