the fed state Flashcards

1
Q

what is the fed state?

A

The ‘well fed’ state, is the 2-4 hour period after a normal meal.
These fuels are oxidized for the bodys energy needs
- Excess is transported to storage sites
- Readily available substrates
 Therefore an ‘anabolic’ state
 Increased triacylglycerol and glycogen synthesis
Oxidation or storage is determined by the insulin/glucagon ratio

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2
Q

carbohydrate metabolism

A

digestion, absorption and transportation, to convert carbohydrates into a format which can be used for energy.
- Most commonly consumed as polysaccharides [e.g. starch, fibre or cellulose] or disaccharides [e.g. lactose, sucrose, galactose], these need to be broken down to monosaccharides

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3
Q

digestion of carbohydrates

A
  • begins in the mouth- alpha-amylase

- continues in small intestine- pancreatic amylase

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4
Q

absorption and transportation of carbohydrates:

A
  • monosaccharides absorbed by intestinal epithelial cells.

- transported to the liver through the hepatic portal vien

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5
Q

glucose oxidation for energy and enters biosynthetic pathways

A
  • Glucose transported via the blood stream to the peripheral tissues- forms the carbon skeleton of most compounds
  • Surplus glucose is initially stored as glycogen in the liver or muscles, before longer term storage [triacylglycerols].
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6
Q

protein metabolism

A

proteins cleaved by pepsin in the stomach. proteolytic enzymes in the small intestine: trypsin, chymotrypsin, elastase, carboxypeptidase A and.

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7
Q

amino acid absorption and storage

A
  • absorbed into intestinal epithelial cells, released into hepatic portal vein.

no AA storage- free AAs absorbed from blood used for protein synthesis and biosynthesis e.g. neurotransmitters and heme. carbon skeleton may be oxidised

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8
Q

fats metabolism

A

TAGs are the major lipids of the diet. fats are not soluble.
- emulsified by bile salts (synthesised in the liver, stored in gall bladder)
- pancreatic lipase converts TAGs to fatty acids & 2-monoacylglycerols
- form micelles contacting with bile salts
Fatty acids absorbed into intestinal epithelial cells and then reformed into TAGs
TAGs combined with proteins, phospholipids, cholesterol into ‘chylomicrons’
- Secreted into the lymphatic system
- Enter bloodstream via thoracic duct to be utilized by different tissues

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9
Q

the liver and metabolism

A

Uniquely situated in metabolism with connection to digestive tract and circulatory system
The first major organ that nutrients meet after they are absorbed from the intestine- hepatic portal vein earlier
- Acts to regulate fluctuations in substrate supplies for cells
- Takes up carbohydrates, lipids, and amino acids- metabolized, stored,

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10
Q

hepatocytes and GLUT 2

A

in carb metabolism, increased glucose uptake by hepatocytes, which have GLUT2 in their membrane. this has a high Km* meaning you need quite a lot of glucose around before the liver starts to take it up- allows ‘priority access’ to glucose e.g. brain.

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11
Q

increased phosphorylation of glucose:

A

Glucokinase creates glucose-6-phosphate, which can be converted to glycogen [glycogenesis]
- It can go via the pentose phosphate pathway [HMP- hexose monophosphate shunt]
- A metabolic pathway parallel to glycolysis,
- Generates NADPH and pentoses and ribose-5-phosphate [a precursor for the synthesis of nucleotides]
The pyruvate produced by glycolysis [break down of glucose] can be converted by acetyl CoA and used to synthesise fatty acids.
Excess glucose is converted to TAG
- Packed into very-low density lipoproteins [VLDL]

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12
Q

increased glycogenesis

A
  • glycogen synthase is activated and converts glucose-6-phosphate to glycogen.
  • the amount of glycogen that the liver can synthesise/store will vary- maximum of ~300g
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13
Q

increased glycolysis

A

more [glucose->pyruvate]
increased insulin-to-glucagon results in increased glycolytic enzymes:
- glucokinase, PFK-1 and pyruvate kinase
- pyruvate dehydrogenase [converting pyruvate to acetyl CoA] is dephosphorylated and active as pyruvate inhibits PDH kinase- increased acetyl CoA

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14
Q

the liver being the site of fatty acid synthesis

A
  • increased during the absorptive state due to acetyl CoA and NADPH availability [from pentose phosphate pathway]. also activation of acetyl CoA Carboxylase:
  • > allosteric activator present, citrate
  • > activated by dephosphorylation
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15
Q

increased acetyl CoA

A
  • pyruvate from glycolysis enters mitochondria
  • citrate leaves due to isocitrate dehydrogenase inhibition
  • cleaved by ATP-citrate lyase [enzyme that catalyses the conversion of citrate to acetyl CoA and oxaloacetate
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16
Q

increased triacylglycerol synthesis:

A
  • Increased acetyl CoA presence and also due to hydrolysis of TAG component from chylomicrons
17
Q

TAG storage

A
  • Packaged in VLDLs and transported to adipose tissues and muscle tissue
    • for energy use and storage
18
Q

amino acid metabolism

A

If AAs are not used for protein synthesis in the liver [which is increased], then they are exported to other tissues for use, or degraded

  • Degradation will involve deamination- urea formed- the urea cycle converts highly toxic ammonia to urea for excretion
  • Carbon skeleton will be degraded to pyruvate, acetyl CoA, or TCA cycle intermediates
19
Q

adipose tissue

A
  • second only to liver in its ability to distribute fuel molecules.
  • increased carbohydrate metabolism.
  • glucose is phosphorylated to glucose 6-P- enters the pentose phosphate pathway, or glycolysis
  • FA and glycerol released from TAGs y lipoprotein lipase [LPL]- an enzyme in capillary walls
20
Q

skeletal muscle

A
  • glucose is used to replenish glycogen stores depleted by exercise
  • AAs taken up for restorative synthesis.

carb metabolism:
- increased insulin-to-glucagon ratio and availability of glucose 6-P favours glycogen synthesis.

Fat metabolism:
- FAs are of secondary importance compared to glucose.

AA metabolism:
- increased uptake of branched chain AAs: leucine, isoleucine, valine, contains transaminase

21
Q

brain tissue

A

Very dependent on glucose, under normal conditions the nervous system requires about 150g per day

    • If levels drop below 40 mg/100 ml: dizzy/light headed
    • Glucose needed as an energy source & precursor for neurotransmitters

• Substrates must be able to pass through blood brain barrier

  • No significant glycogen stores
  • No significant TAG stores
  • Dependent on blood glucose
22
Q

refeeding syndrome

A

occurs about 4 days after refeeding begins. symptoms:
- fluid and electrolyte disorders [hypophosphatemia].
- neurologic, pulmonary, cardiac complications. can lead to death.
patients are at risk if they’ve not fed for 7 days.
during starvation, hormonal and metabolic changes prevent protein/muscle breakdown:
- low insulin, increased glucagon
- adipose tissue release fatty acids and glycerol
- glycogen breakdown and gluconeogenesis, lipid and protein breakdown commence

  • ketone bodies and FAs become the major fuel source.
  • intercellular minerals become depleted
  • during refeeding, shift back to carb metabolism- insulin stimulates glycogen, fat, protein synthesis. sudden demand for minerals and cofactors for glycolytic enzymes.
  • uptake of minerals from extracellular fluid leads to electrolyte/ osmotic disturbances- can lead to cardiac and neurological problems
  • consult experts: monitor vital functions, fluid balance, and plasma electrolytes