1. CONTROL OF APETITE & METABOLISM

2. Glucose Homeostasis NORMAL SERUM GLUCOSE 80-120 mg/dl SERUM GLUCOSE SERUM GLUCOSE ISLET  -CELLS LIVER & MUSCLE METABOLIC DEMANDS INSULIN GLUCOSE UPTAKE ISLET  -CELLS LIVER & MUSCLE GLUCAGON GLYCOGENOLYSIS GLUCONEOGENESIS CORTISONE & EPINEPHRINE MEALS GH

3. HYPOTHALAMUS: ARCUATE NUCLEUS ANTERIOR PITUITARY RELEASING HORMONES ENERGY RESERVES AND METABOLISM –OREXIGENIC/ANOREXIGENIC NEURONS –INCREASE/DECREASE METABOLISM –RECEPTORS FOR PERIPHERAL SIGNALS

4. ARCUATE NUCLEUS TWO TYPES OF NEURONS MELANOCORTIN –POMC –αMSH –INHIBITS FEEDING BEHAVIOR –INCREASES METABOLISM NEUROPEPTIDE-Y (NPY) –NPY –AGOUTI-RELATED PEPTIDE (AgRP) COMPETITIVE INHIBITOR OF MELANOCORTIN RECEPTORS –STIMULATES FEEDING BEHAVIOR –DECREASES METABOLISM –INHIBITS MELANOCORTIN NEURONS

5. ARCUATE NUCLEUS αMSH METABOLIC RATE FEEDING BEHAVIOR (-) (+) NPY (+)(-)

6. ENERGY BALANCE INDICATORS LONG-TERM ENERGY STORES (ADIPOSE) –LEPTIN –INSULIN SHORT-TERM ENERGY STORES (SATIETY) –GHRELIN –PEPTIDE YY –CHOLECYSTOKININ (CCK) –GLP-1

7. Leptin Produced by fat cells –Level of leptin produced is directly related to how much fat is in the fat cell. Peptide Anorexogenic Increases metabolism

8. Leptin Deficiency

9. ARCUATE NUCLEUS αMSH METABOLIC RATE FEEDING BEHAVIOR (-) (+) NPY (+) (-) LEPTIN INSULIN PEPTIDE YY CCK GLP-1(?) GHRELIN

10. CONTROL OF FOOD INTAKE AND METABOLISM CCK