Protein control: (leyland) carb metabolism 1 Flashcards
Metabolic pathways are controlled which 3 core ways?
Control of amount of enzymes
Control on substrate availability
Control catalytic activity of enzymes
Changes in metabolism in the fed state?
(2-4 hours after eating)
Transient increase in plasma glucose, amino acids and TAGs (Triacylglygerols)
Insulin release from pancreas
Fuel stores created
Changes in metabolism in fasted state?
(begins if no further fuel ingested after fed state)
Plasma levels of glucose, aa’s and TAGs fall
Fall in insulin secretion and increase in glucagon release
Degradation of fuel stores begins
Properties of glucagon? Where/when is it synthesised/released and what does it do~?
Synthesised in pancreatic alpha-cells
Hormone of FASTED state
Action can be considered catabolic
Signals through G-protein coupled receptor
properties of insulin? Where/when is it synthesised/released and what does it do?
Synthesised in pancreatic beta-cells
Hormone of FED state
Action can be considered anabolic
Signals through tyrosin kinase receptor
Phases of insulin release?
2 phase release
- Release from granules
- synthesis
how is insulin modified after synthesis?
Post-translationally modified
Preproinsulin (signal sequence cleaved in ER)
- > Proinsulin (further cleavage of C peptide)
- > mature insulin (functional form that binds to receptor)
4 major pathways of glucose utilisation ?
Storage (glycogen, starch, sucrose)
oxidation via glycolysis (pyruvate)
oxidation via pentose-phosphate pathway (ribose-5-phosphate)
synthesis of structural polymers (extracellular matrix and cell wall polysaccharides)
General overview of processing of dietry carbohydrates?
Digestion in mouth and lumen
-> breakage of glycosidic bonds to form monosaccharides
absorption and release of monosaccharides by glucose transporters (GLUT)
Describe step-by step process/cycle on insulin-enhanced transport of glucose into myocytes
glucose transporters ‘stored’ in cell within vesicles
when insulin interacts with its receptor, vesicles move to surface and fuse with plasma membrane -> increase in GLUT in membrane (GLUT4 in adipocytes and muscle)
When insulin level drops, GLUTs are removed from membrane via endocytosis forming small vesicles
small vesicles fuse with endosome
patches of endosome enriched with GLUTs bud off to form GLUT filled vesicles (cycle can then repeat)
What is the key metabolic intermediate that starts many glucose derived metabolic pathways?
Glucose-6-phosphate (G6P)
- starting point of many pathways
Net products of glycolysis?
2 ATP, 2 NADH, 2 Pyruvate
Key steps of regulation in glycolysis?
hexokinase
phosphofructokinase-1
pyruvate kinase
Describe/explain isozyme regulation of hexokinase
Hexokinase phosphorylates glucose to G6P
-> add phosphate to hydroxyl group at C6 (via hydrolysis of ATP)
Reaction has highly negative delta G -> irreversible under usual conditions
Hexokinase 4 (glucokinase) in liver has kM of ~5mM compared to HKI-III of ~0.2mM
Meaning glucokinase is not fully active in resting state (resting blood glucose conc. 4-5mM)
-> fed state increases blood glucose -> glucokinase activity increases and aids with glucose storage i.e increasing glucose storage mobilisation in fed state
Resting blood glucose conc.?
4-5mM
