KETOSIS
DR ROHINI C SANE
PROFESSOR
DEPARTMENT OF BIOCHEMISTRY
DY PATIL MEDICAL COLLEGE MAURITIUS
TYPES OF KETONE BODIES
 ACETONE ,
 ACETO ACETIC ACID
 BETA HYDROXY BUTYRIC ACID
PROPERTIES OF KETONE BODIES
 WATER SOLUBLE
 ENERGY YEILDING (ACETONE CANNOT BE METABOLISED )
KETOGENESIS
Acetyl Co A
Co ASH
Acetyl Co A
KETONEMIA
KETOSIS
 SERUM NORMAL CONCENTRATION---- 1 mg/ml
 Urine-----Trace (Rotheras Test)
 KETONEMIA----( INCREASED CONCENTRATION OF SERUM KETONE BODIES
>100mg / dl)
 KETONURIA-----(INCREASED CONCENTRATION IN URINE >500mg /dl)
 KETOSIS---- KETONEMIA + KETONURIA
 RATE OF SYNTHESIS > RATE OF UTILIZATION
 DIEBETIS MELITUS / STARVATION
FACTORS AGGREVATING KETOSIS
DECREASED CONCENTRATION OF OAA (AS GLUCONEOGENESIS---INCREASED )
DECREASED ACETYL Co A UTILISATION
DECREASED TCA
INCREASED CONCENTRATION OF ACETYL Co A
FACTORS AGGREVATING KETOSIS
INCREASED FREE FATTY ACIDS
DECREASED ACETYL Co A CARBOXYLASE
DECREASED MALONYL Co A
INCREASED CARNITINE PALMITOYL TRANSFERASE
INCREASED ACYL CO A OXIDATION
INCREASED ACETYL COA
FACTORS AGGREVATING KETOSIS
INSULIN / GLUCAGON RATIO DECREASED
INCREASED LIPOLYSIS IN ADIPOSE TISSUE
INCREASED ACETYL Co A
KETONE BODIES
FACTORS AGGREVATING KETOSIS
 KETOGENIC AMINO ACIDS
 LEUCINE
 LYSINE
 TYROSINE
STARVATION
BETA OXIDATION ENZYMES (INCREASED) INCREASED HORMONE
SENSITIVE LIPASE I
ACTIVITY
Acetyl Co A
KETONE BODIES HORMONES
FFA
Acetyl Co A
KETONE BODIES (BRAIN 48HR-20%
7 DAYS-60%
40 DAYS 70% )
STARVATION
MANIFESTATIONS
 DISPLACEMENT OF VISCERAL ORGANS (ADIPOSE TISSUE
THINS OUT )
 SKIN HANGS LOOSE
 DECREASED ACETYL Co A CARBOXYLASE
 DECREASED CITRATE SYNTHETASE
 INCREASED TRANSLOCATION OF CITRATE TO CYTOSOL
 DECREASED FATTY ACID SYNTHESIS
 METABOLIC KETOACIDOSIS
 HYPERVENTILATION
 BREATH ---ACETONE –FRUITY ODOUR
 DECREASED BICARBONATE
 OSMOTIC DIURESIS
 DEHYDRATION ,KETONURIA
 LOSS OF SODIUM AGGRIVATING DEHYDRATION
 INCREASED ACIDITY IN URINE
 INCREASED AMMONIUM SECRETION &EXCRETION OF AMMONIUM
CHLORIDE
 FATTY LIVER( CARBOHYDRATE DECREASED ---DECREASED ALPHA
GLYCEROL P ----DECREASED VLDL )------ACCUMULATION FAT IN LIVER
 COMA
 DEATH
EFFECTS OF KETOSIS
TREATMENT OF KETOSIS ( STARVATION)
 INSULIN
 GLUCOSE
 ASPARTATE ----OAA---TCA-----ACETYL COA
 CORRECTION OF ACIDOSIS& BICARBONATE
TREATMENT OF DIEBETIS KETOACIDOSIS
 INSULIN
 ASPARTATE
 GLUCAGON STIMULATES KETOGENESIS
 INSULIN INHIBITS KETOGENESIS

Ketosis

  • 1.
    KETOSIS DR ROHINI CSANE PROFESSOR DEPARTMENT OF BIOCHEMISTRY DY PATIL MEDICAL COLLEGE MAURITIUS
  • 2.
    TYPES OF KETONEBODIES  ACETONE ,  ACETO ACETIC ACID  BETA HYDROXY BUTYRIC ACID
  • 3.
    PROPERTIES OF KETONEBODIES  WATER SOLUBLE  ENERGY YEILDING (ACETONE CANNOT BE METABOLISED )
  • 4.
  • 5.
  • 6.
    KETOSIS  SERUM NORMALCONCENTRATION---- 1 mg/ml  Urine-----Trace (Rotheras Test)  KETONEMIA----( INCREASED CONCENTRATION OF SERUM KETONE BODIES >100mg / dl)  KETONURIA-----(INCREASED CONCENTRATION IN URINE >500mg /dl)  KETOSIS---- KETONEMIA + KETONURIA  RATE OF SYNTHESIS > RATE OF UTILIZATION  DIEBETIS MELITUS / STARVATION
  • 7.
    FACTORS AGGREVATING KETOSIS DECREASEDCONCENTRATION OF OAA (AS GLUCONEOGENESIS---INCREASED ) DECREASED ACETYL Co A UTILISATION DECREASED TCA INCREASED CONCENTRATION OF ACETYL Co A
  • 8.
    FACTORS AGGREVATING KETOSIS INCREASEDFREE FATTY ACIDS DECREASED ACETYL Co A CARBOXYLASE DECREASED MALONYL Co A INCREASED CARNITINE PALMITOYL TRANSFERASE INCREASED ACYL CO A OXIDATION INCREASED ACETYL COA
  • 9.
    FACTORS AGGREVATING KETOSIS INSULIN/ GLUCAGON RATIO DECREASED INCREASED LIPOLYSIS IN ADIPOSE TISSUE INCREASED ACETYL Co A KETONE BODIES
  • 10.
    FACTORS AGGREVATING KETOSIS KETOGENIC AMINO ACIDS  LEUCINE  LYSINE  TYROSINE
  • 11.
    STARVATION BETA OXIDATION ENZYMES(INCREASED) INCREASED HORMONE SENSITIVE LIPASE I ACTIVITY Acetyl Co A KETONE BODIES HORMONES FFA Acetyl Co A KETONE BODIES (BRAIN 48HR-20% 7 DAYS-60% 40 DAYS 70% )
  • 12.
    STARVATION MANIFESTATIONS  DISPLACEMENT OFVISCERAL ORGANS (ADIPOSE TISSUE THINS OUT )  SKIN HANGS LOOSE  DECREASED ACETYL Co A CARBOXYLASE  DECREASED CITRATE SYNTHETASE  INCREASED TRANSLOCATION OF CITRATE TO CYTOSOL  DECREASED FATTY ACID SYNTHESIS
  • 13.
     METABOLIC KETOACIDOSIS HYPERVENTILATION  BREATH ---ACETONE –FRUITY ODOUR  DECREASED BICARBONATE  OSMOTIC DIURESIS  DEHYDRATION ,KETONURIA  LOSS OF SODIUM AGGRIVATING DEHYDRATION  INCREASED ACIDITY IN URINE  INCREASED AMMONIUM SECRETION &EXCRETION OF AMMONIUM CHLORIDE  FATTY LIVER( CARBOHYDRATE DECREASED ---DECREASED ALPHA GLYCEROL P ----DECREASED VLDL )------ACCUMULATION FAT IN LIVER  COMA  DEATH EFFECTS OF KETOSIS
  • 14.
    TREATMENT OF KETOSIS( STARVATION)  INSULIN  GLUCOSE  ASPARTATE ----OAA---TCA-----ACETYL COA  CORRECTION OF ACIDOSIS& BICARBONATE
  • 15.
    TREATMENT OF DIEBETISKETOACIDOSIS  INSULIN  ASPARTATE  GLUCAGON STIMULATES KETOGENESIS  INSULIN INHIBITS KETOGENESIS