1. Anatomy & Physiology II
Fuel Homeostasis
Anatomy & Physiology II
Tony Serino, Ph.D.
Biology Department
College Misericordia

2. Energy Metabolism
Metabolic Rate (MR) –total rate of energy use in body (Kcal/min) -calorie = amount of heat needed to raise 1g of water one degree Celsius -1 Kcal (1000 calories) = 1 C (nutritional calorie)
BMR –(basal MR) MR of conscious, relaxed person hours after eating standardized for STP, diet and body size; represents the minimum energy required for individual to remain alive
Estimated by heat production, O2 consumption, or CO2 produced

3. Acquisition of Energy and Nutrients
GI tract mechanically and chemically digests food into their chemical “building blocks” for absorption into internal environment
Proteins into amino acids
CHO into monosaccharides
Fats into fatty acids and glycerol
Most of the absorbed material is first processed by the liver

4. Review of Metabolic Pathways

5. Nutritional States of the Body
Absorptive State
Body is assimilating nutrients and is able to use the energy of this food to survive
Lasts about 4 hours (represents time for food to pass through small intestine)
Post-absorptive State (Fasting State)
Occurs after meal fully absorbed

6. Absorptive State

7. Absorptive State Summary
Energy source for body is absorbed glucose
Glucose utilization is favored (burn or store)
Glycogenesis in skeletal muscles and liver: (Glucose  glycogen)
Lipogenesis in adipose and liver: (FA  fat; also excess AA and glucose converted to FA in liver)
Skeletal muscle and liver favor protein anabolism: (AA  protein)
Dominated by insulin

8. Post-Absorptive State

9. Post-Absorptive State Summary
Body energy provided by stored reserves
Glycogenolysis in muscle and liver releasing glucose to blood (glycogen  glucose)
Protein catabolism (esp. in muscle) puts AA in blood
Gluconeogenesis in liver (creation of glucose from non-glycogen sources)
Lactate, pyruvate, glycerol, and AA
Lipolysis (breakdown of fat  FA and glycerol)
FA used as energy source by most cells except brain
Liver can combine Co-A with FA to form ketones
Dominated by glucagon

10. Fuel Homeostasis Regulated by Pancreas
Both an exocrine and endocrine gland
Located in middle of upper right abdominal quadrant
Islets of Langerhans secrete hormones

11. Islet of Langerhans b-cells secrete insulin a-cells secrete glucagon
d-cells secrete somatostatin
f-cells secrete PP (pancreatic polypeptide)

13. Insulin Regulation Stimulated to be secreted by: Inhibited by:
Increase blood glucose
Increase blood AA
Increase GI hormone levels in blood
Increase parasympathetic activity
Inhibited by:
Decrease blood glucose
Increase sympathetic activity
Somatostatin

14. Insulin Effects Message: increase glucose utilization
Increase uptake of glu in all cells except brain and liver (increase glucose transporter proteins)
Increase FA and AA uptake
Increases glycolysis, glycogenesis, lipogenesis, and protein synthesis
Net: decrease glu, AA and FA in blood; increase fat , glycogen and protein production

16. Glucagon Regulation Stimulated by: Inhibited by:
Decrease blood glucose
Increase blood AA
Increase sympathetic stimulation
Epinephrine secretion
Inhibited by:
Increase blood glucose
Increase parasympathetic stimulation
Somatostatin secretion

17. Glucagon Effects
Increases cytoplasmic cAMP which triggers kinase activity to activate enzymes
Increases lipolysis, glycogenolysis, gluconeogenesis
Net: increases blood glucose, FA, glycerol and ketones
Most cells survive on FA and ketone metabolism (glucose sparing action)

18. Exercise Effects Essentially a Fasting State but protein sparing
Skeletal muscle differs from normal response:
Increases uptake and use of glucose
No protein catabolism (after excerise; increase protein synthesis

19. Diabetes
Disease state characterized by polyuria, polydipsia, polyphagia
Diabetes Insipidus –triggered by decrease production of ADH in post. pituitary
Diabetes Mellitus –due to hyposecretion secretion of insulin or insulin hyporesponsiveness
Type I (Insulin dependent or Juvenile) results from loss of b-cells in pancreas (maybe autoimmune disease) (10% 0f diabetics)
Type II (insulin independent or Adult onset) results from loss of insulin membrane receptors in target tissues (Ab attachment to receptor or a chronic down regulation) (90% of diabetics)
Chronic islets stimulation may result in hypertrophy and cell death; and thus insulin dependency

20. Organ Response to Insulin Deficiency