- ุฏ. ุงูุนุณุงู 2026
- ุฏ. ุงูุนุณุงู 2026
- ุชูุฑูุบ 2026ุฏ. ุฑุคู
- Imp Notes
- ู ูุฎุต 2026MZ
- ู ูุฎุต 2026ุฏ.ูุฏู
- ุชูุฑูุบ 2026
๐ General Brain Metabolism
๐ง Brain = 2% of body weight but consumes:
20โ25% of total body oxygen.
60% of total body glucose.
Main & first fuel = Glucose.
Glucose level effect:
70 mg/dL โ all cells work normally.
50 mg/dL โ some cells stop functioning.
40 mg/dL โ only Brain + RBCs work.
<40 mg/dL โ RBCs only continue working.
๐ Comparison: Muscles vs. Brain vs. RBCs
Muscles:
Can use glucose, fatty acids, glycogen.
Have multiple energy sources & can rest.
Brain:
Cannot rest โ must work continuously.
Depends only on glucose & ketone bodies.
RBCs:
Only use glucose (no mitochondria, no nucleus).
Depend on glycolysis + PPP.
Last cells to function at very low glucose.
๐ Brain Structure Notes
Glial Cells: act as insulators like electric wire covering.
Gray Matter: neuronal cell bodies (soma).
White Matter: axons, rich in lipids โ white color.
๐ Energy Sources
-Source Pathway End Product Carbohydrates (Glucose)Glycolysis โ Pyruvate โ Krebs Cycle โ ETCโATP
-Proteins โ amino acids โ Gluconeogenesis or Ketogenesis.โ Glucose / Ketone Bodies โ Fats โ Beta-oxidation โ NADH, FADH โ ETCATP
๐จ Clinical Note:
Acetone โ evaporates in breath โ fruity smell in prolonged fasting or uncontrolled diabetes.
Beta-hydroxybutyrate โ measured to check for ketoacidosis.โ ุนุดุงู ูู ู ุด ู ุชููุฑ ูู ูู ุงูู ุนุงู ู ูุณุชุฎุฏู ูุง ุงูุงุณูุชูู
๐ Fasting State Sequence
Early Phase:
Body uses Glycogen first.
Liver Glycogen: maintains blood glucose.
Muscle Glycogen: local use only.
Astrocytes: small glycogen store for brain cells.
After 8โ14 hours:
Gluconeogenesis (GNG) starts โ glucose from non-carbohydrate sources (mainly amino acids).
Maintains blood glucose between 60โ115 mg/dL.
Prolonged Fasting:
Ketone bodies production increases โ alternative brain fuel.
Types: Acetoacetate, Beta-hydroxybutyrate, Acetone.
๐ฃ Brain & Lipid Metabolism
Brain does NOT use beta-oxidation for energy.
Lipids in brain are used for:
Myelin sheath.
Cell membranes.
Neurotransmitters.
Special Oxidations (non-energy):
Alpha-oxidation โ defect โ Refsum Disease.
Peroxisomal oxidation โ defect โ Zellweger Syndrome.
Brain synthesizes Very Long Chain Fatty Acids (VLCFAs) internally โ BBB prevents their entry.
๐ Pentose Phosphate Pathway (PPP)
Glucose-6-phosphate โ PPP โ produces:
NADPH:
Antioxidant.
Regenerates Glutathione.
Fatty acid synthesis.
Glucuronic acid synthesis.
Ribose-5-phosphate โ nucleotide synthesis.
Glucuronic Acid โ detoxification & conjugation.
๐ Hormonal Regulation
State Main Hormone Action Effect Fed Insulin Dephosphorylation โ activates enzymesโ Glycogen synthesis, โ Lipogenesis
Fasting Glucagon Phosphorylation โ activates catabolic enzymesโ Glycogenolysis, โ Lipolysis, โ Ketogenesis
GLUT 1 & GLUT 3 in brain & RBCs are insulin-independent.
๐จ Clinical Importance
Prolonged fasting/uncontrolled diabetes โ fruity breath smell (acetone).
Beta-hydroxybutyrate used to monitor diabetic ketoacidosis.
RBCs highly sensitive to glucose shortage โ early hypoglycemia signs.
Brain defects:
Refsum Disease โ alpha-oxidation defect.
Zellweger Syndrome โ peroxisomal defect.
๐ General Brain Metabolism
๐ง Brain = 2% of body weight but consumes:
20โ25% of total body oxygen.
60% of total body glucose.
Main & first fuel = Glucose.
Glucose level effect:
70 mg/dL โ all cells work normally.
50 mg/dL โ some cells stop functioning.
40 mg/dL โ only Brain + RBCs work.
<40 mg/dL โ RBCs only continue working.
๐ Comparison: Muscles vs. Brain vs. RBCs
Muscles:
Can use glucose, fatty acids, glycogen.
Have multiple energy sources & can rest.
Brain:
Cannot rest โ must work continuously.
Depends only on glucose & ketone bodies.
RBCs:
Only use glucose (no mitochondria, no nucleus).
Depend on glycolysis + PPP.
Last cells to function at very low glucose.
๐ Brain Structure Notes
Glial Cells: act as insulators like electric wire covering.
Gray Matter: neuronal cell bodies (soma).
White Matter: axons, rich in lipids โ white color.
๐ Energy Sources
-Source Pathway End Product Carbohydrates (Glucose)Glycolysis โ Pyruvate โ Krebs Cycle โ ETCโATP
-Proteins โ amino acids โ Gluconeogenesis or Ketogenesis.โ Glucose / Ketone Bodies โ Fats โ Beta-oxidation โ NADH, FADH โ ETCATP
๐จ Clinical Note:
Acetone โ evaporates in breath โ fruity smell in prolonged fasting or uncontrolled diabetes.
Beta-hydroxybutyrate โ measured to check for ketoacidosis.โ ุนุดุงู ูู ู ุด ู ุชููุฑ ูู ูู ุงูู ุนุงู ู ูุณุชุฎุฏู ูุง ุงูุงุณูุชูู
๐ Fasting State Sequence
Early Phase:
Body uses Glycogen first.
Liver Glycogen: maintains blood glucose.
Muscle Glycogen: local use only.
Astrocytes: small glycogen store for brain cells.
After 8โ14 hours:
Gluconeogenesis (GNG) starts โ glucose from non-carbohydrate sources (mainly amino acids).
Maintains blood glucose between 60โ115 mg/dL.
Prolonged Fasting:
Ketone bodies production increases โ alternative brain fuel.
Types: Acetoacetate, Beta-hydroxybutyrate, Acetone.
๐ฃ Brain & Lipid Metabolism
Brain does NOT use beta-oxidation for energy.
Lipids in brain are used for:
Myelin sheath.
Cell membranes.
Neurotransmitters.
Special Oxidations (non-energy):
Alpha-oxidation โ defect โ Refsum Disease.
Peroxisomal oxidation โ defect โ Zellweger Syndrome.
Brain synthesizes Very Long Chain Fatty Acids (VLCFAs) internally โ BBB prevents their entry.
๐ Pentose Phosphate Pathway (PPP)
Glucose-6-phosphate โ PPP โ produces:
NADPH:
Antioxidant.
Regenerates Glutathione.
Fatty acid synthesis.
Glucuronic acid synthesis.
Ribose-5-phosphate โ nucleotide synthesis.
Glucuronic Acid โ detoxification & conjugation.
๐ Hormonal Regulation
State Main Hormone Action Effect Fed Insulin Dephosphorylation โ activates enzymesโ Glycogen synthesis, โ Lipogenesis
Fasting Glucagon Phosphorylation โ activates catabolic enzymesโ Glycogenolysis, โ Lipolysis, โ Ketogenesis
GLUT 1 & GLUT 3 in brain & RBCs are insulin-independent.
๐จ Clinical Importance
Prolonged fasting/uncontrolled diabetes โ fruity breath smell (acetone).
Beta-hydroxybutyrate used to monitor diabetic ketoacidosis.
RBCs highly sensitive to glucose shortage โ early hypoglycemia signs.
Brain defects:
Refsum Disease โ alpha-oxidation defect.
Zellweger Syndrome โ peroxisomal defect.