export_endocrine 1 Flashcards
Macromolecules
1) proteins (AAs)
2) carbs (glucose)
3) fats (lipids)
where does energy from food go?
heat loss
1) food assimilation (5-10%)
2) biochemical inefficiency (50%)
3) conversion to high energy bonds (basal metabolic) (20-40%)
4) external work (5-25%)
anabolic state
- digestion/absorption
- some for immediate needs
-rest stores until postabsorptive state (~4 hours after meal)
energy conversion
- chemical (food) to kinetic (exercise)
- between chemical (AA to glucose)
-heat lost in conversions
fxns of carbs
- energy (4kcal/g)
- required by brain, nerves, RBCs
what happens to carbs (glucose?)
- stored as fat/glycogen
- 1/4-1/3 in liver glycogen
- 1/3-1/2 muscle glycogen
- large portion to FA synthesis (later in day)
glucose storage trail…
GI–>liver–>
1) glycogen
2) a-glycerol phosphate
3) FAs
2-3–> triglycerides–>VLDL–>adipose tissue
glucose goes to 4 places…
1) use as energy (brain)
2) liver
3) adipose (–>a-glycerol phosphate or FAs–>triglycerides)
4) muscle (glycogen)
what metabolizes glucose?
glucokinase
products of glucose
1) glycogen
2) a-glycerol phosphate
3) FAs
4) non-essential AAs
5) nucleic acids
6) energy
what absorbs nutrients and brings them to the liver?
portal vein
how does glucose enter adipose tissue?
via insulin responsive glucose transporter (GLUT4)
insulin after meal
increases with glucose
fructose pathway
liver –> a-gp –> triglycerol –> VLDL
fxns of fat
1) energy (~85% of stored)
2) structure of cell membrane
3) temp regulation
4) signaling molecules
essential FAs and fxns
linolenic and linoleic
-formation of healthy cells
- development of brain and NS
- hormone like substances (BP, immune, etc)
storage of lipids..
GI–> chylomicrons –> adipose tissue –> monoglyceride/FAs –> trigyceride
what breaks down lipids?
bile salts
where do chylomicrons go?
lymphatic system
-hydrolyzed by lipases in adipose and skeletal muscle
how do lipids get to the liver?
from FAs from lipolysis in adipose tissue
what does the liver do with FAs?
packaged into VLDLs then reexported
low insulin and lipids in liver…
ketone bodies from incomplete FA oxidation
what happens to FA in adipose tissue?
FA reesterified into triglycerides
fxns of AAs
- 15% stored energy
- structural component of proteins
- precursors neurotransmitters
- urea from amine groups
nonessential AAs
derived de novo from carbs
important essential AAs for nutrient signaling
- valine
- luecine
-isoluecine
all branching
destinations of AAs (and path):
1 ) liver –> a-ketoacids –> CO2+H20+energy or FAs
2) liver –> NH3 –> urea
3) muscle –>proteins
anabolism
keeping AA for TCA cycle to build on
digestions of proteins:
breakdown by pancreatic proteases into AAs or dipeptides
-transported by specific AA transporters
what can be done with AA in the liver?
- oxidation for gluconeogenesis
- deamination to keto acids (enter TCA and moved to FAs)
-detox to urea
what do muscles use for gluconeogenesis?
AAs
problems during postabsorptive state
1) no new glucose
2) plasma glucose must be stable (60-80 when waking up)
compensation methods in postabsorptive state
1) produce glucose from stores (gluconeogenesis and glycogenolysis)
2) sparing glucose by use of fat for energy
gluconeogenesis
- done in liver, kidney, and intestines
- TAG metabolism releases glycerol –> glucose
- muscle catabolized to AAs
- ala and glu primary AAs that enter pathway directly
hormones that control gluconeogenesis
1) glucagon (inc glucose production)
2) epinephrine (inc “)
3) cortisol (in “)
4) insulin (dec “)
can fats be made into glucose?
NO
-only used as energy as keytone bodies
glycogenolysis
glycogen released from liver as glucose
-or glycogen from muscle through Cori cycle
how does glycogen from muscle turn into glucose (Cori cycle)?
glycogen –> G-6-P –> glycolysis in blood–> pyruvate and lactate –> liver –> gluconeogenesis –> glucose
why store energy as lipids?
1) more energy dense
2) doesn’t need to store with water
3) spares glucose for neurons
can neurons use FAs?
NO
lyposysis
glucose sparing but doesn’t contribute to glucose
how does liver prep for a fast?
FAs –> oxidized –> Acetyl CoA –> ketones
anabolic steriods
insulin, sex steriods, GH, thyroxine
catabolic steroids
glucagon, epinephrine, glucocoricoids, GH, thyroxine
what controls fast/fed state?
insulin
main effects of insulin?
inc glucose oxidation and fat, glycogen, protein synthesis
inc levels of glucagon affect
inc glycogenolysis, gluconeogenesis, ketogenesis
cortisol
turns on PEPCK, necessary for liver to do gluconeogenesis
where is insulin and glucagon released from?
pancreas
B-cell- insulin
a-cell- glucagon
insulin/glucagon in high/low glucose environment?
high- inc insulin, dec glucagon
lox- dec insulin, inc glucagon
when insulin levels are high where does glucose go?
- inc uptake to adipocytes and muscle
- liver stops producing de novo
-liver uptakes
hormones released from GI to pancreas?
- GLP-1 (enhance insulin sec) (from bile)
- GIP
3 types of signals from GI to pancreas
1) hormones
2) neural
3) nutrients
what is GLUT4 translocation?
inc insulin, moves GLUT4 to cell surface, inc intake of glucose into cells
absorptive state overview
- inc insulin
- cell uptake of glucose
- glycogen storage in liver and muscles
- trigly storage in adipose
- uptake of AA and protein synth
post absorptive state overview
- glucagon inc
- stim glycogenolysis in liver (G6P)
- muscle, <3, liver, kidneys use FA and major fuel source
- stim lipolysis and ketogenesis
how much energy for muscles comes from FA metabolism?
85%
effects of glucagon in liver
- inc glycogenolysis
- inc gluconeogenesis
-inc ketogenesis
epinephrine
- released from adrenal medulla
- stimulates cAMP
-inc glucose levels
cortisol
- secreted by adrenal gland
- acts like glucagon
-needed for gluconeogenesis
type 1 diabetes
- destruction of B-cells
- lack of insulin production
type 2 diabetes
-insulin resistance
pancreatectomy
- no insulin or glucagon
- rely on cortisol and epi to inc blood glucose
-if treated with insulin can counteract bc no glucagon
type 1 diabetes effects on glucagon
- inc glucagon
- inc gluconeogenesis and glycogenolysis
- inc FA and glycerol due to unchecked lipolysis
- inc ketones due to incomplete oxidation of FAs
diabetic ketoacidosis
extreme elevated ketone levels
