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FOO > METABOLIC CHANGES IN FASTING AND STARVATION > Flashcards

METABOLIC CHANGES IN FASTING AND STARVATION Flashcards

1
Q

WHAT ARE THE 2 MAIN THINGS THE BODY NEEDS TO DO DURING FASTING/STARVATION AND WHY:

A

1) SPARE GLUCOSE:
- TO CONSERVE IT FOR TISSUES OR CELLS THAT HAVE AN ABSOLUTE OR NEAR ABSOLUTE REQUIREMENT FOR IT, DONE BY SWITCHING FUEL UTILIZATION FROM GLUCOSE TO FATTY ACIDS

2) SYNTHESIZE NEW GLUCOSE:
- DONE USING NON-CARBOHYDRATE SUBSTRATES
- DONE THROUGH GLUCONEOGENESIS

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2
Q

IN WHICH ORGAN ARE THE FATTY ACIDS OXIDIZED TO KETONE BODIES?

A

IN THE LIVER

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3
Q

WHERE CAN GLUCONEOGENESIS OCCUR?

A

MAINLY IN THE LIVER, BUT TO SOME EXTENT IN THE KIDNEYS TOO

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4
Q

WHICH NON CARBOHYDRATE SUBSTRATES CAN BE USED TO FORM GLUCOSE IN GLUCOENEOGENESIS AND HOW DOES THE BODY GET THEM?

A

LACTATE (FROM ANAEROBIC GLYCOLYSIS)
AMINO ACIDS (FROM PROTEOLYSIS MOSTLY IN MUSCLES)
GLYCEROL (RELEASED WITH FATTY ACIDS FROM ADIPOSE TISSUE DUE TO INCREASED LIPOLYSIS CAUSED BY THE DECREASE IN THE INSULIN/GLUCAGON RATIO THAT ACCOMPANIES STARVATION)

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5
Q

WHAT CHANGE IN THE INSULIN/GLUCAGON RATIO ACCOMPANIES STARVATION?

A

THE RATIO IS DECREASED;

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6
Q

WHAT ARE CHYLOMICRONS?

A

LIPOPROTEINS (CONTAIN TRIGLYCERIDES) WHICH ARE SECRETED INTO THE LYMPHATIC SYSTEM OF THE SMALL INTESTINE

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7
Q

WHICH ENZYME HYDROLYSES THE TRIGLYCERIDES WITHIN CHYLOMICRONS (I.E. DEGRADES CIRCULATING TRIGLYCERIDES IN THE BLOODSTREAM)?

A

LIPOPROTEIN LIPASE

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8
Q

WHAT CAN HAPPEN WITH FATTY ACIDS ONCE THEY ARE RELEASED FROM THE TRIGLYCERIDES BY THE LIPOPROTEIN LIPASE?

A

A) THEY CAN BE USED FOR OXIDATION AND ATP FORMATION

B) THEY CAN BE USED IN ADIPOSE TISSUE FOR THE RE-SYNTHESIS AND STORAGE OF TRIGLYCERIDES

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9
Q

WHAT IS THE PRODUCT OF FATTY ACID OXIDATION IN THE MITOCHONDRIA?

A

ACETYL CoA

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10
Q

WHAT HAPPENS TO REMNANTS OF CHYLOMICRONS ONCE THE LIPOPROTEIN LIPASE HAS RELEASED FATTY ACIDS?

A

THEY ARE CLEARED BY THE LIVER AND THE TRIGLYCERIDES LEFT IN THEM ARE USED TO GENERATE FATTY ACIDS WITHIN THE LIVER AND RE-EXPORT THEM IN LIVER’S OWN VERSION; VLDL

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11
Q

WHAT DOES THE LIVER SYTNHESISE USING REMNANTS OF CHYLOMICRONS AND THE TRIGLYCERIDES THAT REMAINED IN THEM?

A

VLDL (VERY LOW DENSITY LIPOPROTEIN)

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12
Q

GIVEN THAT FATTY ACIDS ARE HYDROPHOBIC AND INSOLUBLE IN THE BLOOD PLASMA, THEY NEED TO BE BOUND BY A CARRIER PROTEIN. WHAT IS THE NAME OF THAT PROTEIN?

A

ALBUMIN

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13
Q

ARE FATTY ACIDS SOLUBLE IN BLOOD PLASMA?

A

NO

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14
Q

HOW ARE CHYLOMICRONS AND VLDL HELPFUL TO ALBUMIN?

A

CAPACITY OF ALBUMIN TO BIND FATTY ACIDS IS LIMITED SO ITS USEFUL TO HAVE THOSE LIPOPROTEINS AS LIPID CARRIERS BETWEEN TISSUES

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15
Q

WHAT IS THE STRUCTURE OF A LIPOPROTEIN MOLECULE?

A

THE HYDROPHOBIC CORE OF THE MOLECULE (E.G. TRIGLYCERIDES, CHOLESTEROL ESTERS) IS SHELTERED BY A SHELL OF POLAR, WATER-COMPATIBLE MOLECULES (E.G. PHOSPHOLIPIDS AND CHOLESTEROL)

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16
Q

WHAT DOES THE TERM ‘APOPROTEIN’ REFER TO?

A

THE PROTEIN PORTION OF A MOLECULE OR COMPLEX CONSISTING OF A PROTEIN MOLECULE JOINED TO A NONPROTEIN MOLECULE OR MOLECULES

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17
Q

WHICH APOPROTEIN DO CHYLOMICRONS AND VLDL CONTAIN AND WHAT DOES IT DO?

A

APOB; IT WRAPS ITSELF AROUND LIPID COMPONENTS OF THOSE LIPOPROTEINS AND ‘STITCHES’ THEM TOGETHER

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18
Q

WHERE DOES PROTEOLYSIS MOSTLY OCCUR?

A

IN MUSCLES

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19
Q

WHY IS HDL CONSIDERED THE ‘GOOD’ CHOLESTEROL CONTAINING PARTICLE?

A

BECAUSE IT TAKES CHOLESTEROL FROM TISSUES AND RETURNS IT TO THE LIVER, WHERE IT CAN BE EXCRETED IN BILE

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20
Q

GLUCOSE CAN BE SYNTHESIZED FROM FATTY ACIDS OR LIPIDS CAN BE SYNTHESIZED FROM GLUCOSE, WHICH ONE IS TRUE?

A

LIPIDS CAN BE SYNTHESIZED FROM GLUCOSE

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21
Q

DO THE SYNTHESIS AND OXIDATION OF FATTY ACIDS OCCUR SIMULTANEOUSLY? HOW IS THIS REGULATED?

A

THEY DO NOT OCCUR SIMULTANEOUSLY
THIS IS ACHIEVED THROUGH THE FIRST METABOLITE IN THE FATTY ACID SYNTHESIS (MALONYL-CoA) ACTING INHIBITORY TOWARDS THE FIRST ENZYME THAT ALLOWS FATTY ACIDS INTO THE MITOCHONDRIA WHERE THEY ARE OXIDIZED (CPT1 ENZYME)

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22
Q

WHICH METABOLITE FORMED FROM GLUCOSE IS USED TO SYNTHESISE FATTY ACIDS?

A

ACETYL-CoA

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23
Q

WHERE IN THE CELL DOES THE SYNTHESIS OF FATTY ACIDS OCCUR?

A

IN THE CYTOPLASM

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24
Q

WHERE DOES BETA OXIDATION OCCUR?

A

IN THE MITOCHONDRIAL MATRIX

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25
Q

WHAT IS THE NAME OF THE FIRST ENZYME THAT NEEDS TO ALLOW FATTY ACIDS TO ENTER THE MITOCHONDRIA FOR THEIR OXIDATION?

A

CARNITINE PALMITOYLTRANSFERASE (CPT1)

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26
Q

WHAT IS THE 1ST METABOLITE IN THE FATTY ACIDS SYNTHESIS PATHWAY?

A

MALONYL-CoA

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27
Q

WHAT IS STEATOSIS?

A

ABNORMALLY HIGH BUILD UP OF FAT IN THE LIVER

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28
Q

WHAT IS THE PURPOSE IN INCREASED LIPOLYSIS IN WHITE ADIPOSE TISSUE DURING STARVATION?

A
  • RELEASE OF FATTY ACIDS THAT WILL BE USED BY MUSCLES IN PREFERENCE TO GLUCOSE
  • PROVIDING FATTY ACIDS FOR OXIDATION WITHIN LIVER TO FORM KETONE BODIES WHICH THE BRAIN WILL BE ABLE TO USE
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29
Q

WHAT IS MALONYL-CoA MADE FROM?

A

GLUCOSE

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30
Q

HOW DOES GLUCOSE UTILIZATION INHIBIT FATTY ACID OXIDATION IN THE FED STATE?

A

BECAUSE GLUCOSE UTILIZATION LEADS TO RAISE IN MALONYL-CoA (WHICH IS MADE FROM GLUCOSE). MALONYL-CoA IS THE FIRST METABOLITE OF FATTY ACID SYNTHESIS AND A POTENT INHIBITOR OF CPT1 ENZYME, WHICH IS CRUCIAL FOR TRANSFER OF FATTY ACIDS INTO MITOCHONDRIAL MATRIX WHERE THEY WOULD BE OXIIDIZED. GIVEN THAT CPT1 IS BLOCKED, FATTY ACIDS CANNOT BE OXIDIZED UNNECESSARILY

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31
Q

HOW DO FATTY ACIDS INHIBIT GLUCOSE UTILIZATION IN E.G. MUSCLE DURING STARVATION (I.E. WHEN THEY BECOME THE MAIN SOURCE OF ENERGY)?

A
  • THE HIGH RATE OF FATTY ACID OXIDATION RAISES ACETYL-CoA LEVELS AND INHIBITS PYRUVATE DEHYDROGENASE; THUS STOPPING PYRUVATE FROM BEING OXIDIZED (SO THE OXIDATION FORMED FROM GLUCOSE IS STOPPED)
  • SOME OF THE CITRATE PRODUCED FROM ACETYL-CoA (WHICH IS MOSTLY USED FOR ATP SYNTHESIS) WILL BE RELEASED INTO THE CYTOSOL WHERE IT WIL INHIBIT THE SECOND REACTION OF GLYCOLYSIS CATALYZED BY PHOSPHOFRUCTOKINASE 1 (PFK1)
32
Q

WHAT HAPPENS TO INSULIN CONCENTRATION DURING FASTING?

A

THEY ARE DECREASED

33
Q

WHAT ARE SOME OF THE MECHANISMS THAT ENSURE THAT COMPETITION BETWEEN GLUCOSE AND FATTY ACID UTILIZATION BY MUSCLE IS MINIMISED?

A
  • HIGH RATES OF GLUCOSE LEAD TO PRODUCTION OF MALONYL-CoA WHICH IS RELATED TO LIPOGENESIS AND INHIBITS FATTY ACIDS OXIDATION
  • WHEN GLUCOSE LEVELS ARE LOW AND FATTY ACIDS OXIDIZED AT HIGH RATES, THE ACETLY-CoA WHICH IS PRODUCED INHIBITS PYRUVATE-HYDROGENASE SO THE PYRUVATE GOTTEN FROM GLYCOLYSIS CANNOT BE OXIDIZED
  • CITRATE THAT IS PRODUCED FROM ACETYL-CoA IS PARTIALLY RELEASED IN THE CYTOSOL WHERE IT WILL BLOCK THE PFK1 ENZYME AND BLOCK THE 2ND STEP OF GLYCOLYSIS
34
Q

WHAT ARE THE GLUCAGON LEVELS LIKE DURING FASTING?

A

HIGH

35
Q

WHAT ARE THE SUBSTRATES FOR GLUCONEOGENESIS AND WHERE DO THEY COME FROM?

A

GLYCEROL; ADIPOSE TISSUE

AMINO ACIDS AND LACTATE; MUSCLE

36
Q

WHEN ARE THE AMINO ACIDS FORMED IN MUSCLE?

A

FOLLOWING THE LOSS OF ANTI-PROTEOLYTIC ACTION OF INSULIN

37
Q

WHICH STEPS IN GLYCOLYSIS NEED TO BE BYPASSED WHEN THE LIVER IS TRYING TO CREATE GLUCOSE? (THEY CANNOT BE REVERSED BECAUSE THEY HAVE HIGH ENERGY CHANGES ASSOCIATED WITH THEM)

A
  • GLUCOSE TO G-6-P (CATALYSED BY HEXOKINASE)
  • FRUCTOSE-6-P TO FRUCTOSE-1,6-bP (PHOSPHOFRUCTOKINASE 1)
  • PEP TO PYRUVATE (PYRUVATE KINASE)
38
Q

WHAT IS GLUCOKINASE?

A

A TYPE OF HEXOKINASE EXPRESSED IN HEPATOCYTES

39
Q

WHICH ENZYME IS USED TO BYPASS THE FUNCTION OF GLUCOKINASE (HEXOKINASE) DURING GLUCONEOGENESIS?

A

GLUCOSE-6-PHOSPHATASE

40
Q

WHERE IN THE CELL IS GLUCOKINASE EXPRESSED AND WHERE IS GLUCOSE-6-PHOSPHATASE EXPRESSED?

A

1) CYTOSOL

2) ENDOPLASMIC RETICULUM

41
Q

WHICH FORM DO FATTY ACIDS NEED TO BE IN TO ENTER THE MITOCHONDRIA AND WHICH ENZYME FACILITATES THIS?

A

ACYLCARNITINE ESTERS, CPT1

42
Q

WHICH ENZYME IS USED TO REVERSE THE STEP IN GLYCOLYSIS CATALYSED BY PFK1?

A

FRUCTOSE 1,6-BIPHOSPHATASE (FbPase)

43
Q

WHAT EFFECTS DOES THE METABOLITE FRUCTOSE-2,6-BISPHOSPHATE (F2,6bP) HAS ON ENZYMES PFK1 AND F16bPASE?

A 
ACTIVATES PFK1 (AND GLYCOLYSIS)
INHIBITS F16bPase (AND GLUCONEOGENESIS)
44
Q

HOW IS F2,6bP FORMED?

A

FROM F-6-PHOSPHATE THROUGH PFK2

45
Q

PFK2 IS REGULATED BY WHICH HORMONE?

A

GLUCAGON

46
Q

HOW MANY CARBONS DOES PYRUVATE HAVE?

A

3

47
Q

WHICH HORMONE INHIBITS THE ENZYME PYRUVATE KINASE (I.E. STOPS CONVERSION OF PEP TO PYRUVATE)?

A

GLUCAGON

48
Q

ENZYME RESPONSIBLE FOR PEP TO PYRUVATE CONVERSION?

A

PYRUVATE KINASE

49
Q

WHAT DOES INSULIN DO TO ACETYL CoA CARBOXYLASE, MALONYL CoA LEVELS AND PFK2 AND WHICH EFFECTS DOES THIS HAVE?

A
  • ACTIVATES ACETLY CoA CARBOXYLASE
  • INCREASES MALONYL CoA LEVELS (INHIBITS FATTY ACIDS OXIDATION REQUIRED TO SUPPORT GLUCONEOGENESIS)
  • ACTIVATES PFK2 (WHICH INCREASES F2,6bP LEVELS, ACTIVATES GLYCOLYSIS AND INHIBITS GLUCONEOGENESIS)
50
Q

ROLE OF ACETYL CoA CARBOXYLASE:

A

COVERTING ACETLY CoA TO MALONYL CoA

51
Q

WHERE CAN KETO BODY FORMATION OCCUR?

A

MAINLY IN THE LIVER + MINOR EXTENT IN THE KIDNEY

52
Q

HOW LONG ARE THE LONG CHAIN FATTY ACIDS?

A

MORE THAN 14 CARBON ATOMS

53
Q

TWO MOST COMMON LONG CHAIN FATTY ACIDS AND THEIR NUMBER OF CARBONS?

A

PALMITIC, 16C

OLEATE, 18 C

54
Q

WHICH TRANSPORTER IS INVOLVED WITH FATTY ACID ENTRY INTO THE CELL?

A

CD 36 (cluster of differentiation 36)

55
Q

FATTY ACIDS ARE LET INTO CELLS BY CD 36,
THEN THEY ARE CONVERTED TO CoA ESTERS AND THEN TO ACYLCARNITINE ESTERS BY CPT1 TO BE ABLE TO CROSS THE MITOCHONDRIAL MEMBRANE.
THEN THEY NEED TO BE CONVERTED BACK TO ACYL CoABEFORE SERVING AS SUBSTRATES FOR BETA OXIDATION? WHICH ENZYME IS RESPONSIBLE FOR THIS LAST CONVERSION?

A

CPT2

56
Q

WHERE IS CPT2 LOCATED IN THE CELL?

A

INNER MITOCHONDRIAL MEMBRANE FACING THE MATRIX

57
Q

HOW MANY CARBON ATOMS ARE SPLIT OFF THE FATTY ACID CHAIN AT EACH TURN OF BETA OXIDATION CYCLE TO GIVE RISE TO 1 ACETYL CoA?

A

2

58
Q

WHAT IS GENERATED DURING BETA OXIDATION EXCEPT FOR ACETYL CoA?

A

FADH2 AND NADH

59
Q

ATP PRODUCED THROUGH BETA OXIDATION IS USED TO SUPPORT WHICH REACTION?

A

GLUCONEOGENESIS

60
Q

HOW ARE THE HIGH ENERGY ELECTRON CARRIERS WHICH ARE OXIDIZED IN THE ELECTRON TRANSPORTER CHAIN TO CREATE ATP CREATED THROUGH BETA OXIDATION?

A

BREAKDOWN OF FATTY ACIDS INTO 2 CARBON SEGMENTS CREATING ACETYL CoA GENERATES FADH2 AND NADH AT EVERY TURN OF THE CYCLE
+ THE ACETYL CoA THAT IS PRODUCED CAN GO THROUGH THE CITRIC ACID CYCLE TO PRODUCE MORE OF THE FADH2 AND NADH

61
Q

DO BETA OXIDATION AND GLUCONEOGENESIS OCCUR AT THE SAME TIME?

A

YES, BOTH STIMULATED BY GLUCAGON, BETA OXIDATION CONTINUOUSLY PRODUCES ENERGY NEEDED TO DRIVE GLUCONEOGENESIS

62
Q

ARE KETONE BODIES WATER OR FAT SOLUBLE?

A

WATER SOLUBLE

63
Q

WHICH ORGANS APART FROM THE BRAIN CAN USE KETONE BODIES?

A

SKELETAL MUSCLE AND HEART

64
Q

CAN LIVER USED KETONE BODIES?

A

NO

65
Q

WHAT IS DEAMINATION?

A

SAFE REMOVAL OF AMINO GROUP FROM (NITROGEN ATOM) FROM THE AMINO ACID SO THE CARBON SKELETON CAN BE USED FOR GLUCONEOGENESIS OF KETOGENESIS

66
Q

CAN AMINO ACIDS BE METABOLISED TO ANYTHING APART FROM GLUCOSE?

A

ACETLY CoA (CONTRIBUTE TOWARDS KETOGENESIS)

67
Q

APART FROM STARVATION WHEN INSULIN IS DECREASED, IN WHICH SITUATIONS CAN PROTEOLYSIS BE INCREASED?

A

WHEN INSULIN COUNTER-REGULATORY HORMONES ARE INCREASED IN CASE OF E.G. STRESS OR TRAUMA AND WITH HEAVY EXERCISE AND MUSCLE INJURY

68
Q

IN WHICH FORM IS NITROGEN EXCRETED IN MAMMALS?

A

AS UREA

69
Q

2 MOST COMMONLY USED KETOACIDS IN STARVATION?

A

PYRUVATE WHICH GIVER RISE TO ALANINE WHICH CAN DIRECTLY BE USED IN THE LIVER FOR GLUCONEOGENESIS
ALPHA-KETOGLUTARATE WHICH GIVES RISE TO GLUTAMATE (ALPHA-KETOG. IS AN INTERMEDIATE OF THE TCA CYCLE)

70
Q

WHICH ORGAN IS THE MAJOR SITE OF UREAGENESIS?

A

THE LIVER

71
Q

GLUTAMATE IS CONVERTED TO GLUTAMINE WHERE?

A

IN THE MUSCLE

72
Q

HOW MANY BRANCHED CHAIN AMINO ACIDS ARE THERE AND WHAT ARE THEIR NAMES?

A

3; LEUCINE, ISOLEUCINE, VALINE

73
Q

WHAT DOES IT MEAN IF AN AMINO ACID IS KETOGENIC VS GLUCOGENIC?

A

KETOGENIC; GIVES RISE TO ACETYL CoA

GLUCOGENIS; GIVES RISE TO INTERMEDIATES OF THE TCA

74
Q

WHAT IS THE MAIN AIM OF STARVATION METABOLISM?

A

RETAINING BRAIN FUNCTION IN THE FACE OF A COMPLETE CESSATION OF GLUCOSE INPUT FROM THE DIET

75
Q

DOES STARVATION METABOLISM HAS CATABOLIC OR ANABOLIC PROFILE?

A

CATABOLIC

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