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84 Cards in this Set

  • Front
  • Back
primary energy source of body
synthesis of glucose
Catabolism of glucose

storage form of glucose
25% found in liver
75% found in skelatal m.
made in adipose tissue from glycerol and fatty acid
oxidation of triacylglycerols to make glycerol and fatty acid
polymers of aa
what makes keto acids?
proteins metabolism to aa and then the aa are deaminated to keto acids
absorptive state
ingested nutrients are entering the blood from the GI tract

occurs like 4 hrs after meal

at this pt body either stores or utilizes the nutrients
postabsoptive state
GI tract is empty and energy is supplied by body stores
more than 24 hrs wo eating
primary source of energy from meal
carbs. they are absorbed from GI as monosaccharides
protein absorbtion in gut
absorbed in GI as dipeptides and then hydrolyzed into aa in epithelial cells and are transported into blood
how are lipid aborbed in GI
absorbed into lymph as triacylglycerols in chylomicrons
during absorptive state, what is done to glucose in skelatal m.?
skeletal m. catabolizes glucose for energy bc glucose is the major energy source during the absorptive state

the muscle stores the glucose as glycogen
during absorptive state, what is done to glucose in adipose tissue?
glucose is converted into triacylgycerol bc glucose is the precursor for both glycerol and fa which make triacylglycerol

glucose can also be used as energy
what does liver do with glucose during the absorptive state?
net uptake of glucose during absorptive state

the glucose is transformed into glycerol and fa and complexed with protein to make VLDLs which are secreted in the blood

the VLDLs are broken down as fa and glycerol by lipoprotein lipase in the caps of the adipose and the fa diffuse into adipocytes where they are transformed back into triacylglycerol
What happens in adipose tissue during the absorptive state?
triacylglycerols in chylomicrons are metabolized into fa and glycerol by lipoprotein lipase. th Fa diffuses into the cells and are used to make triacylglycerols for storage.

small amts of triacylglycerol are oxidzied for immediate needs
2 basic storage forms during absorptive state

sources of fatty acids in adipose tissue
glucose which can be converted to glycerol and fa

ingested triacylglycerol via chylomicrons

VLDL synthesis in the liver
during absorptive state, a small amt of fat is used for energy immediately, what does the amount depend on?
depends on the glucose and the fat content in the meal
what are aa entering body used for?
to make proteins
what does liver do to aa during absorptive state?
aa are taken up the liver and metabolized to keto acids by deamination
when liver converts aa into keto acids during absorbtive state. what can be done with the keto acids?
1. keto acids can be used as energy be entering krebs

2. keto acids can be converted into triacylglycerols. so protein intake in excess of metabolic needs will be converted to fat
biproduct of converting protiens into keto acids
urea from the aa grp from transamination
overview of post absorptive state
there is little absorption of glucose from the GI but the body needs glucose still so 2 things must occur

1. gluconeogenisis
2. shift fuel from source from glucose to fat
3 sources of glucose during post absorptive state


during post absorptive state where is glycogenolysis occuring?
in liver and in skeletal m.
how does skeletal m. undergo glycogenolysis during post absorptive state?
glycogen is hydrolyzed to glucose 6 P but muscle does not have enzymes to convert it to glucose so the G-6-P goes through glycolysis to make pyruvate and lactate and these products enter the blood and go to the liver to go through gluconeogenisis to make glucose
how does lipolysis occur during postabsorbtive state?
in adipose, lipolysis of triacylglycerol makes glycerol and fa which enter the blood and go to the liver. the glycerol undergoes gluconeogensis to make glucose
what happens to protein during postabsorbtive state
protein breaks down to make aa. the aa (mainly alanine) is metabolized to keto acied and then converted to glucose by gluconeogenisis
amt of glucose that gluconeogenesis and glycolysis provide per day
750 kcal/day
how does body shift during post absorptive state?
from utilizing glucose to fat utilization so glucose made by liver can be used by CNS
during post absorptive state, what happens to the fa?
Lipolysis-Fa made by lipolysis circulate bound to albumin. the Fa are picked up by cells are oxidized and enter the Krebs at acetyl Co A

ketone syn- in liver, fa are made into ketones the ketones are released into the blood where they are taken up by cells and used as energy
ketones made from Fa
beta hydroxybutyrate and acetone
what used ketones?
brain during fasting
normal fasting glucose level
70-110 mg/dl
minimal glucose levels required by brain
40 mg/dl
Tm of renal proximal tubules for glucose
180 mg/dl
most important hormone involved in control of plasma glucose conc.
when is insulin hi? lo?
hi in absorptive state

lo in post absorptive state
where is insulin made
in pancrease by beta cells in islets of langerhans
islets of langerhans
contains alpha cells which make glucagon

beta cells which make insulin. this is 60-80% of cells in islets

gamma cells which make somatostatin
describe insulin synthesis
starts out as proinsulin (A-B-C) w/signal sequence and is taken up by golgi to be cleaved into insulin (A-B dimer). C chain is corelease
how is insulin measured. Why?
Measure C chain bc it is coreleased with insulin and it has a longer half life. insulin half life is only 5-6 min
amt of insulin released that is metabolised when it goes through liver
insulin target tissue
primarily liver, skeletal m. and adipose tissue
functions of insulin on glucose metabolism
1.stimulates glucose uptake in muscle and adipose tissue bc insulin causes fusion of vesicles with glucose facilitated transported (glut 4) to the plasma membraine

2. stimulates glycogen synthesis in liver and skeletal m.

3. inhibits glycogen metabolism (glycogenolysis) in liver and skeletal m.
insulin actions on aa metabolism
1. increase aa uptake in liver to make keto acids

2. increase aa uptake in muscle

3. increase enzymes for protein synthesis

4. inhibits protein catabolism
insulin actions on lipid metabolism
1. stimulates triacylglycerol synthesis in liver and adipose

2. inhibits lipolysis in adipose

3. stimulates synthesis of lipoprotein lipase on adipose capps to break down the VLDL
insulin affects on liver
promotes formation of glycogen and triacylglycerol and protein synthesis, inhibits glycogenolysis, gluconeogenisis, and protein degradation
insulin affects on muscle
increase glucose and aa transport into muscle.

promotes glycogen formation and protiein synthesis

inhibits protein degradation
insulin affect on adipose
increase glucose transport, promotes glucose breakdown for triaclglycerol synthesis, increase triacyclerol synthesis and synthesis of lipoprotein lipase

inhibits lipolysis
what regulates insulin secretion
plasma glucose
describe how insulin is released from beta cells
beta cells have a ATP dep. K channel which is open by ADP and closed by ATP. during absorptive state, glucose is hi and taken into beta cell by GLUT 2. the glucose is metabolized to ATP which close the K channels causing the cell to depolarize which activated Ca channels. influx of Ca causes secretion of insulin
Desribe how insulin is not released from beta cells
during post absorbitive period there is normal glucose. The K channel is open and B cell is hyperpolarized and little insulin is released
cause insulin to be released

3 kinds

GLP-1 and GIP and amylin
Glucose dependent insulinotropic peptide
GIP is secreted from K cells in duodenum. GIP is stimulated by food intake (carbs/fats) wi mins.

GIP is inactivated by cleavage of first 3 aa by DPP4.

half life of GIP is 5 min
where are GIP receptors found?
islet cells
adipose tissue
effects of GIP
stimulates glucose dep. insulin secretion.

DOES NOT effect gastric empyting or food intake
GIP secretion in pts with Type II diabetes
GIP is normal or slightly increased but the effect on insulin is lost
Glucagon like peptide
GLP 1 is released from L cells in small intestine/colon. released in biphasic manner.first phase is right after ingesion of meal and second phase is 30-60 min after a meal.
what is stimulus of first phase release of GLP-1?

second phase?
neural and hormonal is stimulus for release in first phase

direct effect of nutirents on the L cells in the stimulus for release of the second phase
Where is GLP-1 contained?
in proglucagon peptide.
where are GLP-1 receptors?
islet cells
effects of GLP-1
stimulate glucose dep insulin secretion

increase preproinsulin gene expression

decrease glucagon secretion

enhance beta cell proliferation

decrease gastric empting and GI mobility

promotes satiety
GLP-1 secretion with type II diabetes
GLP-1 is actie but secretion is decreased!
half life of GLP-1
2 min

it is degraded by DPP-4
what is amylin co released with?
insulin from beta cells
coreleased with insulin from beta cells. Its release is stimulated due to increase in glucose. Amylin regulates plasma glucose during fed state, does not affect fasting glucose levels
effects of amylin
decrease gastric emptying

suppresses glucagon secretion

decreases food intake

circulating receptors binds to area postrema in brain and its effects are mediated through the vagus n.
how do autonaumics control insulin release?
pancrease is innervated by symp and parasymp

parasymp increases insulin

symp decreases insulin
how does plasma aa affect insulin release?
plasma aa stimulates secretion of insulin
major glucose counter regulatory control hormone

works in post absorptive state
what organ does glucagon work on?
only the liver
metabolic effects of glucagon
overall effect is to increase plasma glucose levels during post absorptive state by:

increasing glycogen breakdown

increased gluconeogenesis

increase ketone synthesis
why is glucagon released?
decrease plasma glucose

transition from absorptive to post absorptive sate
What causes transition from absorptive to post absorptive state?
increase in glucagon:insulin ratio in plasma
how do autonaumics affect glucagon release?
symp and epi cause glucagon release

parasymp decreases glucagon release
how does symp system control plasma glucose
2 ways

1. indirectly through regulation of insulin and glucagon release

2. direct effect of cell metabolism
metabolic effects of symp system on glucose
increases glycogenolysis in liver and skeletal m.

gluconeogenisis in liver

lipolyisis is adipose and it stimulates hormone sensitive lipase
what hormone does the symp system behave as?
like glucagon
during hypoglycemia, how does autonaumics behave?
during hypoglycemia increase in symp to liver and adipose and release of epi from adrenal medulla.

but during long periods of fasting the nervous system adapts and decreases activity