Chapter 18: The Endocrine System Muse lecture #10 7/5/12

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 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  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 Can be divided into three groups  Amino acid derivatives  Peptide hormones  Lipid derivatives Circulate freely or bound to transport proteins

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

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)

1 Lipid-soluble hormone diffuses into cell Blood capillary Target cell Transport protein Free hormone 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 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 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 protein 2 3 4

Mechanisms of Hormone Action Important Second Messengers  Cyclic-AMP (cAMP) Derivative of ATP  Cyclic-GMP (cGMP) Derivative of GTP  Calcium ions

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

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 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 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 Activated protein kinases Water-soluble hormone Receptor cAMP serves as a second messenger to activate protein kinases G protein Protein kinases cAMP Activated protein kinases Second messenger Activated adenylate cyclase converts ATP to cAMP Activated protein kinases 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 Protein— P ADP Protein ATP Water-soluble hormone Receptor cAMP serves as a second messenger to activate protein kinases G protein Protein kinases cAMP Activated protein kinases Protein— Second messenger Activated adenylate cyclase converts ATP to cAMP Activated protein kinases 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 Water-soluble hormone Receptor cAMP serves as a second messenger to activate protein kinases G protein Protein kinases cAMP Activated protein kinases Protein— Second messenger Phosphodiesterase inactivates cAMP Activated adenylate cyclase converts ATP to cAMP Activated protein kinases 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

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 - The Master 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

Low blood glucose (hypoglycemia) stimulates release of GHRH 1 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 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) 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 Anterior pituitary Low blood glucose (hypoglycemia) stimulates release of High blood glucose (hyperglycemia) stimulates release of hGH GHRH stimulates secretion of hGH by somatotrophs GHIHGHRH 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 Anterior pituitary GHIH inhibits secretion of hGH by somatotrophs Low blood glucose (hypoglycemia) stimulates release of High blood glucose (hyperglycemia) stimulates release of hGH GHRH stimulates secretion of hGH by somatotrophs GHIHGHRH 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 GHIH inhibits secretion of hGH by somatotrophs Low blood glucose (hypoglycemia) stimulates release of High blood glucose (hyperglycemia) stimulates release of Anterior pituitary hGH GHRH stimulates secretion of hGH by somatotrophs GHIHGHRH 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 GHIH inhibits secretion of hGH by somatotrophs Low blood glucose (hypoglycemia) stimulates release of High blood glucose (hyperglycemia) stimulates release of Anterior pituitary hGH GHRH stimulates secretion of hGH by somatotrophs GHIHGHRH 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 Blood glucose level rises to normal (about 90 mg/100 mL) If blood glucose continues to increase, hyperglycemia inhibits release of GHRH GHIH inhibits secretion of hGH by somatotrophs Low blood glucose (hypoglycemia) stimulates release of High blood glucose (hyperglycemia) stimulates release of Anterior pituitary hGH GHRH stimulates secretion of hGH by somatotrophs GHIHGHRH 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 Blood glucose level rises to normal (about 90 mg/100 mL) If blood glucose continues to increase, hyperglycemia inhibits release of GHRH If blood glucose continues to decrease, hypoglycemia inhibits release of GHIH

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 1 Osmoreceptors High blood osmotic pressure stimulates hypothalamic osmoreceptors Osmoreceptors activate the neurosecretory cells that synthesize and release ADH Hypothalamus 1 2 Osmoreceptors High blood osmotic pressure stimulates hypothalamic osmoreceptors Nerve impulses liberate ADH from axon terminals in the posterior pituitary into the bloodstream Osmoreceptors activate the neurosecretory cells that synthesize and release ADH Hypothalamus ADH Osmoreceptors High blood osmotic pressure stimulates hypothalamic osmoreceptors Nerve impulses liberate ADH from axon terminals in the posterior pituitary into the bloodstream Osmoreceptors 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 Osmoreceptors High blood osmotic pressure stimulates hypothalamic osmoreceptors Low blood osmotic pressure inhibits hypothalamic osmoreceptors Nerve impulses liberate ADH from axon terminals in the posterior pituitary into the bloodstream Osmoreceptors 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 Osmoreceptors High blood osmotic pressure stimulates hypothalamic osmoreceptors Low blood osmotic pressure inhibits hypothalamic osmoreceptors Nerve impulses liberate ADH from axon terminals in the posterior pituitary into the bloodstream Osmoreceptors 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

Thyroid Gland Located inferior to larynx 2 lobes connected by isthmus Thyroid follicles produce thyroid hormones  Thyroxine or tetraiodothyronine (T 4 )  Triiodothyronine (T 3 ) 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 Ca 2+ 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 Anterior pituitary Thyroid gland Thyroid hormones TSH TRH Target cells Stimulates Inhibits

Low blood levels of T 3 and T 3 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 T 3 and T 3 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 T 3 and T 3 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 T 3 and T 4 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 T 3 and T 3 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 T 3 and T 4 released into blood by follicular cells Elevated T 3 inhibits 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 T 3 and T 3 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

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

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

Figure 18–15 The Endocrine 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 Glucagon  Released by alpha cells  Mobilizes energy reserves  Affects target cells Stimulates breakdown of glycogen in skeletal muscle and liver cells Stimulates breakdown of triglycerides in adipose tissue Stimulates production of glucose in liver

Negative Feedback Regulation of Glucagon and Insulin

Low blood glucose (hypoglycemia) stimulates alpha cells to secrete 1 GLUCAGON 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 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 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 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 INSULINGLUCAGON 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 INSULINGLUCAGON 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 INSULINGLUCAGON

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

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  Inhibin inhibits FSH

Pineal Gland Attached to roof of 3 rd 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 Thymus  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.

Copyright 2009, John Wiley & Sons, Inc. Hormone Interactions Figure 18–18 The General Adaptation Syndrome.

Mechanisms of Hormone Action Figure 18–4b Effects of Intracellular Hormone Binding.

Mechanisms of Hormone Action Figure 18–3 G Proteins and Hormone Activity.

Mechanisms of Hormone Action The Process of Amplification  Is the binding of a small number of hormone molecules to membrane receptors  Leads to thousands of second messengers in cell  Magnifies effect of hormone on target cell

Endocrine Tissues of Other Systems Adipose Tissue Secretions  Leptin Feedback control for appetite Controls normal levels of GnRH, gonadotropin synthesis  Resistin Reduces insulin sensitivity

Hormone Interactions Hormones Important to Growth  GH  Thyroid hormones  Insulin  PTH  Calcitriol  Reproductive hormones

Endocrine Tissues of Other Systems Heart  Produces natriuretic peptides (ANP and BNP) When blood volume becomes excessive Action opposes angiotensin II Resulting in reduction in blood volume and blood pressure Thymus  Produces thymosins (blend of thymic hormones) That help develop and maintain normal immune defenses

The endocrine matrix Hormone - what gland secretes it? What is it’s target? What does it do to its target? Is it a peptide, eicosenoid, or steroid, or catecholamine? It it influenced by another hormone? Does it interact with a system? Triiodothyronine T3 Thyroid epithelial cell increases the basal metabolic rate catecholamine TSH influences secretion