REGULATION OF FAT METABOLISM

Question 1

ESTERIFICATION

Answer 1

GLYCEROL + 3 FATTY ACIDS -> TG

Question 2

ESTERIFICATION IS DEPENDS ON

Answer 2

1. SUPPLY OF THE FATTY ACYL COA
2. SUPPLY OF GLYCEROL 3 PHOSPHATE

Question 3

LIPOLYSIS

Answer 3

TG -> 3 FATTY ACIDS + GLYCEROL

Question 4

STATE THE ROLE OF INSULIN.

Answer 4

• TRANSLOCATION OF GLUT 4 TO PLASMA MEMBRANE
• ACTIVATE LIPOPROTEIN LIPASE TO BREAKDOWN THE TG IN THE CM AND VLDL SO THAT IT CAN BE USED FOR ESTERIFICATION

Question 5

ROLE OF INSULIN IN A WELL FED STATE.

Answer 5

1. INHIBIT THE LIPOLYSIS IN THE ADIPOCYTE BY INHIBITING THE HSL
2. ACTIVATE THE LPL IN THE BLOOD SO BREAKDOWN OF TG IN THE BLOOD CAN OCCUR HENCE PROVIDING MORE FA FOR ESTERIFICATION
3. STIMULATE THE TRANSPORT OF GLUCOSE FROM THE BLOOD INTO THE ADIPOCYTE VIA THE GLUT 4

Question 6

OTHER ACTIONS OF INSULIN

Answer 6

INCREASE THE ACTIVITY OF:
- PYRUVATE DH
- ACETYL COA CARBOXYLASE
- GLYCEROL 3 PHOSPHATE DH
- ACYTRANSFERASE

Question 7

ROLE OF HSL

Answer 7

DURING FASTING, THE GLUCAGON IS HIGH -> GLUCAGON WILL BIND TO THE RECEPTOR AND STIMULATE THE ACTIVATION OF THE ADENYLATE CYCLASE -> CAUSING THE CONVERSION OF THE ATP TO CAMP -> HIGH CAMP RESULT IN THE ACTIVATION OF THE PROTEIN KINASE -> PHOSPHORYLATION -> ACTIVATION OF HSL -> DEGRADATION OF TG -> FORMATION OF GLYCEROL + 3 FAs

Question 8

KETONES ARE SYNTHESISED IN THE

Answer 8

LIVER DURING HIGH RATES OF LIPOLYSIS

Question 9

KETOGENESIS OCCUR IN CONDITION

Answer 9

1. LONG TERM STARVATION
2. UNCONTROLLED DIABETES (TYPE 1)

Question 10

KETOGENESIS IS WATER/FAT SOLUBLE

Answer 10

WATER SOLUBLEEX

Question 11

EXAMPLES OF KETONE BODIES.

Answer 11

ACETONE
ACETOACETATE
B- HYDROXYBUTYRATE

Question 12

KETONE BODIES IS USED IN THE

Answer 12

INTESTINE
KIDNEY
BRAIN
MUSCLES

Question 13

KETOGENESIS ABLE TO INCREASED/DECREASED THE BREAKDOWN OF PROTEIN

Answer 13

DECREASED THE BREAKDOWN OF PROTEIN -> REDUCE MUSCLE WASTING

Question 14

SYNTHESIS OF KETONE BODIES BY THE LIVER

Answer 14

DURING FASTING -> LIVER HAVE HIGH AMOUNT OF FA IN THE ADIPOCYTES -> HEPATIC ACETYL COA INCREAES -> INHIBIT THE PYRUVATE DH (PYRUVATE -> ACETYL COA) -> ACTIVATE THE PYRUVATE CARBOXYLASE (PYRUVATE -> OAA) -> OAA INCREASES -> GLUCONEOGESIS -> ACETYL COA CHANNELS INTO KETONE BODIES PRODUCTION

Question 15

EXCESSIVE PRODUCTION OF KETONE BODIES IN DM1

Answer 15

DM1 INSULIN RESISTANT -> INSULIN DEFICIENCY -> FA IN THE ADIPOCYTE INCREASE -> MOBILISE INTO THE BLOOD -> LIVER -> EXCESS ACETYL COA -> NAD+: NADH POOL DECREASE -> SLOW TCA -> INCREASE PRODUCTION OF KETONE BODIES IN LIVER

Question 16

HOW KETOACIDOSIS DEVELOPED?

Answer 16

ELEVATION OF KETONE BODIES IN BLOOD -> LOSES A PROTON (H+) AS IT CIRCULATE IN THE BLOOD -> BLOOD PH TO BE REDUCED -> EXCRETION OF KETONE BODIES IN THE URINE -> DEHYDRATION -> DEHYDRATION + LOW PH -> KETOACIDOSIS