L33+34: Nutrient Utilization Flashcards

1
Q

what are the 3 phases of fuel metabolism

A
  • absorptive phase: active digestion, abs from gut
  • postabsorptive phase: between meals, no nutrient abs
  • prolonged energy deficiency/food deprivation
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2
Q

during the absorptive phase (Phase I) what is the origina of blood glucose and what tissue is using it

A

exogenous, all tissues

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3
Q

during the post-absorptive phase what is the origin of blood glucose and what tissues are using it

A

heptic glycogen and gluconeogenesis
all tissu except liver

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4
Q

during the prolonged energy deficiency phase (phase III/IV), what is the source of blood glucose and what tissues utilize it

A

hepatic and renal gluconeogenesis
used by brain and RBCs

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5
Q

at what stage are ketone bodies primarily being used to fuel the brain

A

prolonged energy deficiency (final / 4th stage)

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6
Q

what does the brain almost exclusively use as its fuel source

A

glucose

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7
Q

during the absorptive phase, what 3 metabolic fuels are channeled and to what deposit sites

A

glucose - liver
amino acids - liver
TG/FA - liver, adipose tissue

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8
Q

what is the substrate for the krebs cycle

A

acetate

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9
Q

energy is released from the krebs cycle in the form of ?

A

ATP

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10
Q

where is glucose stored and in what form

A

in liver and muscles as glycogen during the absorptive phase

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11
Q

what is the first step in processing of glucose

A

glycolysis

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12
Q

what is the activation process of glycogen during the post-absorptive phase

A

glycogenolysis

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13
Q

excess glucose can be converted into ______ in the ______

A

FAs, liver

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14
Q

T/F: many amino acids are removed from circulation on first pass through the liver

A

T

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15
Q

amino acids get deaminated, this produces ____ and ______

A

keto-analogues and urea

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16
Q

what is the major source of blood urea

A

the liver

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17
Q

the liver selectivley removes ____ which can be used for hepatic _____ and _______ synthesis or for liver metabolism

A

amino acids
hepatic protein
plasma protein synthesis

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18
Q

unlike protein synthesis in the liver which uses serum proteins, protein synthesis in non-hepatic tissue uses ?

A

free amino acids

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19
Q

what are blood proteins produced by

A

liver and other organs

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20
Q

most amino acids can be converted to _____ which serves as a substrate for ______ and _______ synthesis

A

glucose
gluconeogenesis and FA synthesis

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21
Q

when proteins enter the blood as amino acids they become part of the _____ pool

A

amino acid

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22
Q

what is the storage form of amino acids

A

muscle protein

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23
Q

when does a net increase in muscle protein occur

A

when protein synthesis&raquo_space; breakdown

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24
Q

what two pools can amino aicds contribute to

A

glucose and adipose tissue pools

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25
Q

what are the 3 fates of keto-analogues after liver deamination

A
  • metabolized
  • enter gluconeogenesis/glycogenesis
  • enter FA synthesis
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26
Q

in what form are FAs stored

A

as trigylcerides

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27
Q

what makes FAs a good storage material compared to carbohydrates or amino acids

A

they hold twice the caloric value of CH or AA and contain little water weight

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28
Q

lipid pools contain what molecules

A

Free fatty acids (aka non-esterified) and glycerol

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29
Q

why do FAs require special transport vehicles

A

b/c they aren’t water soluble

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30
Q

during the absorptive phase of fuel metabolism, triglycerides are transporter to the _____ and _____

A

liver and fat depots

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31
Q

what is the fate of trigylcerides/FFAs in the liver

A

they are repackages
FFAs get transported for storage or utilization as very low denstiy lipoproteins

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32
Q

what are very low density lipoproteins (VLDL)

A

triglycerides coated with phospholipids, cholesterol and proteins

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33
Q

what do fat cells release during the post-absorptive phase

A

glycerol and FFAs

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34
Q

what is the only VFA that is gluconeogenic

A

proprionate

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35
Q

what can FAs be converted into, what can they NOT be converted into?

A

can be converted into ketone bodies
NOT pyruvate or oxaloacetate

36
Q

what organs use ketone bodies as metabolic fuel during prolonged E deficiency

A

brain and heart muscle

37
Q

what molecules regulate the transfer or metabolic fuels into pools during the absorptive phase

A

insulin & glucagon

38
Q

how does insulin reduce circulating glucose concentrations

A

by stimulating …
* Glu uptake in liver + other tissues
* glycogen synthesis in muscle and liver
* FA synthesis in liver and adipose tissue
* protein synthesis in liver and muscle

39
Q

what cells release insulin

A

pancreatic Beta cells

40
Q

what stimulates release of insulin by pancreatic beta cells

A

increased levels of glucose in circulation

41
Q

what cells secrete glucagon

A

Alpha cells

42
Q

what stimulates glucagon secretion

A

low levels of glucose or high levels of amino acids

43
Q

the presence of what molecule inhibits the release of glucagon

A

insulin

44
Q

when is the inhibiting effect of insulin on glucagon removed

A

at low glucose levels

45
Q

how does insulin promote glucose uptake

A

by increasing the surface exposure of GLUT 4 transporters

46
Q

what enzyme converts glucose to glucose-6-P

A

hexokinase

47
Q

what enzyme converts Glucose-6-P into Glucose-1-P

A

phosphoglucomutase

48
Q

what enzyme converts Glucose-1-P into glycogen

A

Glycogen synthase

49
Q

how does insulin stimulate glycogen synthesis in the liver

A

via the de-phosphorylation of glycogensythase (activated) and glycogenphosphatase (deactivation)

50
Q

how does insulin and glucagon stimulate gluconeogenesis, glycolysis and glycogensynthesis

A

through the de-phos

51
Q

if there is about equal or less than levels of glucose compared to amino acids, what goes on

A

blood glu levels rise only moderately as AA levels rise

glu stimulates beta cells, high AAs stimulates both insulin and glucagon secretion

synthesis of large molecules (glycogens, proteins, TGs) is only moderately stimulated

in the absence of exogenous glucose, AA metabolism contributes to keeping blood glu levels steady

52
Q

high AA levels in the diet stimulate the secretion of what 2 molecules

A

insulin and glucagon

53
Q

high Glu levels in the diet cause the secretion of ?

A

insulin

54
Q

glucagon is stimulated by high levels of _____ and low levels of ____

A

high AA, low Glucose

55
Q

what can amino acids be transformed into

A
  • protein
  • TGs
  • glucose
56
Q

Glucagon stimulates ______ from amino acids, this prevents ??

A

gluconeogenesis
hypoglycemia

57
Q

what molecule stimulates gluconeogenesis

A

GLUCAGON

58
Q

T/F: a large portion of amino acids are deaminated on first pass thro liver

A

T

59
Q

during the absorptive phase, metabolic fuels are channeled to ____ sites and glucose is utilized to maintain ?

A

depot sites
maintain metabolism

60
Q

during the post-absorptive phase, metabolic fuels are mobilized from ?

A

depots

61
Q

both a protein rich diet and ______ phase are characterized by low glucose levels; therefore both conditions will stimulate ?

A

post-absorptive
glucagon

62
Q

at what fuel metabolism stage is there no current nutrient supply

A

post-absorptive

63
Q

during what phase has glucagon been stimulated & insulin secretion inhibited

A

post-abs

64
Q

during this phase, the liver switches from glucose utilization to glucose production

A

post-abs

65
Q

when the liver needs to produce glucose it first utilizes ____ followed by ____?

A

short-term stoage - glycogen used first
then gluconeogenesis

66
Q

During this phase, all tissues are using glucose (even brain), however muscle and fat are using it at a diminished rate

A

post-abs phase

67
Q

what are the 3 major metabolic pools

A
  • aa pool
  • glucose pool
  • glycerol+FA pool
68
Q

how long does glycogen depot last

A

8-12 hrs at rest/moderate exercise
30 mins at high demand/severe exercise

69
Q

what molecule stimulates lipolysis

A

glucagon and Epi/NE

70
Q

what molecules stimulate FA release through beta adrenoreceptors (along w/ stimulating lipolysis)

A

Epi/NE

71
Q

_____ is released from the heart during exercise and stimulates ______

A

natriuretic peptide
lipolysis

72
Q

GH and cortisol reinforce increased _______ during and after prolonged exercise

A

lipolysis

73
Q

how are FAs mobilized and released from adipose tissue

A
  • Hormone sensitive lipase (HSL) - activated by Epi/NE
  • NEFAs are transported as FFAs or bound to albumin in a VLDL and get taken up by skeletal muscle and liver
74
Q

what are NEFAs used for

A
  • E production by many tissues
  • synthesis fo ketone bodies and VLDL
75
Q

what are the forms in which NEFAs can circulate

A
  • as free FAs
  • bound to albumin
  • packed in VLDLs
76
Q

NEFAs bind albumin in blood & are transported to what cells

A

peripheral

77
Q

what is the FA transporter (aka fatty acid translocase)

A

CD36, translocated NEFAs into cells
CD36 is a membrane protein on the surface of many cell types

78
Q

after absorption into peripheral cells, what is the fate of FAs

A

beta oxidation and then Krebs

79
Q

when is uptake of FAs and glucose by cardiac and skeletal muscle cells increased

A

after the translocation of transporter proteins: GLUT 4 in responose to insulin during the absorptive phase and CD36 during the postabsorptive phase

80
Q

when glucose entry into the muscle

A
81
Q

the insulin:glucagon ration in the ______ determines the action of antagnoist enzyme pairs

A

liver

82
Q

during the post-abs phase, glucagon phosphorylates (deactivates) _______ and _______ while it phosphorylates (activates) _______and __________

A

Dephosphorylates: glycogensynthase and phosphofructokinase
Phosphorylates: Fructose 1-6 biphosphatase & glycogenphosphorylase

83
Q

without food for 24 hours the body enters into a state of ?

A

ketosis
all glycogen stores have been exhausted and some organs are starting to use FAs for E

84
Q

why can’t the brain use FAs and what does the brain use then for E once glycogen stores are depleted

A

FAs are too large
brain has to use ketone bodies which can pass the BBB

85
Q

as glucogen stores run out, fuel oxidations shifts from mainly CHOs towards mainly _______ as an oxidative source

A

lipids

86
Q

during prolonged E deficiency, the goal is to preserve ____ and ______ while utilizing _______

A

preserve AAs and glucose, utilize fat

87
Q

what are the 3 mechanisms by which the liver makes use of NEFAs

A
  • complete oxidation
  • esterification to form TGs
  • form ketones