Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrinology > Endocrine Control of Metabolism > Flashcards

Endocrine Control of Metabolism Flashcards

1
Q

How is ATP obtained in the body?

A

ATP can’t be stored - is made as needed via anaerobic and aerobic metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Outline the anaerobic production of ATP

A

Anaerobic metabolism:
Glycolysis: Glucose → pyruvate
Gain 2 ATP for every 1 Glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Outline the aerobic ATP production

A

Aerobic Metabolism:
tcA: Pyruvate → Acetyl CoA in mt. enters tca
1 tca = 30~ ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name the major circulating nutrients in the body used for energy metabolism

A 
Glucose - anaerobic glycolysis 
Fatty acids (FFA, NEFA) - β oxidation (FA → Acetyl CoA)
Amino acids 
Ketone bodies
Lactate

These can be full oxidised to yield energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the stored nutrients of the body?

A

Glycogen
Triglycerides (TG, TAG)
Body proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the normal plasma [glucose]?

A

Plasma [glucose] is constant around 5 mmol L-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the significance of a constant plasma [glucose]?

A

Brain function depends on glucose metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the consequence of too low BGL?

A

Hypoglycemia: ultimately coma and death

< ~2.5 mmol L-1 is critical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What [glucose] is critically classed as too low?

A

< ~2.5 mmol L-1 is critical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What effect does a high BGL have?

A

Hyperglycemia: chronic exposure to raised glucose concentrations leads to protein damage via non-enzymatic glycation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the body’s water content

A

60% of body weight is water
40% of body weight is intracellular water
20% of body weight is extracellular water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the approximate blood glucose of a 70kg male?

A

70 kg male, 14 L extracellular water gives total of 14x5 = 70 mmol glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How much glucose is required for the brain to continue functioning?

A

Brain: ~ 30 mmol hr -1 required to continue working

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How much glucose does skeletal muscle require?

A

Skeletal muscle: ~ 300 mmol hr -1 varies upon activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the 2 sources of plasma glucose?

A

Diet : up to 3000 mmol day-1

Organs that can export glucose into the circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is BGL kept constant even before and after meals?

A

Hormones regulate integration of carbohydrate, fat + protein metabolism to maintain constant plasma [glucose] - prevents plasma [glucose] surging after a meal and plummeting between meals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 2 phases of glucose metabolism?

A

Absorptive

Fasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the absorptive phase of glucose metabolism

A

Storage of nutrients in the absorptive phase (fed state)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the fasting state of glucose metabolism?

A

Release of nutrients in the fasting phase (between meals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the role of hormones on glucose metabolism?

A

Hormones regulate metabolic pathways promoting energy storage or release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the role of insulin on glucose metabolism?

A

Insulin: promotes storage, decreases plasma glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the effects of counter-regulatory hormones on glucose metabolism?

A

promote nutrient release, raise plasma glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name examples of counter-regulatory hormones

A

Glucagon
Adrenaline (epinephrine)
Cortisol, growth hormone (somatotrophin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does insulin promote nutrient storage?

A

Uptake of glucose by skeletal muscle, adipose and other tissues
Glycogen synthesis in liver, skeletal muscle,
Uptake of FA and amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does insulin inhibit nutrient release?

A

Inhibits release of glucose from liver (hepatic glucose production)
Inhibits fat and protein breakdown (lipolysis and proteolysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the effects of glucagon on BGL?

A

Principal effects in liver
Stimulates hepatic glucose production (glycogen breakdown → glucose) and (gluconeogenesis - synthesising glucose from non-carbs e.g.. a.a.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How does adrenaline counter regulate glucose?

A

Adrenaline (and sympathetic NS)
Stimulates hepatic glucose production
Stimulates lipolysis: release of FA from adipose tissue stores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the effect of growth hormone on glucose metabolism?

A

Stimulates hepatic glucose production

Stimulates lipolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the counter regulatory effects of cortisol on glucose metabolism

A

Stimulates hepatic glucose production

Stimulates proteolysis: release of amino acids from body proteins (skeletal muscle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Which metabolic pathways lead to energy release?

A 
Gluconeogenesis
Lipolysis
Ketogenesis 
Beta-oxidation
Glycogenolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is Ketogenesis ?

A

Production of ketone bodies from Acetyl CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Explain how Beta-oxidation releases energy

A

FA to Acetyl Co A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is Lipolysis?

A

Release of FA from TG breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Explain how Gluconeogenesis contributes to energy release

A

De novo synthesis of glucose from non-carbohydrate substrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is Glycogenolysis?

A

Release of glucose from glycogen stores

36
Q

How does metabolism respond to hypoglycemia during a positive energy balance?

A

In times of positive energy balance, insulin stimulates uptake (LPL, GLUT4)

37
Q

Explain the response of metabolism to hypoglycemia during a negative energy balance

A

In times of negative, counter-regulatory hormones stimulate lipolysis and release of FFA to circulation, where they bind to plasma proteins and distributed to tissues for uptake and energy metabolism

38
Q

Where are insulin and glucose secreted from?

A

secretory cells of Islets of Langerhans in pancreas

39
Q

How do the secretory cells respond to ↓plasma [glucose]?

A

↓plasma [glucose] sensed directly by
secretory cells :
- ↑glucagon secretion
- ↓insulin secretion

40
Q

How does the CNS respond to ↓plasma [glucose]?

A

Brainstem detects low plasma [glucose] provoking sympathetic response

  • Stimulates adrenal glands; release adrenaline
  • Direct stimulation of pancreas; release glucagon
  • Direct stimulation of liver; ↑ hepatic glucose output
41
Q

What are the short term responses to hypoglycemia?

A

Release of:
Glucagon
Epinephrine
Sympathetic NS

42
Q

What is the medium term response to hypoglycemia?

A

Ketogenesis
fat reserves provide a partial substitute for glucose, sparing muscle tissue from destruction that would otherwise be needed to provide amino acid substrates for gluconeogenesis

43
Q

What is the long term response to hypoglycemia?

A

Cortisol stimulates proteolysis to supply amino acid substrates for gluconeogenesis

44
Q

What is the defence against hyperglycemia?

A

Insulin

45
Q

How does insulin counteract hyperglycemia?

A

Stimulates glucose uptake by tissues

Inhibits hepatic glucose production

46
Q

What is the consequence of lack of insulin action against hyperglycemia?

A

Lack of insulin action leads to hyperglycemia, diabetes melitus
- Type 1 DM: insulin deficiency
- Type 2 DM: insulin insufficiency combined with insulin
resistance

47
Q

What effect does insulin have on the liver?

A

In the liver Insulin stimulates:

  • Glycogenesis
  • Glycolysis
  • lipogenesis

insulin inhibits:

  • Glycogenolysis
  • gluconeogenesis
48
Q

What does insulin stimulate within adipose tissue?

A

Glucose uptake
Free fatty acid uptake
Lipogenesis

49
Q

What are the effects of insulin on muscle?

A

glucose uptake
amino acid uptake
glycogenesis

50
Q

Which processes does insulin inhibit within adipose tissue?

A

Lipolysis

51
Q

How does glucose enter cells within the body?

A

Glucose enters cell from interstitial fluid via GLUTs (some are insulin dependent)

52
Q

How does glucose enter hepatocytes?

A

Liver cells contain GLUT2 receptors which aren’t insulin dependent

53
Q

How is a [glucose] gradient maintained within hepatocytes?

A

Glucose diffuses down [ ] gradient into hepatocytes and is immediately converted to G6P due to insulin presence - maintains [ ] gradient

54
Q

What is the fate of Glucose (G6P) in hepatocytes?

A

G6P undergoes glycolysis → pyruvate / a. coA → lipolysis to fat or tca for ATP
G6P can also be converted to glycogen via glycogenolysis

55
Q

Why can’t all the glucose metabolised be stored as glycogen?

A

(Liver) glycogen stores have a certain capacity

56
Q

How does liver regulate [glucose] in absence of insulin?

A

In the absence of insulin, gluconeogenesis occurs to generate G6P from other substances

57
Q

Why is the transport of lipids more complex?

A

Lipids = insoluble

usually require esterification to pass in and out of cells and structures

58
Q

What is the fate of lipids from the diet?

A

Digestion:
Pancreatic lipases; breakdown of complex fats → FFA
FFA taken up; packaged into chylomicrons

59
Q

What role does the liver play in FA synthesis?

A

New FA synthesised in liver via lipogenesis packaged into VLDL

60
Q

What are chylomicrons and VLDL?

A

VLDL and chylomicrons are circulating TGs in blood

61
Q

What is the role of lipoproten lipase?

A

Lipoprotein lipase needed for uptake of fats into tissues for either energy metabolism or storage

62
Q

How are fats stored in adipocytes?

A

Chylomicrons taken into adipocytes via lipoprotein lipase which hydrolyses them into FFA stimulated by insulin.
FA re-esterified into TGs for storage

63
Q

What is the fate of excess glucose in circulation?

A

Excess glucose in circulation taken up via GLUT4 and undergoes lipogenesis → FA → esterified for storage

64
Q

What stimulates the uptake of glucose into muscles?

A

Glucose stimulates glucose uptake into muscles via GLUT4

Can be oxidised for energy

65
Q

What is the fate of excess glucose in muscles?

A

If in excess can be stored as muscle glycogen

*muscle glycogen is a private store for muscle only as muscle lacks enzyme that converts G6P → Glucose for export

66
Q

What is the significance of insulin in glucose uptake into muscles?

A

Insulin important for glucose uptake in skeletal muscle

GLUT4 won’t be inserted into membrane in absence of insulin = muscle insulin resistance

67
Q

What physiological activity stimulates glucose uptake into muscles?

A

exercise

68
Q

How do the pancreatic hormones affect gluconeogenesis?

A

Gluconeogenesis stimulated by glucagon, inhibited by insulin

69
Q

What is the significance of glycerol?

A

Glycerol is backbone of lactate and TGs

70
Q

What is the fate of glycerol?

A

Glycerol → glucose via Gluconeogenesis

71
Q

What is the fate of amino acids in the absence of insulin?

A

Amino acids in absence of insulin enter ketogenesis or gluconeogenesis depending on a.a.

72
Q

What is the fate of ketogenic amino acids?

A

A.a. → acetyl Coa if ketogenic

73
Q

Describe what happens to glucogenic amino acids in the absence of insulin?

A

A.a. → pyruvate / tca intermediate if glucogenic
Then undergo Gluconeogenesis → Phosphophenol pyruvate → G6P dephosphorylated in liver so glucose can be exported
Inhibited by insulin

74
Q

what stimulates lipogenesis?

A

If glucagon low or insulin high stimulates lipogenesis

75
Q

What is fatty acid metabolism dependent on?

A

Β oxidation / lipogenesis depend on glucagon and insulin

76
Q

What happens to fatty acids in the liver?

A

FA → *fatty acyl CoA

*has to enter mt. via CPT to be converted to Acetyl CoA

77
Q

What is the fate of fatty acids once in the mitochondria?

A

Once in mt. can undergo oxidation for energy release

Or excess undergoes ketogenesis into ketone bodies

78
Q

What is the effect of insulin on fatty acid metabolism?

A

In insulin presence - acetyl CoA undergoes lipogenesis → malonyl coA
Β oxidation is inhibited in insulin presence

79
Q

What is the use of ketone bodies in the body?

A

Freely transported in blood, reconverted back to acetyl CoA, in brain + other tissues, and metabolised in TCA cycle for energy

80
Q

What is the consequence of insufficient insulin to regulate fatty acid metabolism and gluconegeonesis?

A

In the liver, oxidation of fatty acids and gluconeogenesis can compete for substrates

81
Q

What are the products of Beta-oxidation of FA?

A

Beta-oxidation of FA produces acetyl Co A, which combines with oxaloacetate (OAA) to form citrate, entering the TCA cycle for complete oxidative phosphorylation

82
Q

As well as beta-oxidation of FA, where else is oxaloacetate used in the liver?

A

OAA is also used as a substrate in gluconeogenesis

83
Q

What is the consequence of insufficient OAA?

A

In absence of sufficient OAA, acetyl Co A builds up and is funnelled into ketogenesis

84
Q

What is the effect of excess ketogenesis?

A

Ketone bodies are acids: excess in circulation overwhelm buffering capacity of blood, leading to metabolic acidosis

85
Q

What is the effect of insulin on liver metabolism?

A

Insulin inhibits beta oxidation and ketogenesis

86
Q

What is the consequence of Diabetic Ketoacidosis?

A

Normally ketones (acids) are buffered by blood

Insulin deficiency (type 1 diabetes mellitus) buffering capacity is overwhelmed
~ decreased serum bicarbonate
~ diabetic ketoacidosis
~ deep sighing (Kussmaul) respiration

87
Q

Explain how insufficient insulin leads to acidosis?

A

(insulin not working/ not present) -> accumulation of acetyl Coa and not enough oxaloacetate to keep up and combine with it for tca

Build up of acetyl CoA → excess ketogenesis can lead to increased [ketone bodies]

Normally these can be metabolised but excess leads to acidosis which occurs during diabetic acidosis

Endocrinology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions