Pancreas
ENDOCRINE GLANDS
COURSE OUTLINE
16.5 The Endocrine Pancreas
16.6 Other Endocrine Glands and Hormone-Secreting Tissues
16.7 Three Examples of Endocrine Control of Physiological Variables
UPCOMING SCHEDULE
Next Lecture:
Chapter 19 Blood
Canvas Quizzes:
Endocrine Quiz II: Thyroid and Parathyroid Glands - due February 1, 11:59 PM
Endocrine Quiz III: Adrenal & Pancreas - due February 3, 11:59 PM
Endocrine Quiz IV: All of Chapter 16 - due February 3, 11:59 PM
Mastering Assignments:
Finish Chapter 16 - Dynamic Study Module – Sections 4 – 7 (due January 30)
Finish Chapter 16 – Interactive Reading – The Endocrine System (due February 1, 11:59 PM)
ENDOCRINE ORGANS
Anterior Pituitary Gland
Thyroid Gland
Parathyroid Glands
Thymus Gland
Adrenal Cortex
Pancreas
Ovaries (female)
Testes (male)
Neuroendocrine Organs:
Hypothalamus
Pineal Gland
Posterior Pituitary Gland
Adrenal Medulla
KEY CONCEPTS TO KNOW
Gland
Hormone(s)
Target Tissue(s)
Physiological Effects
Hypo- & Hypersecretion
THE PANCREAS
STRUCTURE OF THE PANCREAS
The pancreas is a club-shaped organ located in the abdominal cavity, mostly posterior to the stomach. It has:
Head
Body
Tail
Contains two main types of cells:
Pancreatic Islets (endocrine)
Acinar Cells (exocrine) that secrete enzymes and other products into small ducts delivered to the digestive tract
CELL TYPES IN PANCREATIC ISLETS
Alpha Cells: Secrete Glucagon
Beta Cells: Secrete Insulin
Delta Cells: Secrete Somatostatin (same as produced by the hypothalamus)
GROWTH HORMONE (GH)
Growth Hormone (GH): Also known as Somatotropin.
Produced by Somatotrophs.
Peak secretion occurs during sleep.
Regulates growth; target tissues include:
Skeletal and cardiac muscle
Adipose
Liver
Cartilage
Bone
Growth Hormone-Releasing Hormone (GHRH) stimulates release of GH.
Growth Hormone-Inhibiting Hormone (Somatostatin) inhibits GH.
ASSOCIATED HORMONES
TRH (Thyrotropin-Releasing Hormone): Stimulates Prolactin release.
Prolactin promotes breast development and milk production; inhibited by Dopamine (Prolactin-Inhibiting Factor).
TSH (Thyroid-Stimulating Hormone): Stimulates thyroid hormone secretion.
CRH (Corticotropin-Releasing Hormone):
Stimulates Adrenocorticotropic Hormone (ACTH) production.
Promotes adrenal gland development and secretion of steroid hormones.
GnRH (Gonadotropin-Releasing Hormone): Stimulates release of FSH and LH.
FSH engages in testosterone binding and estrogen production.
LH stimulates testosterone and estrogen/progesterone production.
PANCREATIC HORMONES
GLUCAGON
Promotes reactions that raise glucose and metabolic fuel levels in the blood.
Targets liver, muscle, and adipose tissue, causing:
Glycogenolysis: Breakdown of glycogen into glucose.
Gluconeogenesis: New glucose formation in the liver.
Protein breakdown in muscle for glucose increase.
Fat release from adipose tissue for gluconeogenesis.
KETONE BODIES
Formation of Ketone Bodies from fatty acids in the liver.
Ketone bodies are fuels for muscle and brain under extreme calorie restriction or starvation.
High levels can lead to Ketoacidosis when acidity increases blood pH.
GLUCAGON SECRETION TRIGGER
Triggered by:
Decrease in blood glucose concentration
Sympathetic nervous system stimulation
Ingested proteins
Inhibited by:
Elevated blood glucose levels
Somatostatin
INSULIN
Promotes uptake of nutrients, lowering blood glucose levels.
Secreted primarily from Beta Cells and helps store nutrients.
Targets:
Liver
Cardiac & skeletal muscle
Parts of brain
Actions include:
Promotes feelings of satiety.
Maintains glucose concentrations within a narrow range.
Stimulated by rising blood glucose, inhibited by somatostatin.
DISORDERS OF INSULIN
HYPERGLYCEMIA
Defined by insufficient insulin secretion or decreased insulin sensitivity.
Commonly causes:
Type 1 and Type 2 Diabetes Mellitus.
Damages blood vessels and increases risks of heart attacks and wounds.
Leads to complications like Peripheral Neuropathy and blindness.
HYPOGLYCEMIA
Occurs due to high insulin levels, reducing blood glucose.
Symptoms include:
Weakness, dizziness, rapid breathing, nausea, sweating.
Severe cases can cause confusion, hallucinations, seizures, coma, and even death.
TYPE 1 DIABETES MELLITUS
Affects 5-10% of diabetes cases in the U.S.
Caused by immune system destruction of Beta Cells leading to:
Inability of target cells to absorb glucose.
Increased ketone production from glucagon action.
SYMPTOMS
Glucosuria: Loss of glucose in urine.
Ketonuria: Loss of ketones in urine.
Leads to: Frequent urination, excessive thirst, and potential for diabetic ketoacidosis.
TYPE 2 DIABETES MELLITUS
Affects up to 95% of adult diabetes cases.
Involves insulin resistance due to:
Beta cells' decreased responsiveness to glucose.
Target cells’ reduced response to insulin.
Often manageable with lifestyle changes; may require oral hypoglycemics or insulin therapy.
BLOOD GLUCOSE REGULATION
INCREASING BLOOD GLUCOSE LEVELS
Stimulus: Blood glucose increases (normal range is 70−99 mg/dl).
Can occur from feeding or cortisol response.
Receptor: Beta cells detect increased glucose concentration.
Control Center: Beta cells increase insulin secretion.
Effector/Response: Insulin increases glucose uptake by cells and storage of glucose.
Return to Normal: Upon normalization, beta cells decrease insulin production.
DECREASING BLOOD GLUCOSE LEVELS
Stimulus: Blood glucose decreases below normal range (70−99 mg/dl).
Receptor: Alpha cells detect decreased glucose.
Control Center: Alpha cells increase glucagon secretion, insulin secretion decreases.
Effector/Response: Glucagon raises blood glucose through glycogen breakdown and gluconeogenesis.
Return to Normal: Alpha cells adjust glucagon levels once normal range is restored.
GONADS AND HORMONES
TESTES: TESTOSTERONE
Sex steroid hormone produced primarily in the testes.
Influenced by GnRH from the hypothalamus leading to secretion of LH and FSH from the anterior pituitary.
Effects:
Anabolic: Stimulates bone growth and increases muscle mass.
Androgenic: Development of male secondary sex characteristics (e.g., deeper voice, facial hair).
OVARIES: ESTROGENS AND PROGESTERONE
Estrogens and Progesterone are vital for female reproductive health.
Regulated through feedback loops involving GnRH, LH, FSH.
Effects include development of female secondary sex characteristics and regulation of menstrual cycle.
Progesterone supports preparation for pregnancy and fetal development.
THYMUS
Irregularly shaped organ in the mediastinum.
Site for T lymphocyte maturation, secretes Thymosin and Thymopoietin.
Larger and more active in infants; atrophy occurs in adults, replaced mainly with fat.
PINEAL GLAND - MELATONIN
Part of the epithalamus in the diencephalon.
Secretes melatonin, regulating sleep-wake cycles based on ambient light.
Effectiveness of melatonin supplements for sleep enhancement is debated.
ADIPOSE TISSUE: LEPTIN
Leptin: Protein hormone released by adipocytes.
crosses the blood-brain barrier, interacts with the hypothalamus to induce satiety and prevent overeating.
Amount of leptin relates to adipose tissue quantity, complex feeding regulation mechanisms are at play.
HEART: ATRIAL NATRIURETIC PEPTIDE (ANP)
Produced by cardiac muscle in response to stretch.
Causes vasodilation to lower blood pressure and blood volume.
KIDNEYS AND ENDOCONCRINE ROLES
Erythropoietin (EPO) production in response to low blood oxygen, stimulates red bone marrow.
Renin: Converts angiotensinogen to angiotensin-1, part of the renin-angiotensin-aldosterone system that controls blood pressure.
Activation of Vitamin D, converting it to Calcitriol, stimulated by parathyroid hormone.
HORMONE-SECRETING TISSUES
Pineal Gland: Melatonin - Regulates sleep-wake cycle.
Adipose Tissue: Leptin - Induces satiety.
Heart: Atrial Natriuretic Peptide (ANP) - causes vasodilation, decreases blood pressure, and promotes natriuresis.
Kidneys: Erythropoietin, Renin, Vitamin D.