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Endocrinology > Endocrine Control of Metabolism > Flashcards

Endocrine Control of Metabolism Flashcards

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1
Q

How is ATP obtained in the body?

A

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

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2
Q

Outline the anaerobic production of ATP

A

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

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3
Q

Outline the aerobic ATP production

A

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

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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

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5
Q

What are the stored nutrients of the body?

A

Glycogen
Triglycerides (TG, TAG)
Body proteins

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6
Q

What is the normal plasma [glucose]?

A

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

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7
Q

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

A

Brain function depends on glucose metabolism

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8
Q

What is the consequence of too low BGL?

A

Hypoglycemia: ultimately coma and death

< ~2.5 mmol L-1 is critical

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9
Q

What [glucose] is critically classed as too low?

A

< ~2.5 mmol L-1 is critical

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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

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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

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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

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13
Q

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

A

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

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14
Q

How much glucose does skeletal muscle require?

A

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

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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

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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

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17
Q

What are the 2 phases of glucose metabolism?

A

Absorptive

Fasting

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18
Q

Describe the absorptive phase of glucose metabolism

A

Storage of nutrients in the absorptive phase (fed state)

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19
Q

What is the fasting state of glucose metabolism?

A

Release of nutrients in the fasting phase (between meals)

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20
Q

What is the role of hormones on glucose metabolism?

A

Hormones regulate metabolic pathways promoting energy storage or release

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21
Q

What is the role of insulin on glucose metabolism?

A

Insulin: promotes storage, decreases plasma glucose

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22
Q

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

A

promote nutrient release, raise plasma glucose

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23
Q

Name examples of counter-regulatory hormones

A

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

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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

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25
How does insulin inhibit nutrient release?
Inhibits release of glucose from liver (hepatic glucose production) Inhibits fat and protein breakdown (lipolysis and proteolysis)
26
What are the effects of glucagon on BGL?
Principal effects in liver Stimulates hepatic glucose production (glycogen breakdown → glucose) and (gluconeogenesis - synthesising glucose from non-carbs e.g.. a.a.)
27
How does adrenaline counter regulate glucose?
Adrenaline (and sympathetic NS) Stimulates hepatic glucose production Stimulates lipolysis: release of FA from adipose tissue stores
28
what is the effect of growth hormone on glucose metabolism?
Stimulates hepatic glucose production | Stimulates lipolysis
29
Describe the counter regulatory effects of cortisol on glucose metabolism
Stimulates hepatic glucose production | Stimulates proteolysis: release of amino acids from body proteins (skeletal muscle)
30
Which metabolic pathways lead to energy release?
``` Gluconeogenesis Lipolysis Ketogenesis Beta-oxidation Glycogenolysis ```
31
What is Ketogenesis ?
Production of ketone bodies from Acetyl CoA
32
Explain how Beta-oxidation releases energy
FA to Acetyl Co A
33
What is Lipolysis?
Release of FA from TG breakdown
34
Explain how Gluconeogenesis contributes to energy release
De novo synthesis of glucose from non-carbohydrate substrates
35
What is Glycogenolysis?
Release of glucose from glycogen stores
36
How does metabolism respond to hypoglycemia during a positive energy balance?
In times of positive energy balance, insulin stimulates uptake (LPL, GLUT4)
37
Explain the response of metabolism to hypoglycemia during a negative energy balance
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
Where are insulin and glucose secreted from?
secretory cells of Islets of Langerhans in pancreas
39
How do the secretory cells respond to ↓plasma [glucose]?
↓plasma [glucose] sensed directly by secretory cells : - ↑glucagon secretion - ↓insulin secretion
40
How does the CNS respond to ↓plasma [glucose]?
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
What are the short term responses to hypoglycemia?
Release of: Glucagon Epinephrine Sympathetic NS
42
What is the medium term response to hypoglycemia?
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
What is the long term response to hypoglycemia?
Cortisol stimulates proteolysis to supply amino acid substrates for gluconeogenesis
44
What is the defence against hyperglycemia?
Insulin
45
How does insulin counteract hyperglycemia?
Stimulates glucose uptake by tissues | Inhibits hepatic glucose production
46
What is the consequence of lack of insulin action against hyperglycemia?
Lack of insulin action leads to hyperglycemia, diabetes melitus - Type 1 DM: insulin deficiency - Type 2 DM: insulin insufficiency combined with insulin resistance
47
What effect does insulin have on the liver?
In the liver Insulin stimulates: - Glycogenesis - Glycolysis - lipogenesis insulin inhibits: - Glycogenolysis - gluconeogenesis
48
What does insulin stimulate within adipose tissue?
Glucose uptake Free fatty acid uptake Lipogenesis
49
What are the effects of insulin on muscle?
glucose uptake amino acid uptake glycogenesis
50
Which processes does insulin inhibit within adipose tissue?
Lipolysis
51
How does glucose enter cells within the body?
Glucose enters cell from interstitial fluid via GLUTs (some are insulin dependent)
52
How does glucose enter hepatocytes?
Liver cells contain GLUT2 receptors which aren't insulin dependent
53
How is a [glucose] gradient maintained within hepatocytes?
Glucose diffuses down [ ] gradient into hepatocytes and is immediately converted to G6P due to insulin presence - maintains [ ] gradient
54
What is the fate of Glucose (G6P) in hepatocytes?
G6P undergoes glycolysis → pyruvate / a. coA → lipolysis to fat or tca for ATP G6P can also be converted to glycogen via glycogenolysis
55
Why can't all the glucose metabolised be stored as glycogen?
(Liver) glycogen stores have a certain capacity
56
How does liver regulate [glucose] in absence of insulin?
In the absence of insulin, gluconeogenesis occurs to generate G6P from other substances
57
Why is the transport of lipids more complex?
Lipids = insoluble | usually require esterification to pass in and out of cells and structures
58
What is the fate of lipids from the diet?
Digestion: Pancreatic lipases; breakdown of complex fats → FFA FFA taken up; packaged into chylomicrons
59
What role does the liver play in FA synthesis?
New FA synthesised in liver via lipogenesis packaged into VLDL
60
What are chylomicrons and VLDL?
VLDL and chylomicrons are circulating TGs in blood
61
What is the role of lipoproten lipase?
Lipoprotein lipase needed for uptake of fats into tissues for either energy metabolism or storage
62
How are fats stored in adipocytes?
Chylomicrons taken into adipocytes via lipoprotein lipase which hydrolyses them into FFA stimulated by insulin. FA re-esterified into TGs for storage
63
What is the fate of excess glucose in circulation?
Excess glucose in circulation taken up via GLUT4 and undergoes lipogenesis → FA → esterified for storage
64
What stimulates the uptake of glucose into muscles?
Glucose stimulates glucose uptake into muscles via GLUT4 | Can be oxidised for energy
65
What is the fate of excess glucose in muscles?
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
What is the significance of insulin in glucose uptake into muscles?
Insulin important for glucose uptake in skeletal muscle | GLUT4 won’t be inserted into membrane in absence of insulin = muscle insulin resistance
67
What physiological activity stimulates glucose uptake into muscles?
exercise
68
How do the pancreatic hormones affect gluconeogenesis?
Gluconeogenesis stimulated by glucagon, inhibited by insulin
69
What is the significance of glycerol?
Glycerol is backbone of lactate and TGs
70
What is the fate of glycerol?
Glycerol → glucose via Gluconeogenesis
71
What is the fate of amino acids in the absence of insulin?
Amino acids in absence of insulin enter ketogenesis or gluconeogenesis depending on a.a.
72
What is the fate of ketogenic amino acids?
A.a. → acetyl Coa if ketogenic
73
Describe what happens to glucogenic amino acids in the absence of insulin?
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
what stimulates lipogenesis?
If glucagon low or insulin high stimulates lipogenesis
75
What is fatty acid metabolism dependent on?
Β oxidation / lipogenesis depend on glucagon and insulin
76
What happens to fatty acids in the liver?
FA → *fatty acyl CoA | *has to enter mt. via CPT to be converted to Acetyl CoA
77
What is the fate of fatty acids once in the mitochondria?
Once in mt. can undergo oxidation for energy release | Or excess undergoes ketogenesis into ketone bodies
78
What is the effect of insulin on fatty acid metabolism?
In insulin presence - acetyl CoA undergoes lipogenesis → malonyl coA Β oxidation is inhibited in insulin presence
79
What is the use of ketone bodies in the body?
Freely transported in blood, reconverted back to acetyl CoA, in brain + other tissues, and metabolised in TCA cycle for energy
80
What is the consequence of insufficient insulin to regulate fatty acid metabolism and gluconegeonesis?
In the liver, oxidation of fatty acids and gluconeogenesis can compete for substrates
81
What are the products of Beta-oxidation of FA?
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
As well as beta-oxidation of FA, where else is oxaloacetate used in the liver?
OAA is also used as a substrate in gluconeogenesis
83
What is the consequence of insufficient OAA?
In absence of sufficient OAA, acetyl Co A builds up and is funnelled into ketogenesis
84
What is the effect of excess ketogenesis?
Ketone bodies are acids: excess in circulation overwhelm buffering capacity of blood, leading to metabolic acidosis
85
What is the effect of insulin on liver metabolism?
Insulin inhibits beta oxidation and ketogenesis
86
What is the consequence of Diabetic Ketoacidosis?
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
Explain how insufficient insulin leads to acidosis?
(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)

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