1. GROWTH & METABOLISM Part 2 – Hormonal Regulation
LECTURE 17
CH 19

2. Islets of Langerhans Beta cells secrete insulin
Alpha cells secrete glucagon
Delta cells secrete somatostatin most of the pancreas consists of acini cells.
--blood glucose homeostasis
--glucose is the brain’s primary energy source
--w/o glucose: weakness/dizziness  coma, death --high glucose leads to tissue damage

3. Under what conditions is insulin secreted?
Insulin is secreted when blood glucose levels are too high.
Fasting plasma glucose: mg/dl
Absorptive state rises to mg/dl
Insulin acts to remove excess glucose from the blood after a carbohydrate-rich meal.
---the parasympathetic nervous system stimulates insulin release --glucose taken orally stimulates insulin release faster than injected glucose

4. How is insulin secreted by the pancreatic islets?
GLUT 2 channels
Cellular resp.  ATP
ATP-gated K+ channels close
Depolarization causes action pot.
Ca2+ channels open, Ca2+ enters
Exocytosis of insulin

5. INSULIN STIMULATES THE PRODUCTION OF GLUT CARRIERS
Skeletal (primarily)and cardiac muscle, liver, and adipose cells Promotes production and storage of glycogen and fat, inhibits breakdown of fat and muscle proteins Inhibits the liver from secreting glucose; induces the formation of fat-forming enzymes Promotes cellular uptake of amino acids and their incorporation into protein anabolic

6. During Fasting, Glucose Is Made in the Liver
Catabolism release of glucose glycogenolysis gluconeogenesis fatty acid release
Use of fatty acids for energy by skeletal muscles liver and adipose stress hyperglycemia

7. Feeding and Fasting

8. Diabetes mellitus Type I Diabetes mellitus Type II
-- child-onset (juvenile onset), “IDDM” (insulin- dependent diabetes).
-- an autoimmune disease --environmental factors
-- β attacked by immune syst.
--insulin needed 2-3x/day
--abnormally high glucagon --hyperglycemia; ketoacidosis can lead to coma/death
Diabetes mellitus Type II
-- non-insulin dependent -- patients produce insulin -- receptors are not working --glucagon stimulated
-- patients may be obese or normal weight
-- exercise stimulates cells to make more insulin receptor proteins
--strong genetic component
See table 19.5

9. Oral Glucose Tolerance Test
Tests ability of beta cells to release insulin and ability of insulin to reduce blood glucose levels normal – blood glucose returns to normal w/in 2 h Diabetic – remains at 200 mg/dL

10. Regulation of Metabolism by Epinephrine or Glucagon
beta receptor stimulates glycogenolysis in liver & lipolysis in adipose tissue

11. Stress  ACTH  adrenal cortex
Regulation of metabolism by glucocorticoids

12. --↑ metabolic heat -- influences BMR
--stimulates production of uncoupling proteins, ↓𝐴𝑇𝑃 --stimulating cell resp.
--↑ metabolic heat -- influences BMR
-- thyroxine is required for development of the CNS, otherwise cretinism.
All organs
--hypothyroidism – O2 consumption
is less than 30% of normal
--hyperthyroidism O2>30% of normal both lead to protein/muscle breakdown

13. Metabolic Effects of Growth Hormone
GHRH 
Inhibited by somatostatin
ANABOLIC EFFECT
CATABOLIC EFFECT
GH Stimulates cells to take up amino acids
somatomedins

14. Progression of Acromegaly
Due to excessive secretion of Growth Hormone; gigantism. After epiphyseal plates have sealed, height does not increase but elongation of jaw, face, hands and feet occurs
acromegaly
acromegaly
Dwarfism is regulated by multiple genes, not just GH

15. Regulation of Calcium and Phosphate
Blood calcium is required for muscles and membrane permeability It is maintained by PTH, 1,25- dihydroxyvitamin D3, and calcitonin. Skeleton is our Ca2+ and Phosphate storage (hydroxyapatite crystals) taken from blood by osteoblasts (bone deposition). Osteoclasts then break down bone (bone resorption) when blood levels are low.

16. Bone Resorption by Osteoclasts
Bone is demineralized due to acid secretion by the osteoclast. Enzymes get rid of collagen.

17. Normal Bone vs. Osteoporosis
-- Osteoporosis occurs when resorption exceeds deposition -- Peak bone mass occurs when people are in their 30s
--by age 50 or 60, the rate of resorption exceeds deposition
--estrogen stimulates apoptosis of osteoclasts

18. Vitamin D is a hormone INACTIVE D3 INACTIVE D3 ACTIVE D3
D3 allows active transport of Ca2+ into the small intestine
Stimulated by PTH
ACTIVE D3

19. Negative feedback control of parathyroid hormone secretion

20. Negative Feedback Control of Calcitonin

21. Terms to know:
Osteoblasts – bone forming cells Osteocytes – mature bone cells Osteoclasts – cells that break down bone Bone resorption – the desolving of bone Bone deposition – bone remodeling; making bone Absorption – nutrients taken into the blood from the small intestine Re-absorption – molecules re-claimed from the kidney filtrate and sent back to the blood
You do not need to know about RANK

22. SUMMARY
Know this