Chapter 18: The Endocrine System Muse lecture #14 7/1/10

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

Introduction to the Endocrine System Regulates long-term processes Growth Development Reproduction Uses chemical messengers to relay information and instructions between cells

Endocrine Glands 2 kinds of glands Endocrine glands include 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

Endocrine locations

Hormone Activity Hormones affect only specific target tissues with specific receptors Receptors constantly synthesized and broken down Down-regulation Up-regulation

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

Chemical classes of hormones Lipid-soluble – use transport proteins Steroid Thyroid Nitric oxide (NO) Water-soluble – circulate in “free” form Amine Peptide/ protein Eicosanoid

Hormones Figure 18–2 A Structural Classification of Hormones

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

Lipid-soluble and Water-soluble Hormones

Mechanisms of Hormone Action Hormones and Plasma Membrane Receptors Catecholamines and peptide hormones Are not lipid soluble Unable to penetrate plasma membrane Bind to receptor proteins at outer surface of plasma membrane (extracellular receptors)

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

Mechanisms of Hormone Action Important Second Messengers Cyclic-AMP (cAMP) Derivative of ATP Cyclic-GMP (cGMP) Derivative of GTP Calcium ions Copyright 2009, John Wiley & Sons, Inc.

Mechanisms of Hormone Action Hormones and Plasma Membrane Receptors G Protein Enzyme complex coupled to membrane receptor Involved in link between first messenger and second messenger Binds GTP Activated when hormone binds to receptor at membrane surface and changes concentration of second messenger cyclic-AMP (cAMP) within cell: increased cAMP level accelerates metabolic activity within cell

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

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

Hypothalamus and Pituitary Gland

Pituitary Gland Figure 18–9 Pituitary Hormones and Their Targets.

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

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

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

Pituitary Gland Figure 18–8a Feedback Control of Endocrine Secretion

Negative Feedback Regulation

Effects of hGH and IGFs

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

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

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)

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 osmo- receptors 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

Thyroid Gland

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

Hypothalamus TRH Anterior pituitary TSH Thyroid gland Thyroid hormones Stimulates Target cells Inhibits

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

Parathyroid Glands

Roles of Calcitonin, Parathyroid hormone, Calcitrol in Calcium Homeostasis

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

Adrenal Glands

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

Pancreas

Pancreas Insulin Is a peptide hormone released by beta cells Affects target cells Accelerates glucose uptake Accelerates glucose utilization and enhances ATP production Stimulates glycogen formation Stimulates amino acid absorption and protein synthesis Stimulates triglyceride formation in adipose tissue

Pancreas

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

Stimulates glucose uptake by cells Insulin Tissue cells Stimulates glycogen formation Pancreas Glucose Glycogen Blood glucose falls to normal range. Liver Stimulus Blood glucose level Stimulus Blood glucose level Blood glucose rises to normal range. Pancreas Liver Glucose Glycogen Stimulates glycogen breakdown 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

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

Pineal Gland Functions of Melatonin Inhibiting reproductive functions Protecting against damage by free radicals Setting circadian rhythms

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

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

Hormone Interactions General Adaptation Syndrome (GAS) Also called stress response How body responds to stress-causing factors Is divided into three phases: Alarm phase Resistance phase Exhaustion phase Figure 18–18

Stress Response

Hormone Interactions Figure 18–18 The General Adaptation Syndrome.

Hormone Interactions Figure 18–18 The General Adaptation Syndrome.

Mechanisms of Hormone Action Figure 18–4b Effects of Intracellular Hormone Binding. Copyright 2009, John Wiley & Sons, Inc.

Mechanisms of Hormone Action Figure 18–3 G Proteins and Hormone Activity. Copyright 2009, John Wiley & Sons, Inc.