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BIOC192 2024 > Lecture 31 > Flashcards

Lecture 31 Flashcards

1
Q

What is metabolic homeostasis

A

The body’s ability to maintain various metabolic processes to ensure molecules essential for life are kept at an optimal level

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2
Q

What does metabolic homeostasis require?

A

The interplay of the digestive system, endocrine system, nervous system and many different signal transduction events

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3
Q

What is the preferred fuel type for the brain?

A

Glucose but can use ketone bodies as well

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4
Q

What is the preferred fuel type for skeletal muscle?

A

Fatty acids, however, can use all especially when exercising

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5
Q

What does skeletal muscle store and export?

A

Stores glycogen
Exports lactate and alanine

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6
Q

What is the preferred fuel type for cardiac muscle?

A

Fatty acids

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7
Q

What is the preferred fuel type for the adipose tissue?

A

Fatty acids

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8
Q

What fuel is stored in and transported from adipose tissue?

A

Stores triacylglycerols
Exports fatty acids and glycerol

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9
Q

What is the preferred fuel type for the liver?

A

Amino acids, glucose and fatty acids

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10
Q

What fuel is stored in and exported from the liver?

A

Stores glycogen
Exports triacylglycerols, glucose, ketone bodies

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11
Q

What is the prefered fuel for RBCs and why?

A

Glucose as RBCs lack mitochondria for any other metabolic pathway to occur

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12
Q

What fuel is exported from RBCs?

A

Lactate

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13
Q

Why can the brain not use FAs?

A

They cannot cross the blood-brain barrier

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14
Q

What is insulin?

A

A peptide hormone synthesised in and secreted by the pancreatic beta cells in response to high blood glucose levels

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15
Q

What does insulin do?

A

Acts on the liver, muscle and adipose tissues to promote glucose transport into cells to be used for energy or stored as glycogen

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16
Q

What happens to the body without insulin?

A

It starves

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17
Q

What is type 1 diabetes?

A

An early onset form of diabetes, diagnosed by symptoms, blood glucose and glycated haemoglobin

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18
Q

What are common symptoms of diabetes?

A

Glycosuria (glucose in urine) and the presence of ketones in the blood

19
Q

What causes type 1 diabetes?

A

An autoimmune condition leading to the loss of pancreatic beta cells and therefore no insulin secretion

20
Q

What is preproinsulin?

A

Initial form of insulin synthesised from transcription and translation in the ER, containing the A-chain, B-chain, C-peptide, and a signal sequence

21
Q

What is the signal sequence?

A

A chain that helps direct the protein into the ER but is removed by signal peptidase, leaving proinsulin

22
Q

What is proinsulin?

A

The A-chain, B-chain, and C-peptide of insulin. It is folded and stabilised by disulfide bonds and moves to the Golgi and is packaged into secretory granules. Proprotein convertase enzymes in the granules cleave proinsulin to release active insulin (A-chain and B-chain) and C-peptide.

23
Q

What is the C-peptide?

A

A chain released during the cleavage of proinsulin along with insulin, has a longer half-life than insulin and can be used as a marker of insulin secretion

24
Q

What is the c-peptide important for?

A

Distinguishing between endogenous insulin and exogenous insulin

25
Q

How does glucose stimulate insulin secretion from beta-cells?

A

GLUT1 transports glucose into pancreatic beta cells, glucose is metabolised via glycolysis and the CAC to increase ATP levels. Increased ATP:ADP ratio inhibits ATP-gated K+ channels triggering membrane depolarisation and the opening of voltage-gated Ca2+ channels. The calcium influx induces exocytosis of insulin-containing secretory vesicles

26
Q

When are glucose levels the highest?

A

About an hour after eating

27
Q

When are insulin levels the highest?

A

About two hours after eating

28
Q

What is the incretin effect?

A

The phenomenon where oral glucose intake stimulates a greater insulin response compared to an equivalent amount of glucose administered intravenously

29
Q

Why does oral insulin work better?

A

Due to the action of gut-derived hormones; GLP-1

30
Q

Why does insulin have to be taken intravenously?

A

Gets broken down in GI tract

31
Q

What is GLP-1 in the L-cells of the intestine an example of?

A

A different way of processing the same protein (similar to insulin)

32
Q

What is GLP-1?

A

A peptide hormone that is synthesised in the intestine in response to nutrient arrival.

33
Q

What is GLP-1 made from?

A

Glucagon via convertase enzyme

34
Q

What does GLP-1 do?

A

Acts through its receptor (GLP-1R) to stimulate insulin secretion

35
Q

How is GLP-1 used to treat type 2 diabetes?

A

Agonists are developed

36
Q

How does GLP-1 promote weight loss?

A

Slows gastric emptying and reduces appetite

37
Q

What is GLUT4?

A

An insulin-regulated glucose transporter into fat and muscle cells

38
Q

Where is GLUT4 found in muscle and adipose cells?

A

Intracellular storage vesicles called GSV vesicles

39
Q

What happen when insulin binds to its receptor?

A

A phosphorylation cascade is activated that regulates the trafficking of GLUT4 vesicles to the plasma membrane by regulating vesicle trafficking proteins

40
Q

What does AS160 do?

A

‘Regulates a GTPase protein Rab10 which is involved in the trafficking of vesicles’ (on the slide)

It binds to the GSV vesicle preventing it from moving to the plasma membrane to allow glucose into the cells. AKT phosphorylates it, releasing it from GSV

41
Q

What is IRS?

A

Insulin receptor substrate

42
Q

What is PIP2 and PIP3?

A

Membrane phospholipids

43
Q

What is the insulin receptor an example of?

A

A tyrosine kinase receptor

44
Q

What is the difference between GLUT1 and GLUT4?

A

GLUT1 is found on pancreatic beta cells and is NOT sensitive to insulin, it allows facilitative diffusion of glucose into beta-cells

GLUT4 is found in skeletal muscle and adipose tissue, its expression is regulated by insulin and it allows facilitative diffusion of glucose into muscle and adipose cells

BIOC192 2024 (36 decks)

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