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Flashcards in Pancreas Deck (50)
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1

Pancreas

nTissue

 

uAcini

___ glands that secrete __ ___

 

uIslets of Langerhans

FSecrete___ into the blood

 

Pancreas: Endo and exocrine gland

Acinar cells secrete digestive enzymes and bicarb but we are going to focus on the endocrine portion of the gland

Pancreas

nTissue

uAcini

Fexocrine glands that secrete digestive juices

uIslets of Langerhans

FSecrete hormones into the blood

 

Pancreas: Endo and exocrine gland

Acinar cells secrete digestive enzymes and bicarb but we are going to focus on the endocrine portion of the gland

2

Pancreas

nAlpha cells

___ (20%)

 

nBeta cells

___(70%)

 

nDelta cells

___ (10%)

 

nF cells

___ ____

 

Somatostatin: Inhibitory

Pancreas

nAlpha cells

uGlucagon (20%)

nBeta cells

uInsulin (70%)

nDelta cells

uSomatostatin (10%)

nF cells

uPancreatic polypeptide

 

Somatostatin: Inhibitory

3

This shows the blood supply for the pancreas

The blood supply moves from the___ to ___

Interior: Most of the ___ cells

When insulin released from beta cells blood caries the insulin to the outside

Ouside is where you find most of the ___ cells

When insulin comes from the inside, it will shut down the production of ____  by alpha cells.

___  also has impact on glucagon secretion. (inhibitor)

This shows the blood supply for the pancreas

The blood supply moves from the interior to the exterior

Interior: Most of the Beta cells

When insulin released from beta cells blood caries the insulin to the outside

Ouside is where you find most of the alpha cells

When insulin comes from the inside, it will shut down the production of glucagon by alpha cells.

Glucose also has impact on glucagon secretion. (inhibitor)

4

Insulin 

nHistory:

uDiscovered in 1921 by Banting and Best

nChemistry

uSynthesized by the ___ cells of the pancreas from ____   (single chain of 110 amino acid).

uThe 24-amino acid N-terminal of preproinsulin is ___ to form proinsulin, after___ through the membrane of the rough   endoplasmic reticulum (RER). 

nHistory:

uDiscovered in 1921 by Banting and Best

nChemistry

uSynthesized by the B cells of the pancreas from preproinsulin   (single chain of 110 amino acid).

uThe 24-amino acid N-terminal of preproinsulin is cleaved to form proinsulin, after translocation through the membrane of the rough   endoplasmic reticulum (RER). 

5

Endogenous Synthesis of insulin

This is the mRNA from insulin gene

There is a signal sequence and the A, C, and B domains

mRNA gets tlating

As it moves thru ER, the __ ___ gets cleaved

With the signal sequence its _____

Once its cleaved you get _____

Form pro insulin

This has A and B chain connected by a C peptide

Further processing occurs in golgi

In trans golg __ ___ iis cleaved by prohormone convertase

Once its cleaved you have packaging of mature ___ with ___ ___ in a vesicle

Vesicle also has ___ which is important for insulin stabilization and  fcn

For every mole of insulin, you have a mol of C peptide.  C peptide doesn’t have much biological fcn

__ ___ can be used to ___ how much insulin is in the body

Same molar ratio

This is the mRNA from insulin gene

There is a signal sequence and the A, C, and B domains

mRNA gets tlating

As it moves thru ER, the Signal sequence gets cleaved

With the signal sequence its preproinsulin

Once its cleaved you get pro insulin

Form pro insulin

This has A and B chain connected by a C peptide

Further processing occurs in golgi

In trans golgi, C peptide iis cleaved by prohormone convertase

Once its cleaved you have packaging of mature insulin with C peptide in a vesicle

Vesicle also has Zn which is important for insulin stabilization and  fcn

For every mole of insulin, you have a mol of C peptide.  C peptide doesn’t have much biological fcn

C peptide can be used to asses how much insulin is in the body

Same molar ratio

6

Human proinsulin and its conversion to insulin.

This is insulin

A chain has ___ chain disulfide bond

Connected to B chain by ___ chain disulfide bond

___  is the aa that forms disulfide bonds

Human proinsulin and its conversion to insulin.

This is insulin

A chain has intra chain disulfide bond

Connected to B chain by INTER chain disulfide bond

Cysteine is the aa that forms disulfide bonds

7

Insulin 

nRegulation of insulin secretion

uTightly regulated to allow ___ conc. of glucose in both fasting and fed state

uSecretion of insulin promoted by

___

__ __

__ __

__ __

___ __ ___

___ ___ ___ ___, VIP, gastrin, secretin, cholecystokinin, enteroglucagon
β2-AR and vagal nerve stimulation ­ release

 

Brain depends on glucose for E so glucose has to available. If not, you go into a coma.

Glucose is primary stimulant for insulin release

___ stimulate the production of insulin

Insulin's major fcn is to store nutrients

GIP and GLP. These two are___

Incretins stimulate ____ production by the Beta cells

Symp NS can stimulate (thru __ recep) or inhibit (thru ___ recep) insulin secretion 

Insulin 

nRegulation of insulin secretion

uTightly regulated to allow stable conc. of glucose in both fasting and fed state

uSecretion of insulin promoted by

F glucose

F amino acids,

Ffatty acids,

Fketone bodies,

FGIP (gastric inhibitory polypeptide), (incretins)

F GLP-1 (glucagon-like intestinal peptide 1), VIP, gastrin, secretin, cholecystokinin, enteroglucagon
β2-AR and vagal nerve stimulation ­ release

 

Brain depends on glucose for E so glucose has to available. If not, you go into a coma.

Glucose is primary stimulant for insulin release

Nutrients stimulate the production of insulin

Insulin's major fcn is to store nutrients

GIP and GLP. These two are incretins.

Incretins stimulate insulin production by the Beta cells

Symp NS can stimulate (thru B recep) or inhibit (thru alpha recep) insulin secretion 

8

Glucose [] vs time

If glucose given orally

As glucose gets absorbed in the intestine, glucose level rises

As glucose level rises you have __ ___ in insulin

 

If same amount of glucose was given by IV

Way ___ insulin is released

The difference is bc of those molecules we talked about. GLP and GIP

They are released from the intestines go to the __ ___ and stimulate ___ insulin release
Even though glucose is the main stimulant, GLP and GIP contribute too.

You see that difference here

 

Type I: Diabetic Patient in B

Baseline for glucose is much ___ here than a normal patient

__ ___ insulin release because the beta cell has been ___ 

If after 2 hrs. glucose levels are above 200 mg/dL you are a diabetic

 

C:

Person receives glucose. Response is a rapid ___e in insulin.

The insulin that is release, this is insulin that was ___ within the Beta cells

Second phase of release is more sustained (this is ___ and ___ ___ d insulin) This will remain high until glucose level falls

Glucose [] vs time

If glucose given orally

As glucose gets absorbed in the intestine, glucose level rises

As glucose level rises you have massive increase in insulin

If same amount of glucose was given by IV

Way less insulin is released

The difference is bc of those molecules we talked about. GLP and GIP

They are released from the intestines go to the Beta cells and stimulate more insulin release
Even though glucose is the main stimulant, GLP and GIP contribute too.

You see that difference here

Type I: Diabetic Patient in B

Baseline for glucose is much higher here than a normal patient

Hardly any insulin release because the beta cell has been destroyed

If after 2 hrs. glucose levels are above 200 mg/dL you are a diabetic

C:

Person receives glucose. Response is a rapid increase in insulin.

The insulin that is release, this is insulin that was preformed within the Beta cells

Second phase of release is more sustained (this is preformed and newly formed insulin) This will remain high until glucose level falls

9

Insulin 

uRegulation of insulin

FAny condition that ___ the ____nervous system (e.g. severe burns, hypoxia, hypothermia, surgery) ____the secretion of insulin via activation of ___

uGlucose is the ___stimulus for insulin release and require___ nto the β-cells (via ___) and ___.

u

____ acts as the glucose sensor 

uRegulation of insulin

FAny condition that activates the autonomic nervous system (e.g. severe burns, hypoxia, hypothermia, surgery) suppress the secretion of insulin via activation of α2-AR.

uGlucose is the principal stimulus for insulin release and requires   entry into the β-cells (via GLUT2) and metabolism.

u

uGlucokinase acts as the glucose sensor 

10

Regulation  of Insulin Release

How does glucose stimulate insulin release?

Glucose has to be ___ by the Beta cell before it can cause release.

Glucose will pass thru a glucose transporter.

GLUT 2: ___

GLUT4: ____

Glucose is metabolized by ___

Glucose forms___

ATP binds __ channels

K channel ___

Membrane potential ___ ( ____ ) 

___ channels in membrane are voltage gated

Ca channels ___

Ca moves___ cell ___ its gradient

The increase in Ca triggers ___ of vesicles to release insulin


Sulfaurida drugs can bind to K channel and ___ it just like ___

Diabetic take this drug, ___  released

How does glucose stimulate insulin release?

Glucose has to be metabolized by the Beta cell before it can cause release.

Glucose will pass thru a glucose transporter.

GLUT 2: pancreas

GLUT4: muscle, adipose tissue

Glucose is metabolized by Glycolysis.

Glucose forms ATP

ATP binds K channels

K channel closes

Membrane potential rises..Depolarized

Ca channels in membrane are voltage gated

Ca channels open

Ca moves into cell along its gradient

The increase in Ca triggers exocytosis of vesicles to release insulin


Sulfaurida drugs can bind to K channel and close it just like ATP

Diabetic take this drug, insulin released

11

Molecular Mechanism of Insulin Action

Insulin is also required for____

How does it regulate growth and metabolism?

It has 2 different signaling cascades that allow it to do that

 

Metabolic Effect: 

Insulin Receptor

A chain is seen extracellularly

B chain is transcellular

B chain has Tyrosine kinase activity

Insulin binds to its receptor

Conf change

Activation of B chain

B chain phosphorylates A

A phosphorylates B

Once you have P group on receptor, the P groups act as binding sites for other proteins. (____, 1/2/3/4)

In turn these recruit other proteins like PI3 kinase, Protein dependent kinase and ____ (Protein Kinase B)

Akt: PKB: When Akt activated, it signals to___ ___ normally found in the cell to move into the membrane to let glucose into the cell

If you disrupt this, lot of glucose in blood but it __ __ ___ the cell

 

Growth Effect

P group attracts ____, Ras, MEK and  __ ___

MAP kinase can phosphorylate __ ___ that lead to gene expression and growth regulation

Insulin is also required for growth

How does it regulate growth and metabolism?

It has 2 different signaling cascades that allow it to do that

Metabolic Effect: 

Insulin Receptor

A chain is seen extracellularly

B chain is transcellular

B chain has Tyrosine kinase activity

Insulin binds to its receptor

Conf change

Activation of B chain

B chain phosphorylates A

A phosphorylates B

Once you have P group on receptor, the P groups act as binding sites for other proteins. (IRS, 1/2/3/4)

In turn these recruit other proteins like PI3 kinase, Protein dependent kinase and AKT (Protein Kinase B)

Akt: PKB: When Akt activated, it signals to glucose transporters normally found in the cell to move into the membrane to let glucose into the cell

If you disrupt this, lot of glucose in blood but it can’t get into the cell

Growth Effect

P group attracts Grb2, Ras, MEK and  Map Kinase

MAP kinase can phosphorylate tx factors that lead to gene expression and growth regulation

12

Molecular Mechanism of Insulin Resistance

Obesity is driving the epidemic of Type II diabetes

How are they related?

Obestity...Excess of ___ or ___

Mitochondria cannot deal with the oxidation of all the fa.

Excess___ and ____ (byproducts of fa oxidation)

Excess of these ___ the mitochondria

These fa byprod are activators of ___ __ ___

Normally the___ proteins are phosphorylated on __ residues

But they also have a phosphorylation site for ___

Excess of these DAG and fatty acyl coA activate more than normal activation of these ___kinases

These phosphorylate IRS Serine residue

This __ ___phosphorylation

Now it doesn’t work

Insulin cant send the signal to __ ___ to get into the cell

Signal gets interrupted

Serine phosphorylation also marks these IRS proteins for ___

Less IRS, less ability to signal to the glucose transporters, less glucose taken up-à __ ___ (Type _ diabetes)

Obesity is driving the epidemic of Type II diabetes

How are they related?

Obestity...Excess of Fa or their byproducts

Mitochondria cannot deal with the oxidation of all the fa.

Excess DAG and fatty acyl coA (byproducts of fa oxidation)

Excess of these leave the mitochondria

These fa byprod are activators of serine Thr kinases

Normally the IRS proteins are phosphorylated on Y residues

But they also have a phosphorylation site for serine

Excess of these DAG and fatty acyl coA activate more than normal activation of these Serine kinases

These phosphorylate IRS Serine residue

This Blocks Y phosphorylation

Now it doesn’t work

Insulin cant send the signal to GLUT transporters to get into the cell

Signal gets interrupted

Serine phosphorylation also marks these IRS proteins for degradation

Less IRS, less ability to signal to the glucose transporters, less glucose taken up-à insulin resistance (Type 2 diabetes)

13

Insulin Pharmacology

nClinical uses of insulin

uPatients with type I diabetes

uGestational diabetes not controlled by ___t alone

uEmergency treatment (___.) of ____ diabetic emergencies (e.g. diabetic ketoacidosis)

uEmergency treatment of ___: ___is given with glucose to ____ extracellular K+ by directing it into cells.

uMany type ___ diabetic patients ultimately require insulin treatment

 

 

People with gestational diabetes, not controlled by diet. Need to be given insulin

People with diabetic ketoacidosis have to be given __ __ ____

Insulin can also help get K ___ cells

If there are high levels of K in the blood, insulin is given along with glucose to get K into cells

Insulin has action on the __ __ ___ that takes K into cells

Many type 2 diabetics require insulin when the oral agents no longer work

Insulin Pharmacology

nClinical uses of insulin

uPatients with type I diabetes

uGestational diabetes not controlled by diet alone

uEmergency treatment (i.v.) of hyperglycemic diabetic emergencies (e.g. diabetic ketoacidosis)

uEmergency treatment of hyperkalemia: insulin is given with glucose to lower extracellular K+ by directing it into cells.

uMany type 2 diabetic patients ultimately require insulin treatment

 

 

People with gestational diabetes, not controlled by diet. Need to be given insulin

People with diabetic ketoacidosis have to be given fast acting insulin

Insulin can also help get K into cells

If there are high levels of K in the blood, insulin is given along with glucose to get K into cells

Insulin has action on the Na/K pump that takes K into cells

Many type 2 diabetics require insulin when the oral agents no longer work

14

Effect of Insulin on Liver

nPromotes ___ of glucose as glycogen and conversion of glucose to ____

nPromote __ ___

transcription of ___

­__ ___

___ ____

__ __ ___

nPromotes storage of glucose as glycogen and conversion of glucose to triglycerides

nPromote glycogen synthesis

u­ transcription of glucokinase

u­glycogen synthase

u¯glycogen phosphorylase

u¯glucose-6-phosphatase

15

Effect of Insulin on Liver

nPromote___ and carbohydrate oxidation

u­ activity of ___

u­___

u__ ___

uPromote metabolism via __ ___ shunt

u­ __ ___

uInhibit ___

u

nPromote glycolysis and carbohydrate oxidation

u­ activity of glucokinase

u­phosphofructokinase

uPyruvate kinase

uPromote metabolism via hexose monophosphate shunt

u­ pyruvate dehydrogenase

uInhibit gluconeogenesis

u

16

Effect of Insulin on Liver

nPromote __ ___ of fat by ­__ __ ____ and __ __ ___

nPromote ___ ___  and inhibit ___ ___

nPromote synthesis and storage of fat by ­acetyl CoA carboxylase and fatty acid synthase

nPromote protein synthesis and inhibit protein breakdown

17

Metabolic Effects of Insulin on Liver

Insulin has 4 major actions in the liver:

 

Stimuate __ ___ in the liver

Store aa as protesins


__ __e as glycogen

Gà G6P by glucokinase. Insulin stimulates that enzyme

Insulin also stimulates glycogen synthase so more glycogen gets produced.

 

Stimulates ___

Stimulates certain critical enzymes. PFK and Pyruvate Kinase

 

Stimulate conversion of ___ ___ to ___

Excess glucose stored as fat.

Stimulates enzyme Aceryl coA carboxylase which takes Acetyl CoAàmalonyl coA

Malonyl coA inhibits movement of fa to mitochondria for oxidation and allows it to be converted to triglycerides

Metabolic Effects of Insulin on Liver

Insulin has 4 major actions in the liver:

Stimuate protein synthesis in the liver

Store aa as protesins


Stores glucose as glycogen

Gà G6P by glucokinase. Insulin stimulates that enzyme

Insulin also stimulates glycogen synthase so more glycogen gets produced.

Stimulates glycolysis

Stimulates certain critical enzymes. PFK and Pyruvate Kinase

Stimulate conversion of Acetyl coA into TAG

Excess glucose stored as fat.

Stimulates enzyme Aceryl coA carboxylase which takes Acetyl CoAàmalonyl coA

Malonyl coA inhibits movement of fa to mitochondria for oxidation and allows it to be converted to triglycerides

18

Insulin Action in Muscle

nPromotes ___ of glucose and its storage as ___

u­ ___ transporter to plasma and ­ glucose ___

u­ transcription of ___ and activate __ ___

uPromote ___ and carbohydrate oxidation

uPromote ___ synthesis and ¯ protein breakdown

nPromotes uptake of glucose and its storage as glycogen

u­ Glut4 transporter to plasma and ­ glucose uptake

u­ transcription of hexokinase and activate glycogen synthase

uPromote glycolysis and carbohydrate oxidation

uPromote protein synthesis and ¯ protein breakdown

19

Metabolic Effects of Insulin on Muscle

4 actions in muscle too!

1)Stimulates movement of __ ___ into the membrane so you can have more glucose coming into the cell. We didn’t see that in the liver bc transport of glucose into the liver is not insulin dependent.

2)Store Glucose as ____Stimulate glycogen synthase

3)Stimulate ___

4)Stimulate usage of__ as ___

4 actions in muscle too!

1)Stimulates movement of GLUT transporters into the membrane so you can have more glucose coming into the cell. We didn’t see that in the liver bc transport of glucose into the liver is not insulin dependent.

2)Store Glucose as Glycogen. Stimulate glycogen synthase

3)Stimulate glycolysis.

4)Stimulate usage of ketones as fuel

20

Insulin Action in Adipocytes

nPromote uptake of glucose and its conversion to___ for storage

u­ ____ transporter to plasma and ­ glucose uptake

uPromote ___ and formation of____

uPromote esterification of ____

uWith free fatty acids to form___e for storage

uPromote ___s of lipoprotein lipase

u

nPromote uptake of glucose and its conversion to triglyceride for storage

u­ Glut4 transporter to plasma and ­ glucose uptake

uPromote glycolysis and formation of α-glycerophosphate

uPromote esterification of α-glycerophosphate

uWith free fatty acids to form triglyceride for storage

uPromote synthesis of lipoprotein lipase

u

21

Insulin Action in Adipocytes

1)Stimulates__ ___ ____s into the membrane to let more glucose in

2)Stimulate breakdown of glucose by ____.. Difference here. Product of glycoylsis is __ __ ___e. It goes from PEP and then insulin stimulates the conversion to AGP. This can then be combined with fa to make triglycerides

1)Where does fa come from? Diet

1)Insulin stimulates production of__ _____e. Made within adipose but exported to endothellial cells where it sits on surface of endothelial cell waiting for chylomicrons, fat containing molecules coming from the liver. When it gets there LPL breaks that into __. Fa then go back into the adipocytes where it combines with AGP  to from __

3)Inhbit breakdown of Triglycerides

1)Stimulates movement of transporters into the membrane to let more glucose in

2)Stimulate breakdown of glucose by glycolysis. Difference here. Product of glycoylsis is alpha-glycerol-phosphate. It goes from PEP and then insulin stimulates the conversion to AGP. This can then be combined with fa to make triglycerides

1)Where does fa come from? Diet

1)Insulin stimulates production of lipoprotein lipase. Made within adipose but exported to endothellial cells where it sits on surface of endothelial cell waiting for chylomicrons, fat containing molecules coming from the liver. When it gets there LPL breaks that into fa. Fa then go back into the adipocytes where it combines with AGP  to from TG

3)Inhbit breakdown of Triglycerides

22

Insulin 

nAdverse Effects

uMost common is _____ (sweating, hunger, paresthesias, palpitations, tremor, anxiety) ____symptoms occur first followed by loss of concentration, confusion, weakness, drowsiness, blurred vision, loss of consciousness (n_____ symptoms)

uWeight ___

___  (due to insulin’s ____ action)

____ (due to ___ actions of high local concentrations of insulin.

u

 

If you have patient sweating while the AC is on, it could be that they are hypoglycemic.

Don’t leave hypoglycemic patient alone.

Ask someone to stay with the patient

Weight gain because stores nutrients

Insulin 

nAdverse Effects

uMost common is hypoglycemia (sweating, hunger, paresthesias, palpitations, tremor, anxiety) autonomic symptoms occur first followed by loss of concentration, confusion, weakness, drowsiness, blurred vision, loss of consciousness (neuroglycopenic symptoms)

uWeight gain

uEdema (due to insulin’s antinatriuretic action)

ulipohypertrophy (due to lipogenic actions of high local concentrations of insulin.

u

 

If you have patient sweating while the AC is on, it could be that they are hypoglycemic.

Don’t leave hypoglycemic patient alone.

Ask someone to stay with the patient

Weight gain because stores nutrients

23

Treatment of Hypoglycemia

nAdminister __ ___ sugars such as fruit juice, soda, table sugar by mouth who are able to ___

__ ___ of ___ if patient is unable to swallow

__ ___ if in hospital setting

n

If patient is unconcious or cant open mouth, give IM injection of glucagon.

In hospital setting you can give IV glucose but...

You usually don’t have IV glucose in a dental office!!


Give glucagon if they cant open their mouth

Treatment of Hypoglycemia

nAdminister readily absorbable sugars such as fruit juice, soda, table sugar by mouth who are able to swallow.

nI.M. injection of glucagon if patient is unable to swallow

nIV glucose if in hospital setting

n

If patient is unconcious or cant open mouth, give IM injection of glucagon.

In hospital setting you can give IV glucose but...

You usually don’t have IV glucose in a dental office!!


Give glucagon if they cant open their mouth

24

Nutritional State and Regulation of Blood Glucose

GH Cortisol Glucagon EP

Blood Glucose 

FA                       

AA                    

MP                   

 

 

MP: Muscle protein

All four of these oppose action of insulin.

But when nutrients are available (we eat), insulin is king during that period. The other 4 have very little effect 

Nutritional State and Regulation of Blood Glucose

GH Cortisol Glucagon EP

Blood Glucose ↑       ↑         ↑       ↑

FA                     ↑      ↑         ↑       ↑        

AA                    ↓      ↑         N       N

MP                    ↑      ↓         N       N

 

 

MP: Muscle protein

All four of these oppose action of insulin.

But when nutrients are available (we eat), insulin is king during that period. The other 4 have very little effect 

25

Somatostatin

Somatostatin

uProduced by__ cells of the stomach and duodenum; hypothalamus, and d cells of the pancreas

uAct on pancreas to ___ _____secretion

 

Pancreatic Polypeptide

uProduced by ___ cells of pancreas

uInhibit ___ ____secretion and __ __ ___

n

 

Somatostatin: Inhibit insulin and glucagon secretion and exocrine secretion

Somatostatin

nSomatostatin

uProduced by D cells of the stomach and duodenum; hypothalamus, and d cells of the pancreas

uAct on pancreas to ¯ endocrine/exocrine secretion

nPancreatic Polypeptide

uProduced by F cells of pancreas

uInhibit pancreatic enzyme secretion and gall bladder contraction

n

 

Somatostatin: Inhibit insulin and glucagon secretion and exocrine secretion

26

Glucagon

nChemistry

u  Proglucagon-derived peptides are encoded by  ___le mammalian proglucagon ___

u

uProglucagon is cleaved by __ ____ (PC) in a__ ___c manner to yield ___ hormones

u

uIn the ___ cells of the pancreas proglucagon is cleaved to yield a 29 amino acid peptide called ___

u

uGlucagon is cleaved just before secretion. Glucagon and ___ ____ are present in a ____   relationship in the islets.
 

 

Works with insulin to maintain blood glucose levels

Insulin and glucagon form a regulatory couple and oppose each other in actions

Glucagon

nChemistry

u  Proglucagon-derived peptides are encoded by a single mammalian proglucagon gene.

u

uProglucagon is cleaved by prohormone convertase (PC) in a tissue specific manner to yield different hormones

u

uIn the alpha cells of the pancreas proglucagon is cleaved to yield a 29 amino acid peptide called glucagon. 

u

uGlucagon is cleaved just before secretion. Glucagon and pancreatic polypeptide are present in a reciprocal   relationship in the islets.
 

 

Works with insulin to maintain blood glucose levels

Insulin and glucagon form a regulatory couple and oppose each other in actions

27

Processing of Glucagon

Glucagon formed from this peptide

In the alpha cell, glucagon is cleaved to be ____

In the ____, it is cleaved differently. You don’t get glucagon but you get ____

Glucagon formed from this peptide

In the alpha cell, glucagon is cleaved to be glucagon

In the intestine, it is cleaved differently. You don’t get glucagon but you get GLP1

28

Factors affecting glucagon secretion

nGlucagon and insulin form a ____ couple. Glucagon is ___glycemic: it acts on liver and adipose tissue to ____ blood glucose and fatty acid concentrations.

n

uHypoglycemia( [glucose] < 50 mg/dL)____ glucagon secretion. 

uHyperglycemia ( [glucose] > 200 mg/dL) ____ glucagon secretion.

u↑ fatty acid ____ insulin secretion and ___ glucagon  secretion

u↑ Amino acids stimulate the release of_______

u

u Exercise, glucocorticoids, gastrin, arginine, alanine, gastrin,   VIP, GIP Cholecystokinin (CCK), ____ glucagon release, while fatty acids, secretin,  somatostatin, ____ glucagon release. 

uStress ___ glucagon secretion via the ___c nervous system

u

n

 

Hypoglycemia: Stimulates Glucagon Secretion

Hyperglycemia: That is when insulin is king

High protein diet favors secretion of ____

High carb diet favors secretion of ___

Mixed meal, get secretion of both

Need both glucagon and insulin

If you have high protein diet and secrete only insulin. It will take all carb and move it into cell bc most of diet is protein

If too  much carb goes into the cell what will you get? Hypoglycemia

So to prevent hypoglycemia you need to secrete glucagon

Factors affecting glucagon secretion

nGlucagon and insulin form a regulatory couple. Glucagon is hyperglycemic: it acts on liver and adipose tissue to raise blood glucose and fatty acid concentrations.

n

uHypoglycemia( [glucose] < 50 mg/dL) stimulates glucagon secretion. 

uHyperglycemia ( [glucose] > 200 mg/dL) suppresses glucagon secretion.

u↑ fatty acid stimulate insulin secretion and ↓ glucagon  secretion

u↑ Amino acids stimulate the release of both insulin and glucagon. (E)

u

u Exercise, glucocorticoids, gastrin, arginine, alanine, gastrin,   VIP, GIP Cholecystokinin (CCK), stimulate glucagon release, while fatty acids, secretin,  somatostatin, inhibit glucagon release. 

uStress stimulate glucagon secretion via the sympathetic nervous system

u

n

 

Hypoglycemia

Stimulates Glucagon Secretion

Hyperglycemia: That is when insulin is king

High protein diet favors secretion of glucagon

High carb diet favors secretion of insulin

Mixed meal, get secretion of both

Need both glucagon and insulin

If you have high protein diet and secrete only insulin. It will take all carb and move it into cell bc most of diet is protein

If too  much carb goes into the cell what will you get? Hypoglycemia

So to prevent hypoglycemia you need to secrete glucagon

29

Factors affecting glucagon secretion

Control of Glucagon Secretion

Increase Glucagon Secretion        Decrease Glucagon

                                                                 Secretion

Amino acids                                                 fatty acids

Exercise                                                       Secretin

Glucocorticoids                                             Somatostatin

  Gastrin

  Arginine

  Alanine

  Vasoactive intestinal peptide (VIP)

  Gastrin intestinal peptide (GIP)

  Cholecystokinin (CCK)
 

Factors affecting glucagon secretion

Control of Glucagon Secretion

Increase Glucagon Secretion        Decrease Glucagon

                                                                 Secretion

Amino acids                                                 fatty acids

Exercise                                                       Secretin

Glucocorticoids                                             Somatostatin

  Gastrin

  Arginine

  Alanine

  Vasoactive intestinal peptide (VIP)

  Gastrin intestinal peptide (GIP)

  Cholecystokinin (CCK)

30

Factors affecting glucagon secretion

uDuring mixed meals, both ___ and ___ are secreted.

n

n High protein diets favor ___ and ___comes from glycogenolysis and gluconeogenesis.

u High carbohydrate diets favor____ secretion.
 

uDuring mixed meals, both glucagon and insulin are secreted.

n

n High protein diets favor glucagon and glucose comes from glycogenolysis and gluconeogenesis.

u High carbohydrate diets favor insulin secretion.