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Presemester DENT > Glucose Metabolism & Homeostasis I and II > Flashcards

Glucose Metabolism & Homeostasis I and II Flashcards

1
Q

What concentration is glucose kept at?

A

5mM

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2
Q

What are the 5 phases of glucose homeostasis?

A

Phase I: Meal provides carbohydrates right after the meal.

Phase II: Glycogen stores broken down in the liver (6-8 hours post meal) Gluconeogenesis in liver starts

Phase III: Hepatic gluconeogenesis

Phase IV: Gluconeogenesis and production of ketone bodies

Phase V: Gluconeogenesis and more ketone body production

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3
Q

What are normal fasting glucose levels?

A

3.5 - 5.5 mM

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4
Q

What are normal fed glucose levels?

A

5.5 - 7 mM

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5
Q

Where is glucose utilized most?

A

In the brain

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6
Q

Why does the brain hold no glycogen stores?

A

1 gram of glycogen requires 3 grams of water as well.

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7
Q

What happens if the concentration of blood glucose is low?

A

Causes brain dysfunction and coma.

Extended period of very low blood glucose can cause irreversible damage to brain or death

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8
Q

What happens to insulin levels at 5mM?

A

Insulin levels drop

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9
Q

What happens to adrenaline/glucagon at 3.9 mM?

A

Their levels increase

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10
Q

What does insulin release do in muscle and fat tissue?

A

Stimulates glucose uptake in muscle and fat. Converts glucose to glucose-6-phosphate.

Insulin stimulates production of TAG in fat tissue.

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11
Q

What does insulin release do in liver tissue?

A

Stimulates glycogen synthase, inactivates glycogen phosphorylase. Stimulates production of glycogen from glucose 6-phosphate

In the liver, insulin stimulates conversion of excess glucose to fat. Acetyl-CoA -> TAG, exported by VLDL

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12
Q

How is glucose uptake in the liver increased by insulin?

A

Increasing expression of glucokinase

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13
Q

What does insulin do to glycolysis?

A

It increases glycolysis to increase acetyl-CoA production which is important for fat production.

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14
Q

How does insulin affect the liver glycogen storage?

A

Glycogen synthase (activated via dephosphorylation)

Glycogen phosphorylase (inactivated via dephosphorylation)

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15
Q

How does insulin increase glycogen storage in liver and muscle/fat cells?

A

In liver it increases activation/inactivation of metabolic enzymes required for glycogen synthesis.

In muscle it increases amount of glucose entering the muscle cells. (glucose transporters are only available in the presence of insulin)

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16
Q

What does glucagon do?

A

Works via cAMP to increase glucose in blood. It does this by activating glycogen phosphorylase and inhibiting glycogen synthase.

In liver it reduces Phosphofructokinase activity (decreases F2,6BP and therefore glycolysis) while stimulating gluconeogenesis.

Inhibits pyruvate kinase (Prevents pyruvate production from Phosphoenol pyruvate to prevent production of acetyl-CoA and buildup of phosphoenol pyruvate favours gluconeogenesis)

Stimulates PEPCK for gluconeogenesis

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17
Q

What does glucagon do in adipose tissue?

A

Via cAMP cascades it:

Activates TAG hydrolysis and phosphorylates perilipin to expose lipid droplet to lipases.

Activates hormone sensitive lipase.

This results in fatty acid transport to other tissues so that glucose is spared for the brain.

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18
Q

What does adrenaline do to glucagon levels?

A

Stimulates the same cAMP cascades that glucagon does in fat and liver. However, it also:

Stimulates glucagon secretion itself and inhibits insulin secretion.

Breaks down muscle glycogen as well as liver glycogen.

Stimulates glycolysis and therefor lactate formation.

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19
Q

How does meal influence glucose levels in the blood?

A

Immediately after meal glucose levels increase dramatically.

2 or more hours after meal blood glucose begins to drop (glycogen is secreted liver glycogen releases glucose)

4 hours after meal more glucagon, more TAG hydrolysis, FA become fuel for muscle and liver

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20
Q

What happens to macronutrients in the well-fed liver?

A

Glucose, amino acids, and TAGs enter the liver and are processed, pancreas is signalled to produce insulin. Glucose goes to the brain, TAGs go the muscles and to adipose tissue, amino acids are used to produce proteins, alpha-ketoacids and urea.

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21
Q

What happens during prolonged fasting?

A

Muscle begins to be used for fuel. (liver deaminates or transaminates amino acids)

FAs are oxidised to acetyl CoA but oxaloacetate depleted to make glucose so forms ketone bodies which are exported to other tissues.

22
Q

What happens to amino acids during prolonged fasting?

A

Amino groups are converted to urea.

C skeletons of glucogenic AAs converted to pyruvate, then glucose via gluconeogenesis.

Provides glucose for the brain

23
Q

What happens to fuel in the liver during prolonged fasting?

A

Protein degradation yields glucogenic amino acids.

Urea is exported to the kidneys and excreted in urine.

Oxaloacetate is diverted to gluconeogenesis

Glucose is exported to the brain via the bloodstream.

Ketone bodies are exported via the bloodstream to the brain (build up of acetyl CoA due to lack of oxaloacetate leads to this)

Fatty acids are oxidised as fuel producing Acetyl-CoA

24
Q

What are the different precursors for gluconeogenesis?

A

Lactate (from RBCs)

Glycerol (From TAG; FA cant be used because acetyl CoA to pyruvate can’t happen)

Amino acids (removal of amine group, can enter as pyruvate or oxaloacetate)

25
Q

What happens to muscle mass during starvation?

A

Rapid muscular wasting between 18 - 48 hours after final meal. This wasting occurs very rapidly due to maximum GNG activity in the liver/kidneys. Urea production at this stage is also at a maximum.

As starvation continues the body depends less on GNG and more on ketosis for energy.

26
Q

What are the stages of starvation?

A

Stage 1: Low glucose situation (typically post meal) there is a rise in glucagon and drop in insulin levels..

Stage 2: 24 hours after last meal, fat is primary energy source. Liver breaks down fatty acids into ketone bodies. After a week the brain uses ketones for energy.

Stage 3: Fat reserves are depleted, proteins become primary source of energy and muscle rapidly deplete. Nonessential proteins are used up first.

27
Q

What happens to metabolism during stage 1 of starvation?

A

There is a rise in glycogen degradation. (glycogen phosphorylase activity increases)

There is a drop in glucose utilisation by muscle.

There is an increase in gluconeogenesis in the liver

There is an increase in triglyceride degradation in the liver and adipose tissue.

There is a decrease in fatty acid synthesis and increase in β-oxidation in adipose tissue and liver.

28
Q

What happens when glycogen is depleted? How does the brain get energy?

A

In the liver there is an elevated rate of GNG using lactate, glycerol, and amino acids

29
Q

What happens to metabolism during stage 3 of starvation?

A

Kidneys take over gluconeogenesis from the liver and once essential proteins are used up the essential proteins get used until eventually the cell function stops.

30
Q

What overall effect does stage 3 starvation have on the body?

A

Pancreas reduces insulin secretions

Metabolic rate is decreased

Many organs begin to shrink

Villi in gut shrink

Total body shutdown and death

31
Q

When does stage 2 of starvation end?

A

24 days later

32
Q

What cells in the body produce glucagon?

A

Alpha cells (islets of langerhans)

33
Q

What cells in the body produce insulin?

A

Beta cells (also islets of langerhans in the pancreas)

34
Q

Which cells produce somatostatin?

A

Delta cells (also islets of langerhans in the pancreas)

35
Q

How is insulin secreted in response to blood glucose?

A

Glucose enters beta-cells via GLUT2 and enters glycolysis -> ETC [ATP increases]

ATP binds ATP-gated K+ channels causing them to close. This results in plasma membrane depolarizing.

Depolarization triggers opening of Ca2+ channels which increases Ca2+ in the cytosol.

Increase in Ca2+ concentration triggers insulin release by exocytosis.

36
Q

How does insulin mature and get stored into vesicles?

A

24 AA-long signal sequence targets proinsulin to the ER where the storage vesicles form.

proinsulin is cleaved to release mature peptide.

Ca2+ activates proteases that cleave the C-peptide from proinsulin in the storage vesicles.

37
Q

How do we test for insulin levels?

A

Tests of insulin levels measure the C-peptide

38
Q

Is insulin’s half life short or long?

A

Short

39
Q

What does insulin look like?

A

alpha and beta chain bound together by disulfide bonds.

40
Q

How is insulin produced?

A

Initially folded into a long chain of protein with a signal sequence targetting it to the ER.

Signal sequence is cleaved off at the ER leaving proinsulin.

The loop is cleaved off to turn proinsulin into insulin + C-peptide.

41
Q

What kind of receptor is the insulin receptor?

A

A tyrosine kinase receptor. When insulin binds it causes autophosphorylation.

The activated receptor then phosphorylates intracellular proteins.

42
Q

What is the substrate for the insulin receptor (cytosolic side enzyme)?

A

Insulin receptor substrate (aka IRS-1)

43
Q

Where is GLUT1 located?

A

RBCs

44
Q

Where is GLUT2 located?

A

Liver

Islet beta cells

Low affinity for glucose high transport capacity

45
Q

Where is GLUT3 located?

A

Brain

46
Q

Where is GLUT4 located?

A

Muscle

Fat

Regulated by insulin

47
Q

What does insulin do to GLUT4 in muscle and fat?

A

Stimulates uptake and storage of glucose.

Insulin stimulates GLUT4 translocation to the plasma membrane through action of insulin and insulin stimulates fusion of GLUT4 vesicles with the plasma membrane.

When insulin levels fall GLUT4 transporters are recycled back into the cytoplasm.

48
Q

How are insulin effects reversed once the blood glucose has decreased?

A

Decreased blood glucose results in decreased insulin production and increased glucagon production changing flux through the 2 pathways is what’s important.

The relative levels determine what happens.

49
Q

What does glucagon do in cells?

A

Stimulates liver cells to hydrolyse glycogen to produce glucose

Stimulates lipolysis and usage of FA for energy supply

Decreases AA uptake in muscle

Increases AA uptake by liver which deaminates amino acids converting them to carbohydrates.

50
Q

Is glucagon a receptor tyrosine kinase?

A

No, it acts through cAMP

Presemester DENT (16 decks)

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