Phys Hormones Ii

Front 1

monosaccharides

Back 1

glucose
galactose
fructose

Front 2

primary energy source of body

Back 2

monosaccarides

Front 3

synthesis of glucose

Back 3

gluconeogensis

Front 4

Catabolism of glucose

Back 4

glycolysis

Front 5

polysaccharides

Back 5

glycogen

storage form of glucose
25% found in liver
75% found in skelatal m.

Front 6

triacylgycerols

Back 6

made in adipose tissue from glycerol and fatty acid

Front 7

lipolysis

Back 7

oxidation of triacylglycerols to make glycerol and fatty acid

Front 8

proteins

Back 8

polymers of aa

Front 9

what makes keto acids?

Back 9

proteins metabolism to aa and then the aa are deaminated to keto acids

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absorptive state

Back 10

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

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postabsoptive state

Back 11

GI tract is empty and energy is supplied by body stores

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fasting

Back 12

more than 24 hrs wo eating

Front 13

primary source of energy from meal

Back 13

carbs. they are absorbed from GI as monosaccharides

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protein absorbtion in gut

Back 14

absorbed in GI as dipeptides and then hydrolyzed into aa in epithelial cells and are transported into blood

Front 15

how are lipid aborbed in GI

Back 15

absorbed into lymph as triacylglycerols in chylomicrons

Front 16

during absorptive state, what is done to glucose in skelatal m.?

Back 16

skeletal m. catabolizes glucose for energy bc glucose is the major energy source during the absorptive state

the muscle stores the glucose as glycogen

Front 17

during absorptive state, what is done to glucose in adipose tissue?

Back 17

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

Front 18

what does liver do with glucose during the absorptive state?

Back 18

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

Front 19

What happens in adipose tissue during the absorptive state?

Back 19

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

Front 20

2 basic storage forms during absorptive state

Back 20

glycogen

triacylglycerol

Front 21

sources of fatty acids in adipose tissue

Back 21

glucose which can be converted to glycerol and fa

ingested triacylglycerol via chylomicrons

VLDL synthesis in the liver

Front 22

during absorptive state, a small amt of fat is used for energy immediately, what does the amount depend on?

Back 22

depends on the glucose and the fat content in the meal

Front 23

what are aa entering body used for?

Back 23

to make proteins

Front 24

what does liver do to aa during absorptive state?

Back 24

aa are taken up the liver and metabolized to keto acids by deamination

Front 25

when liver converts aa into keto acids during absorbtive state. what can be done with the keto acids?

Back 25

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

Front 26

biproduct of converting protiens into keto acids

Back 26

urea from the aa grp from transamination

Front 27

overview of post absorptive state

Back 27

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

Front 28

3 sources of glucose during post absorptive state

Back 28

glycogenolysis

lipolysis

protein

Front 29

during post absorptive state where is glycogenolysis occuring?

Back 29

in liver and in skeletal m.

Front 30

how does skeletal m. undergo glycogenolysis during post absorptive state?

Back 30

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

Front 31

how does lipolysis occur during postabsorbtive state?

Back 31

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

Front 32

what happens to protein during postabsorbtive state

Back 32

protein breaks down to make aa. the aa (mainly alanine) is metabolized to keto acied and then converted to glucose by gluconeogenisis

Front 33

amt of glucose that gluconeogenesis and glycolysis provide per day

Back 33

750 kcal/day

Front 34

how does body shift during post absorptive state?

Back 34

from utilizing glucose to fat utilization so glucose made by liver can be used by CNS

Front 35

during post absorptive state, what happens to the fa?

Back 35

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

Front 36

ketones made from Fa

Back 36

beta hydroxybutyrate and acetone

Front 37

what used ketones?

Back 37

brain during fasting

Front 38

normal fasting glucose level

Back 38

70-110 mg/dl

Front 39

minimal glucose levels required by brain

Back 39

40 mg/dl

Front 40

Tm of renal proximal tubules for glucose

Back 40

180 mg/dl

Front 41

most important hormone involved in control of plasma glucose conc.

Back 41

insulin

Front 42

when is insulin hi? lo?

Back 42

hi in absorptive state

lo in post absorptive state

Front 43

where is insulin made

Back 43

in pancrease by beta cells in islets of langerhans

Front 44

islets of langerhans

Back 44

contains alpha cells which make glucagon

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

gamma cells which make somatostatin

Front 45

describe insulin synthesis

Back 45

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

Front 46

how is insulin measured. Why?

Back 46

Measure C chain bc it is coreleased with insulin and it has a longer half life. insulin half life is only 5-6 min

Front 47

amt of insulin released that is metabolised when it goes through liver

Back 47

60%

Front 48

insulin target tissue

Back 48

primarily liver, skeletal m. and adipose tissue

Front 49

functions of insulin on glucose metabolism

Back 49

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.

Front 50

insulin actions on aa metabolism

Back 50

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

Front 51

insulin actions on lipid metabolism

Back 51

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

Front 52

insulin affects on liver

Back 52

promotes formation of glycogen and triacylglycerol and protein synthesis, inhibits glycogenolysis, gluconeogenisis, and protein degradation

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insulin affects on muscle

Back 53

increase glucose and aa transport into muscle.

promotes glycogen formation and protiein synthesis

inhibits protein degradation

Front 54

insulin affect on adipose

Back 54

increase glucose transport, promotes glucose breakdown for triaclglycerol synthesis, increase triacyclerol synthesis and synthesis of lipoprotein lipase

inhibits lipolysis

Front 55

what regulates insulin secretion

Back 55

plasma glucose

Front 56

describe how insulin is released from beta cells

Back 56

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

Front 57

Desribe how insulin is not released from beta cells

Back 57

during post absorbitive period there is normal glucose. The K channel is open and B cell is hyperpolarized and little insulin is released

Front 58

incretin

Back 58

cause insulin to be released

3 kinds

GLP-1 and GIP and amylin

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Glucose dependent insulinotropic peptide

Back 59

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

Front 60

where are GIP receptors found?

Back 60

islet cells
adipose tissue
heart
brain

Front 61

effects of GIP

Back 61

stimulates glucose dep. insulin secretion.

DOES NOT effect gastric empyting or food intake

Front 62

GIP secretion in pts with Type II diabetes

Back 62

GIP is normal or slightly increased but the effect on insulin is lost

Front 63

Glucagon like peptide

Back 63

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.

Front 64

what is stimulus of first phase release of GLP-1?

second phase?

Back 64

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

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Where is GLP-1 contained?

Back 65

in proglucagon peptide.

Front 66

where are GLP-1 receptors?

Back 66

islet cells
kidney
lung
heart
neurons

Front 67

effects of GLP-1

Back 67

stimulate glucose dep insulin secretion

increase preproinsulin gene expression

decrease glucagon secretion

enhance beta cell proliferation

decrease gastric empting and GI mobility

promotes satiety

Front 68

GLP-1 secretion with type II diabetes

Back 68

GLP-1 is actie but secretion is decreased!

Front 69

half life of GLP-1

Back 69

2 min

it is degraded by DPP-4

Front 70

what is amylin co released with?

Back 70

insulin from beta cells

Front 71

amylin

Back 71

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

Front 72

effects of amylin

Back 72

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.

Front 73

how do autonaumics control insulin release?

Back 73

pancrease is innervated by symp and parasymp

parasymp increases insulin

symp decreases insulin

Front 74

how does plasma aa affect insulin release?

Back 74

plasma aa stimulates secretion of insulin

Front 75

glucagon

Back 75

major glucose counter regulatory control hormone

works in post absorptive state

Front 76

what organ does glucagon work on?

Back 76

only the liver

Front 77

metabolic effects of glucagon

Back 77

overall effect is to increase plasma glucose levels during post absorptive state by:

increasing glycogen breakdown

increased gluconeogenesis

increase ketone synthesis

Front 78

why is glucagon released?

Back 78

decrease plasma glucose

transition from absorptive to post absorptive sate

Front 79

What causes transition from absorptive to post absorptive state?

Back 79

increase in glucagon:insulin ratio in plasma

Front 80

how do autonaumics affect glucagon release?

Back 80

symp and epi cause glucagon release

parasymp decreases glucagon release

Front 81

how does symp system control plasma glucose

Back 81

2 ways

1. indirectly through regulation of insulin and glucagon release

2. direct effect of cell metabolism

Front 82

metabolic effects of symp system on glucose

Back 82

increases glycogenolysis in liver and skeletal m.

gluconeogenisis in liver

lipolyisis is adipose and it stimulates hormone sensitive lipase

Front 83

what hormone does the symp system behave as?

Back 83

like glucagon

Front 84

during hypoglycemia, how does autonaumics behave?

Back 84

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