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PHYSIOLOGY III > L33+34: Nutrient Utilization > Flashcards

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
what are the 3 fates of keto-analogues after liver deamination
* metabolized * enter gluconeogenesis/glycogenesis * enter FA synthesis
26
in what form are FAs stored
as trigylcerides
27
what makes FAs a good storage material compared to carbohydrates or amino acids
they hold twice the caloric value of CH or AA and contain little water weight
28
lipid pools contain what molecules
Free fatty acids (aka non-esterified) and glycerol
29
why do FAs require special transport vehicles
b/c they aren't water soluble
30
during the absorptive phase of fuel metabolism, triglycerides are transporter to the _____ and _____
liver and fat depots
31
what is the fate of trigylcerides/FFAs in the liver
they are repackages FFAs get transported for storage or utilization as very low denstiy lipoproteins
32
what are very low density lipoproteins (VLDL)
triglycerides coated with phospholipids, cholesterol and proteins
33
what do fat cells release during the post-absorptive phase
glycerol and FFAs
34
what is the only VFA that is gluconeogenic
proprionate
35
what **can** FAs be converted into, what can they NOT be converted into?
can be converted into ketone bodies NOT pyruvate or oxaloacetate
36
what organs use ketone bodies as metabolic fuel during prolonged E deficiency
brain and heart muscle
37
what molecules regulate the transfer or metabolic fuels into pools during the absorptive phase
insulin & glucagon
38
how does insulin reduce circulating glucose concentrations
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
what cells release insulin
pancreatic Beta cells
40
what stimulates release of insulin by pancreatic beta cells
increased levels of glucose in circulation
41
what cells secrete glucagon
Alpha cells
42
what stimulates glucagon secretion
low levels of glucose or high levels of amino acids
43
the presence of what molecule inhibits the release of glucagon
insulin
44
when is the inhibiting effect of insulin on glucagon removed
at low glucose levels
45
how does insulin promote glucose uptake
by increasing the surface exposure of GLUT 4 transporters
46
what enzyme converts glucose to glucose-6-P
hexokinase
47
what enzyme converts Glucose-6-P into Glucose-1-P
phosphoglucomutase
48
what enzyme converts Glucose-1-P into glycogen
Glycogen synthase
49
how does insulin stimulate glycogen synthesis in the liver
via the de-phosphorylation of glycogensythase (activated) and glycogenphosphatase (deactivation)
50
how does insulin and glucagon stimulate gluconeogenesis, glycolysis and glycogensynthesis
through the de-phos
51
if there is about equal or less than levels of glucose compared to amino acids, what goes on
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
high AA levels in the diet stimulate the secretion of what 2 molecules
insulin and glucagon
53
high Glu levels in the diet cause the secretion of ?
insulin
54
glucagon is stimulated by high levels of _____ and low levels of ____
high AA, low Glucose
55
what can amino acids be transformed into
* protein * TGs * glucose
56
Glucagon stimulates ______ from amino acids, this prevents ??
gluconeogenesis hypoglycemia
57
what molecule stimulates gluconeogenesis
GLUCAGON
58
T/F: a large portion of amino acids are deaminated on first pass thro liver
T
59
during the absorptive phase, metabolic fuels are channeled to ____ sites and glucose is utilized to maintain ?
depot sites maintain metabolism
60
during the post-absorptive phase, metabolic fuels are mobilized from ?
depots
61
both a protein rich diet and ______ phase are characterized by low glucose levels; therefore both conditions will stimulate ?
post-absorptive glucagon
62
at what fuel metabolism stage is there no current nutrient supply
post-absorptive
63
during what phase has glucagon been stimulated & insulin secretion inhibited
post-abs
64
during this phase, the liver switches from glucose utilization to glucose production
post-abs
65
when the liver needs to produce glucose it first utilizes ____ followed by ____?
short-term stoage - glycogen used first then gluconeogenesis
66
During this phase, all tissues are using glucose (even brain), however muscle and fat are using it at a diminished rate
post-abs phase
67
what are the 3 major metabolic pools
* aa pool * glucose pool * glycerol+FA pool
68
how long does glycogen depot last
8-12 hrs at rest/moderate exercise 30 mins at high demand/severe exercise
69
what molecule stimulates lipolysis
glucagon and Epi/NE
70
what molecules stimulate FA release through beta adrenoreceptors (along w/ stimulating lipolysis)
Epi/NE
71
_____ is released from the heart during exercise and stimulates ______
natriuretic peptide lipolysis
72
GH and cortisol reinforce increased _______ during and after prolonged exercise
lipolysis
73
how are FAs mobilized and released from adipose tissue
* 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
what are NEFAs used for
* E production by many tissues * synthesis fo ketone bodies and VLDL
75
what are the forms in which NEFAs can circulate
* as free FAs * bound to albumin * packed in VLDLs
76
NEFAs bind albumin in blood & are transported to what cells
peripheral
77
what is the FA transporter (aka fatty acid translocase)
CD36, translocated NEFAs into cells CD36 is a membrane protein on the surface of many cell types
78
after absorption into peripheral cells, what is the fate of FAs
beta oxidation and then Krebs
79
when is uptake of FAs and glucose by cardiac and skeletal muscle cells increased
after the translocation of transporter proteins: **GLUT 4** in responose to insulin during the absorptive phase and **CD36** during the postabsorptive phase
80
when glucose entry into the muscle
81
the insulin:glucagon ration in the ______ determines the action of antagnoist enzyme pairs
liver
82
during the post-abs phase, glucagon **phosphorylates (deactivates)** _______ and _______ while it **phosphorylates (activates)** _______and __________
Dephosphorylates: glycogensynthase and phosphofructokinase Phosphorylates: Fructose 1-6 biphosphatase & glycogenphosphorylase
83
without food for 24 hours the body enters into a state of ?
ketosis all glycogen stores have been exhausted and some organs are starting to use FAs for E
84
why can't the brain use FAs and what does the brain use then for E once glycogen stores are depleted
FAs are too large brain has to use ketone bodies which can pass the BBB
85
as glucogen stores run out, fuel oxidations shifts from mainly CHOs towards mainly _______ as an oxidative source
lipids
86
during prolonged E deficiency, the goal is to preserve ____ and ______ while utilizing _______
preserve AAs and glucose, utilize fat
87
what are the 3 mechanisms by which the liver makes use of NEFAs
* complete oxidation * esterification to form TGs * form ketones

PHYSIOLOGY III (31 decks)

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