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ESS1606 Nutrition and metabolism > Carbohydrate metabolism > Flashcards

Carbohydrate metabolism Flashcards

1
Q

glucose uptake

A

into tissues - used for energy in brain

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2
Q

glycogen synthesis

A

triglycerides in adipose tissue

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3
Q

glycogen breakdown

A

glycogenolysis

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4
Q

glycolysis

A

glucose breakdown

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5
Q

gluconeogenesis

A

lactate from liver used

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6
Q

the pancreas

A
  • Secretes hormone insulin into blood in response to an increase in blood glucose
  • Exocrine - release digestive enzymes into ducts
  • Endocrine - hormones - Islets of Langerhans - released into blood stream
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7
Q

what happens when glucose is in the blood?

A

• Some glucose taken up by liver via facilitated transport (uptake) - regulate gluc absorption
• Insulin activates hexokinase (glucokinase) to store glucose as glycogen (glycogen synthesis)
• Liver hexokinase reaction reversible so glucose can also leave liver cell (glycogenolysis and gluconeogenesis) to maintain blood glucose
- Use when not taking carb in diet

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8
Q

why do we need to maintain blood glucose?

A

• Glucose primary fuel source of brain cells (glycolysis), as well as turnover and neurotransmitter synthesis
• 2% of body weight, but consumes 20% of glucose, making it main consumer of glucose for body weight (6 mg/100 g tissue/min or 100-150 g/day)
• Normal diet 300 g/day, and liver stores around 100 g/day
- Astrocytes
- Not regulated by insulin

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9
Q

astrocytes

A

support cells to help neuron function - store glyc

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10
Q

how is most of the remaining glucose taken up

A

by skeletal muscle

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11
Q

skeletal muscle glucose uptake

A

• Glucose enters muscle via facilitated transport (uptake)
• Hexokinase (glucokinase in liver) phosphorylates glucose to maintain gradient
• Unlike liver, glucose-6-phosphate cannot leave cell and enters glycolysis or glycogen synthesis (500 g whole body)
- Doesn’t store as much as liver - can be manipulated with nutrition and ex

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12
Q

glucose transport via GLUT4

A
  • GLUT4 translocated to plasma membrane from intracellular vesicles in response to insulin
  • Muscle contraction also stimulates GLUT4 translocation to plasma membrane
  • Calcium (Ca2+) thought to be main signal
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13
Q

glycogen synthesis

A
  • Glucose-6-phosphate (G6P) converted to glucose-1- phosphate (G1P) by phosphoglucomutase
  • Uridine diphosphate glucose (UDP-glucose) is synthesised from G1P and uridine triphosphate UTP
  • UDP-glucose binds to pre-existing glycogen molecule or glycogenin and UDP is released
  • Glycogenin is a protein at the core of a glycogen molecule that has autocatalytic (add to itself) activity
  • Glycogen synthase and branching enzymes then form proglycogen, which grows into macroglycogen - rate limiting step
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14
Q

how does insulin stimulate glycogen synthesis?

A
  • Switches protein phosphatase on
  • Inactive as phosphorylated - blocks catalytic site
  • Phosphatase removes phosphate
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15
Q

muscle contraction/how does exercise reduce glycogen synthesis?

A
  • Kinase - phoshphorylates

- No food = no insulin = no glyc

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16
Q

how does insulin inhibit glycogen breakdown (glycogenolysis)?

A
  • Glyc phosphorylase - rate limiting step

- Active = phosphorylated§

17
Q

muscle contraction/how does exercise stimulate glycogen breakdown?

A

Insulin levels decrease

18
Q

glycolysis preferential during exercise

A

• Calcium (Ca2+) and adrenaline main signals stimulating glycogenolysis
• Reduced insulin with exercise
• G6P derived from both
glycogenolysis and glucose uptake
• Enters glycolysis pathway (leaves liver by action of glucose-6- phosphatase)

19
Q

gluconeogenesis - liver

A
  • Liver is first and foremost reserve for maintaining blood glucose in postabsorptive period and during fasting
  • Once reserve is exhausted (overnight fast can almost fully deplete liver glycogen stores), glucose must be made from non-carbohydrate precursors
  • Circulating fatty acids and glycerol increase during fasting
  • Unfortunately fatty acids cannot be a precursor as the pyruvate dehydrogenase and pyruvate kinase reactions are irreversible (i.e. acetyl- CoA from fatty acids cannot form glucose)
  • Reversal of glycolysis?
  • Acetyl-CoA from fatty acids plays an important role in inhibiting pyruvate dehydrogenase and diverting pyruvate to oxaloacetate and malate
  • Lack of insulin relieves inhibition of muscle proteolysis to release amino acids, such as alanine
20
Q

reversal of glycolysis

A
  • Pyruvate kinase inhibited by alanine
  • Glycerol is phosphorylated to glycerol-3-P via glycerol kinase
  • Lactate produced at high rates in muscle during exercise, and also continuously in red blood cells
21
Q

different carbohydrate sources for exercise

A

liver

ingested

skeletal muscle

maintain glucose at 5 mmol/l

22
Q

liver carbohydrate source

A

o 100 mmol/kg
o 80-100g
o 320-400 kcals
o Replenished with just food

23
Q

ingested carbohydrate source

A

o Up to 1000g/day

24
Q

skeletal muscle carbohydrate source

A

o 50-100 mmol/kg
o 400-700g
o 1600-2800 kcals
o More than liver as muscles bigger

25
Q

blood glucose at rest

A
  • 80-100g in liver
  • 0.1g/min
  • Sink maintained at 5 mmol/l
  • Glucose uptake in diff tissues at rest 0.1g/min
  • Brain is biggest consumer
26
Q

blood glucose during carbohydrate ingestion

A

Volume of sink increases

27
Q

skeletal muscle glucose uptake increases during exercise

A
  • Muscle contraction also stimulates GLUT4 translocation to plasma membrane
  • Ca2+ main signal
  • Regulated by ex intensity
28
Q

blood glucose during prolonged exercise

A

Reduced volume of sink

29
Q

liver glycogenolysis and glucose output increased during prolonged exercise

A

Exercise increases activation of the sympathetic NS

releases adrenaline

inhibits insulin release

inhibits glycogenolysis

glucagon stimulates glycogenolysis

30
Q

carbohydrate oxidation during prolonged exercise

A
  • Start using other fuels - muscle glyc

• Rate of carb ox cannot fuel muscle contraction - stop ex

31
Q

why does glycogenolysis increase as exercise intensity increases?

A
  • Increased AMP
  • ATP only fuel used for muscle contraction
  • Higher muscle contraction = higher breakdown
32
Q

muscle and liver glycogen stores are finite and become depleted during exercise

A

can only be used for so long

33
Q

blood glucose response to exercise with water or 1.5/min carbohydrate ingestion

A
  • Stimulus greater than use at start

* Didn’t fatigue - maintain blood glucose and carb ox

34
Q

glucose oxidation response to exercise with water or 1.5/min carbohydrate ingestiom

A
  • Stimulus greater than use at start

* Didn’t fatigue - maintain blood glucose and carb ox

35
Q

slowing down the rate of muscle glycogen use during exercise with 0.5/min carbohydrate

A
  • Running
  • ½ marathon pace
  • 0.5g/min - carb 5.5% electrolyte solution - 500ml with 30g carb - tested Lucozade
  • Spared glyc utilisation - run for another half hour - 33%
36
Q

which type of carb is best to ingest?

A
  • 3g/min
  • Can’t ox more than 1g/min
  • Rate of gluc ox stays the same regardless of amount digested
  • W/ fructose (absorbed diff) - can get more into system and oxidise
37
Q

how can glycogen loading increase exercise performance?

A

Ingest carb after ex - load up muscle

38
Q

what is glycogen loading caused by?

A

increase in sensitivity of muscle to insulin

  • Muscle contraction stimulates GLUT4 translocation to plasma membrane
  • End of ex TCA cycle, PDC and glycolysis flux return to near resting, but GLUT4 maintained for several hrs post ex
  • Glyc resynthesis highest in first few hrs post ex, but insulin sensitivity elevated for few days
39
Q

when is glycogen resynthesis highest?

A

in hours after exercise

immediately after

ESS1606 Nutrition and metabolism (19 decks)

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