L33+34: Nutrient Utilization Flashcards
what are the 3 phases of fuel metabolism
- absorptive phase: active digestion, abs from gut
- postabsorptive phase: between meals, no nutrient abs
- prolonged energy deficiency/food deprivation
during the absorptive phase (Phase I) what is the origina of blood glucose and what tissue is using it
exogenous, all tissues
during the post-absorptive phase what is the origin of blood glucose and what tissues are using it
heptic glycogen and gluconeogenesis
all tissu except liver
during the prolonged energy deficiency phase (phase III/IV), what is the source of blood glucose and what tissues utilize it
hepatic and renal gluconeogenesis
used by brain and RBCs
at what stage are ketone bodies primarily being used to fuel the brain
prolonged energy deficiency (final / 4th stage)
what does the brain almost exclusively use as its fuel source
glucose
during the absorptive phase, what 3 metabolic fuels are channeled and to what deposit sites
glucose - liver
amino acids - liver
TG/FA - liver, adipose tissue
what is the substrate for the krebs cycle
acetate
energy is released from the krebs cycle in the form of ?
ATP
where is glucose stored and in what form
in liver and muscles as glycogen during the absorptive phase
what is the first step in processing of glucose
glycolysis
what is the activation process of glycogen during the post-absorptive phase
glycogenolysis
excess glucose can be converted into ______ in the ______
FAs, liver
T/F: many amino acids are removed from circulation on first pass through the liver
T
amino acids get deaminated, this produces ____ and ______
keto-analogues and urea
what is the major source of blood urea
the liver
the liver selectivley removes ____ which can be used for hepatic _____ and _______ synthesis or for liver metabolism
amino acids
hepatic protein
plasma protein synthesis
unlike protein synthesis in the liver which uses serum proteins, protein synthesis in non-hepatic tissue uses ?
free amino acids
what are blood proteins produced by
liver and other organs
most amino acids can be converted to _____ which serves as a substrate for ______ and _______ synthesis
glucose
gluconeogenesis and FA synthesis
when proteins enter the blood as amino acids they become part of the _____ pool
amino acid
what is the storage form of amino acids
muscle protein
when does a net increase in muscle protein occur
when protein synthesis»_space; breakdown
what two pools can amino aicds contribute to
glucose and adipose tissue pools
what are the 3 fates of keto-analogues after liver deamination
- metabolized
- enter gluconeogenesis/glycogenesis
- enter FA synthesis
in what form are FAs stored
as trigylcerides
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
lipid pools contain what molecules
Free fatty acids (aka non-esterified) and glycerol
why do FAs require special transport vehicles
b/c they aren’t water soluble
during the absorptive phase of fuel metabolism, triglycerides are transporter to the _____ and _____
liver and fat depots
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
what are very low density lipoproteins (VLDL)
triglycerides coated with phospholipids, cholesterol and proteins
what do fat cells release during the post-absorptive phase
glycerol and FFAs
what is the only VFA that is gluconeogenic
proprionate
what can FAs be converted into, what can they NOT be converted into?
can be converted into ketone bodies
NOT pyruvate or oxaloacetate
what organs use ketone bodies as metabolic fuel during prolonged E deficiency
brain and heart muscle
what molecules regulate the transfer or metabolic fuels into pools during the absorptive phase
insulin & glucagon
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
what cells release insulin
pancreatic Beta cells
what stimulates release of insulin by pancreatic beta cells
increased levels of glucose in circulation
what cells secrete glucagon
Alpha cells
what stimulates glucagon secretion
low levels of glucose or high levels of amino acids
the presence of what molecule inhibits the release of glucagon
insulin
when is the inhibiting effect of insulin on glucagon removed
at low glucose levels
how does insulin promote glucose uptake
by increasing the surface exposure of GLUT 4 transporters
what enzyme converts glucose to glucose-6-P
hexokinase
what enzyme converts Glucose-6-P into Glucose-1-P
phosphoglucomutase
what enzyme converts Glucose-1-P into glycogen
Glycogen synthase
how does insulin stimulate glycogen synthesis in the liver
via the de-phosphorylation of glycogensythase (activated) and glycogenphosphatase (deactivation)
how does insulin and glucagon stimulate gluconeogenesis, glycolysis and glycogensynthesis
through the de-phos
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
high AA levels in the diet stimulate the secretion of what 2 molecules
insulin and glucagon
high Glu levels in the diet cause the secretion of ?
insulin
glucagon is stimulated by high levels of _____ and low levels of ____
high AA, low Glucose
what can amino acids be transformed into
- protein
- TGs
- glucose
Glucagon stimulates ______ from amino acids, this prevents ??
gluconeogenesis
hypoglycemia
what molecule stimulates gluconeogenesis
GLUCAGON
T/F: a large portion of amino acids are deaminated on first pass thro liver
T
during the absorptive phase, metabolic fuels are channeled to ____ sites and glucose is utilized to maintain ?
depot sites
maintain metabolism
during the post-absorptive phase, metabolic fuels are mobilized from ?
depots
both a protein rich diet and ______ phase are characterized by low glucose levels; therefore both conditions will stimulate ?
post-absorptive
glucagon
at what fuel metabolism stage is there no current nutrient supply
post-absorptive
during what phase has glucagon been stimulated & insulin secretion inhibited
post-abs
during this phase, the liver switches from glucose utilization to glucose production
post-abs
when the liver needs to produce glucose it first utilizes ____ followed by ____?
short-term stoage - glycogen used first
then gluconeogenesis
During this phase, all tissues are using glucose (even brain), however muscle and fat are using it at a diminished rate
post-abs phase
what are the 3 major metabolic pools
- aa pool
- glucose pool
- glycerol+FA pool
how long does glycogen depot last
8-12 hrs at rest/moderate exercise
30 mins at high demand/severe exercise
what molecule stimulates lipolysis
glucagon and Epi/NE
what molecules stimulate FA release through beta adrenoreceptors (along w/ stimulating lipolysis)
Epi/NE
_____ is released from the heart during exercise and stimulates ______
natriuretic peptide
lipolysis
GH and cortisol reinforce increased _______ during and after prolonged exercise
lipolysis
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
what are NEFAs used for
- E production by many tissues
- synthesis fo ketone bodies and VLDL
what are the forms in which NEFAs can circulate
- as free FAs
- bound to albumin
- packed in VLDLs
NEFAs bind albumin in blood & are transported to what cells
peripheral
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
after absorption into peripheral cells, what is the fate of FAs
beta oxidation and then Krebs
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
when glucose entry into the muscle
the insulin:glucagon ration in the ______ determines the action of antagnoist enzyme pairs
liver
during the post-abs phase, glucagon phosphorylates (deactivates) _______ and _______ while it phosphorylates (activates) _______and __________
Dephosphorylates: glycogensynthase and phosphofructokinase
Phosphorylates: Fructose 1-6 biphosphatase & glycogenphosphorylase
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
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
as glucogen stores run out, fuel oxidations shifts from mainly CHOs towards mainly _______ as an oxidative source
lipids
during prolonged E deficiency, the goal is to preserve ____ and ______ while utilizing _______
preserve AAs and glucose, utilize fat
what are the 3 mechanisms by which the liver makes use of NEFAs
- complete oxidation
- esterification to form TGs
- form ketones
