Rose: Endocrine Pancreas Flashcards by Sarah Carlson

Where is glucose stored for future energy needs after feeding?

Liver and muscle= stored as glycogen (lasts 12 hrs)

adipose tissue= stored as TG (unlimited)

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Does the brain store energy?

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How does the body store glucose in the fed state?

as glycogen and TG

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What processes occur after eating?

LIPOGENESIS: 
glucose> 
2 pyruvates> 
citrate>
FFA+ glycerol>
TG

GLYCOGENESIS:
glucose>
glycogen

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What is the role of insulin in the FED state?

inhibits intracellular lipases (hydrolyze TG)> inhibits brkdwn of fat/adipose
Facilitates entry of glucose into adipocytes and liver> promotes accumulation of TG in fat cells

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What is glucose used for in adipose?

used to synthesize glycerol

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What is glucose used for in the liver?

FA (only once glycogen stores are maximal)

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What happens to liver derived FA?

packaged as lipoproteins>
enter circulation as FA>
picked up by Adipose>
combined w/ glycerol>
TG

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What procceses increase in the FED state when INSULIN predominates?

↑ glucose oxidation (= glycolysis)
↑ glycogen synthesis
↑ fat synthesis
↑ protein synthesis

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What processes increase in the FASTED state when GLUCAGON predominates?

↑ glycogenolysis
↑ gluconeogenesis
↑ ketogenesis

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What pancreatic islet hormones regulate glucose levels?

β cell (70%): Insulin and amylin

α cell (20%): Glucagon is dominant with fasting

δ cell (5%): Somatostatin

ε cell (<1%): Ghrelin

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What inhibits insulin secretion during fight/flight?

SNS

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What type of innervation is involved in the cephalic phase of insulin secretion?

PNS

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What hormone dominates in the Fasted state? What biochemical process dominates in the fastest state?

glucagon

gluconeogenesis

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What is gluconeogenesis?

glucose production from noncarbohydrate sources, glycerol, and amino acids

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What is the preferred energy source for the brain?

Glucose

ketones in starvation

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What gets broken down in the fasted state to maintain glucose levels??

1st- Glycogen breakdown in liver & muscle → glucose (reserves depleted in 24 hrs)

2nd – Adipose TGs are catabolized to glycerol and FFAs

3rd – glycerol made into glucose (gluconeogenesis in the liver) and FFAs, acetoacetate and b-hydroxybuterate can be made in the liver.

4th- muscle wasting (proteins catabolized> AA> gluconeogenesis in the liver> Glucose)

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How are ketones metabolized?

Ketones converted to acetyl CoA → energy in the citric acid cycle in tissues including brain and muscle

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What can be measured as an indicator of endogenous insulin production in diabetic pts?

C peptide (connecting peptide)

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What is the t1/2 of insulin and where is it metabolized?

circulates FREE in the plasma for

metabolized by the kidney and liver

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What type of receptor is the insulin receptor?

tyrosine kinase

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What does amylin do?

Copackaged/secreted w/ insulin from beta cell>

inhibits glucagon secretion at the level of the alpha cell

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How does amylin affect satiety?

induces satiety by:

↓ food intake, delay gastric emptying, and inhibiting secretion of digestive enzymes, stomach acid, and bile ejection

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What hormone promotes liver gluconeogenesis, glycogenolysis and lipolysis?

Glucagon

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Where is glucagon produced?

alpha cell of pancreas synthesized as proglucagon> spliced into glucagon

What leads to increased glucagon?

hypoglycemia AA (protect from hypoglycemia after a protein meal) SNS and vagal stimulation (tempers insulin affects)

What leads to decreased glucagon?

hyperglycemia | amylin

What type of receptor is the glucagon receptor?

GPCR

What does somatostatin do?

inhibits production of pancreatic hormones (insulin, glucagon, ghrelin)

What stimulates somatostatin?

increase in insulin

What inhibits STT?

ghrelin

How does STT affect the GI tract?

decreases the rate of food absorption

When is Ghrelin active and what does it do?

Increases w/ fasting> | promotes glucagon secretion and inhibits insulin and STT

What are incretins?

GI hormones that promote insulin release after eating

What do incretins (GI HORMONES) do?

DECREASE gastric emptying> SLOWs rate of absorption of nutrients into blood stream *may also directly decrease food intakes

What stimulates insulin in a high glucose situation?

GLP-1

Where is GLP-1 produced?

PROGLUCAGON GENE> cleaved in intestinal cells> GLP-1> secreted from L cells of lower SI and colon

What is GLP-1 degraded by?

dipeptidyl peptidase-4

What produces GIP?

K cells of duodenum and jejunum

What is the t1/2 like for GIP and GLP-1?

mins

What are the 4 phases of insulin secretion?

1) Cephalic Phase- PNS info from sight and smell 2) Oral Phase- PNS info and carb sugar stimulation of sweet receptors 3) GI Phase o The “incretins” 4) Blood Glucose Phase o ↑ in blood glucose triggers β cell release of insulin o ↓ in blood glucose triggers α cell release of glucagon

How

1) Cephalic Phase- parasympathetic info from sight and smell 2) Oral Phase- parasympathetic info and carb sugar stimulation of sweet receptors 3) GI Phase o The “incretins” — GIP: produced in response to hyperosmolarity d/t glucose in gut; Amt of insulin secreted is greater when glucose is administered orally than IV — GLP-1 (remember: derived from a proglucagon gene) 4) Blood Glucose Phase o ↑ in blood glucose triggers β cell release of insulin o ↓ in blood glucose triggers α cell release of glucagon

What happens to the incretins during the GI phase?

GIP: produced in response to hyperosmolarity d/t glucose in gut; Amt of insulin secreted is greater when glucose is administered orally than IV GLP-1 (remember: derived from a proglucagon gene)

What is the incretin effect? What causes it?

When you get a larger response from oral vs. IV glucose. D/t the oral and intestinal phases of insulin secretion (parasympathetic and incretin signals)

What controls nutrient intake and nutrient influx to the blood by inhibiting food intake and gastric emptying (also inhibits glucagon secretion)?

Beta cell secretion of amylin and insulin

What is made in the distal small bowel and colon in response to glucose and acts on receptors in beta pancreatic cells and the brain?

GLP-1

What is made by intestinal K cells in response to glucose and acts on receptors in beta pancreatic cells and in the brain.

GIP

What increases insulin secretion when there are high levels of glucose?

GIP

What do epsiolon cells do?

secrete ghrelin> | promotes glucagon stimulation (hunger signal that coincides w/ low glucose)

What inhibits secretion of insulin, glucagon, and ghrelin and is stimulated by insulin release (part of neg. feedback to ensure hormones do not overshoot)?

STT

How do you prevent hypoglycemia?

glucagon

What are the two types of glucose transporters involved in maintaining glucose homeostasis?

SGLTs and GLUTs

How do SGLTs work and where are they located?

Active transporters/symporters in the gut/kidney that derive energy for transport from the Na gradient across the membrane.

What is one way to block glucose reabsorption?

block SGLT1 or SGLT2

How does SGLT2 allow for the passive diffusion of glucose out of the cell and DOWN the gradient?

Na+ equilibrium maintained by Na+/K+ ATPase on basolateral surface Na+ DOWN gradient allows for glucose to be transported UP it's gradient into the cell

Where is SGLT located?

KIDNEY

What type of transporters are GLUTs?

facilitated transporters

What are the 3 classes of Gluts?

I, II, and III

What GLUT transporter is responsible for the LOW level basal uptake of glucose that occurs in MOST cells?

GLUT 1

What GLUT transporter acts as a "glucose sensor" in the pancreas and initiates the secretion of insulin?

GLUT 2

Where is GLUT 2 located?

Liver, beta cells, kidney, hypothalamus, basolateral membrane small intestine.

What GLUT is located in skeletal and cardiac muscle and fat is and is activated by INSULIN?

GLUT4

What is PULSATILE insulin secretion dependent on?

Calcium!!

How is insulin secretion Ca dependent? Describe the mechanism.

Cholinergic stimulation (ACh) d/t metabolism of nutrients → CLOSES an ATP-sensitive K+ channel → depolarizes pancreatic b-cell → extracellular Ca2+ enters via voltage-dependent Ca2+ channel → stimulates secretion of insulin

Besides CHOLINERGIC stimulation, what are other STIMULATORS of insulin secretion?

Cholinergic stimulation Glucagon (provides “fine tuning” the steady-state levels of blood glucose → prevents wide fluctuations) Amylin, GLP-1, GIP, gastrin, secretin, and CCK

Besides ADRENERGIC stimulation, what are other INHIBITORS of insulin secretion?

Catecholamines | SST

Describe insulin signaling.

1) Insulin binds tyrosine kinase receptor ↑ glucose storage as glycogen or TGs 2) Receptor phosphorylates insulin-receptor substrates (IRS) 3) 2nd messenger pathways alter protein synthesis and existing proteins 4) Membrane transport is modified 5) Cell metabolism is changed

What induces the exocytosis of GLUT4 transporters?

INSULIN | exercise