the fed state Flashcards
what is the fed state?
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
carbohydrate metabolism
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
digestion of carbohydrates
- begins in the mouth- alpha-amylase
- continues in small intestine- pancreatic amylase
absorption and transportation of carbohydrates:
- monosaccharides absorbed by intestinal epithelial cells.
- transported to the liver through the hepatic portal vien
glucose oxidation for energy and enters biosynthetic pathways
- 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].
protein metabolism
proteins cleaved by pepsin in the stomach. proteolytic enzymes in the small intestine: trypsin, chymotrypsin, elastase, carboxypeptidase A and.
amino acid absorption and storage
- 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
fats metabolism
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
the liver and metabolism
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,
hepatocytes and GLUT 2
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.
increased phosphorylation of glucose:
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]
increased glycogenesis
- 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
increased glycolysis
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
the liver being the site of fatty acid synthesis
- 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
increased acetyl CoA
- 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
increased triacylglycerol synthesis:
- Increased acetyl CoA presence and also due to hydrolysis of TAG component from chylomicrons
TAG storage
- Packaged in VLDLs and transported to adipose tissues and muscle tissue
- for energy use and storage
amino acid metabolism
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
adipose tissue
- 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
skeletal muscle
- 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
brain tissue
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
refeeding syndrome
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
