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Control of Metabolism Flashcards

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1
Q

eg of circulating nutrients?

A 
Glucose
Fatty acids (FA, free FA, non esterified FA)
AA
Ketone bodies
Lactate
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2
Q

eg of stored nutrients?

A

Glycogen
Triglycerides
Body proteins

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3
Q

What’s plasma glucose conc?

A

5 mmol L-1

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4
Q

What’s hypoglycemia?

A

plasma glucose conc<2.5 mmol L-1

critical ultimately coma and death

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5
Q

What’s hyperglycemia?

A

chronic exposure to raised glucose conc –> protein damage via non-enzymatic glycation

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6
Q

60/40/20 rule?

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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7
Q

How much glucose does 70kg male need?

A

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

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8
Q

How long does 70mmol glucose last?

A

Brain: ~ 30 mmol hr-1

Skeletal muscle: ~ 300 mmol hr-1

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9
Q

Sources of plasma glucose?

A

Diet

Organs that can export glucose into circulation

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10
Q

How much glucose is from diet?

A

up to 3000 mmol day-1

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11
Q

What prevents plasma glucose surging after a meal + plummeting between meals?

A

Hormones regulate the integration of carbohydrate, fat, protein metabolism to maintain constant plasma glucose levels

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12
Q

What are the 2 phases of metabolism?

A
  • Storage of nutrients in absorptive phase (fed state)

- Release of nutrients in fasting phase (between meals)

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13
Q

Role of insulin?

A

promotes storage, decreases plasma glucose

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14
Q

eg of anabolic hormone

A

insulin

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15
Q

What are counter-regulatory hormones + eg?

A

promote nutrient release, raise plasma glucose
Glucagon
A
Cortisol, growth hormone (somatotrophin)

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16
Q

Effects of insulin?

A

-Stimulates nutrient storage:
Glucose uptake by skeletal muscle, adipose tissue
Glycogen synthesis in liver, skeletal muscle
FA + AA uptake
-Inhibits nutrient release:
Inhibits hepatic glucose production
Inhibits lipolysis+proteolysis

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17
Q

Effect of glucagon?

A

Stimulates hepatic glucose production

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18
Q

Effect of Adrenaline?

A

Stimulates hepatic glucose production + lipolysis

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19
Q

What’s lipolysis?

A

release of FA from TG breakdown from adipose tissue stores

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20
Q

Effect of growth hormone?

A

Stimulates hepatic glucose production + lipolysis

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21
Q

Effect of cortisol?

A

Stimulates hepatic glucose production, lipolysis, proteolysis

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22
Q

What’s proteolysis?

A

release of AA from body proteins (skeletal muscle)

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23
Q

Describe how excess carbohydrate is converted into fat?

A
  • glucose taken out of circulation
  • converted into glycogen for energy storage
  • when glycogen stores are full
  • excess glucose is converted to acetyl coA
  • then fed into lipogenesis to synthesise new FA
  • FA not oxidised for energy so converted to TG for energy storage
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24
Q

Metabolic pathways serving energy storage?

A

Glycogenesis
Lipogenesis
Triglyceride synthesis

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25
What's glycogenesis?
Synthesis of glycogen from glucose
26
What's lipogenesis?
Synthesis of FA from acetyl CoA
27
What's triglyceride synthesis?
Esterification of FA for storage as TG
28
Metabolic pathways serving energy release
``` Glycogenolysis Gluconeogenesis Lipolysis Beta-oxidation Ketogenesis ```
29
What's glycogenolysis
Release of glucose from glycogen stores
30
What's gluconeogenesis
synthesis of glucose from non-carbohydrate substrates
31
What's beta-oxidation
FA to acetyl coA
32
What's ketogenesis?
Production of ketone bodies from acetyl coA
33
Why ketogenesis?
- fasting - FA converted to ketone bodies via beta oxidation - so brain uses energy stored as fat - brain cannot metabolize FA but can metabolize ketone bodies - so partial substitute for glucose
34
Immediate response to hypoglycemia?
Drop in plasma glucose detected in pancreas + brainstem cells: - turn up rate of glucagon secretion from pancreatic α cells + inhibit insulin secretion - sympathetic outflow to directly stimulate liver, adrenal glands, pancreas to increase further glucagon output, stimulate hepatic glucose production
35
Short term defence against hypoglycemia?
Glucagon Adrenaline Sympathetic NS
36
Medium term defence against hypoglycemia?
Ketogenesis : fat reserves are a substitute for glucose, sparing muscle
37
Long term defence against hypoglycemia?
Cortisol stimulates proteolysis to supply amino acid substrates for gluconeogenesis
38
Defences against hyperglycaemia?
Insulin : Stimulates glucose uptake by tissues Inhibits hepatic glucose production
39
What's type 1 DM?
insulin deficiency
40
What's type 2 DM?
insulin insufficiency combined with insulin resistance
41
Major insulin sensitive tissues?
liver, skeletal muscle, adipose tissue
42
Flexible uses of glucose?
- glucose uptake via GLUT - energy, glycolysis, TCA - beyond energy needs, glycogenesis - glycogen stores full, lipogenesis
43
Role of chylomicrons?
carry absorbed digested fat from gut + can transport to liver, adipose tissue
44
How are transported fats broken down?
at endothelial membrane by lipoprotein lipase
45
How are TAGs (VDLP/chylomicrons) broken down?
at endothelial membrane by lipoprotein lipase
46
Describe absorptive state
- blood glucose rising - enters cells via GLUT - glucose phosphorylated to maintain diffusion gradient - G6P into glycolysis ->pyruvate -> ACoA -> TCA - most G6P -> glycogen (glycongenesis) - G6P -> FA (lipogenesis) - FA stored as fat
47
Describe absorptive state
- blood glucose rising - enters cells via GLUT (stimulated by insulin) - glucose phosphorylated to maintain diffusion gradient - G6P into glycolysis ->pyruvate -> ACoA -> TCA - most G6P -> glycogen (glycongenesis) - G6P -> FA (lipogenesis) - FA stored as TAG
48
Describe post-absorptive state
-blood glucose low -insulin release reduced -glucagon released -glycogen -> G6P via glycogenolysis -in liver G6P dephosphorylated -> glucose which diffuses into circulation (stimulated by glucagon) -gluconeogenesis : glycerol -> glucose AA -> glucose via pyruvate
49
How TAGs enter adipocytes?
- TAGS -> FA by lipoprotein lipase - FA diffuse into adipocyte (insulin stimulated) - FA -> TAGs in adipocyte
50
How glucose enters adipocytes?
- GLUT4 on adipocyte membrane (insulin dependent) - glucose -> FA via lipogenesis - FA esterified -> stored as TAG
51
Effect Adrenaline on adipocytes?
promotes breakdown of TAG in adipocytes -> free FA + glycerol exported into circulation
52
Describe metabolic pathway in muscle?
- glucose enters via GLUT4 - glucose phosphorylated to maintain diffusion gradient - G6P into glycolysis -> pyruvate -> TCA - anaerobic : pyruvate -> lactate diffuses into blood and go to liver -> fed into gluconeogenesis - FA can be fed into TCA cycle.
53
Describe how to burn long term fat stores?
- mobilise fats from lipid reserves - TAGs transported in VLDLs to muscle - TAGs -> FA by lipoprotein lipase - FA -> ACoA -> TCA via beta oxidation
54
Role of oxaloacetate?
- Oxidation of ACoA (produced by beta oxidation) to enter TCA - Oxaloacetate to phosphoenol pyruvate for gluconeogenesis
55
Describe ketogenesis
- competition for oxaloacetate between liver FA oxidation + glucongeogenesis - build up of ACoA from liver FA oxidation - ACoA cannot enter Krebs until there's oxaloacetate molecule to bind with - so ACoA -> ketone bodies - ketone bodies enter circulation - used by muscle + brain where reconverted -> ACoA -> Krebs -> energy
56
eg of ketone bodies?
acetoacetate, 3-hydroxybutyrate, acetone
57
Benefit of ketogenesis?
- Reduces demand for AA for gluconeogenesis - Reduces protein breakdown - Conserve limited glucose for brain (when low glucose)
58
Describe FA metabolism in liver?
- glucose -> ACoA - ACoA into mitochondria to cytosol for lipogenesis - 1st step malonyl coA which inhibits beta-oxidation + promotes lipogenesis pathway - beta-oxidation occurs in absence of insulin - produces acetyl coA -> krebs - in excess will undergo ketogenesis
59
What's the lipogenesis pathway?
synthesis of FA which can then be converted into TAG and exported as VLDLs
60
Fate of FA in liver?
- Esterified for transport + storage as TG | - Enter mitochondria for beta-oxidation
61
Describe what happens when FA enters mitochondria for beta-oxidation?
Produces ACoA: - enter TCA cycle OR - enter ketogenesis depending on nutritional / hormonal status
62
How ketone bodies can cause metabolic acidosis?
- liver oxidation of FA + gluconeogenesis competes for substrates - beta-oxidation of FA produces ACoA - ACoA + oxaloacetate = citrate - citrate enters TCA for complete oxidative phosphorylation - oxaloacetate used as a substrate in gluconeogenesis too - insufficient oxaloacetate - ACoA builds up --> ketogenesis - ketone bodies are acids so excess in circulation overwhelm buffering capacity of blood - metabolic acidosis
63
How diabetic ketoacidosis occurs in DM 1?
- lack of insulin - gluconeogenesis occurs - using oxaloacetate there's beta oxidation - FA -> ACoA - build up of ACoA - ketogenesis --> ketone bodies. - lower blood pH - buffering system is overwhelmed - diabetic ketoacidosis.
64
Metabolic disturbances in DM 1?
-hyperglycemic, because glucose absorbed from the gut is not taken up by the tissues (as this is an insulin dependent process, so accumulates in blood) -simultaneously body making glucose by gluconeogenesis due to lack of insulin -increase in blood sugar -osmotic problems: *Glycosuria : glucose filtrated from blood into tubule, usually it would be reabsorbed but the glucose concentrations are higher than the capacity for reabsorption -> glucose in urine. *Osmotic diuresis : high osmolarity in tubule means less water reabsorption -> dehydration -> polyurea, thirst *Kidney impairment : can't excrete H+ --> acidosis -> adds to problem of ketoacidosis = Coma and Death

ENDO (10 decks)

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