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