Biochemistry Final

Calvin Cycle

used by photosynthetic organisms to fix CO2 to yield hexose sugars as fuel

R5P→3-phosphoglycerate→1,3-BPG→GAP→ F6P→hexose sugars

Transketolase

Enzyme that transfers a 2C unit from a ketose to an aldose (used in both Calvin Cycle and PPP, Thiamine Pyrophosphate coenzyme [TPP])

Ex. F6P+GAP→ erythrose 4-phosphate+xylulose 5-phosphate

Transaldolase (Aldolase)

Enzyme that catalyzes an aldol condensation between DHAP and an aldehyde (seemingly transfers 3C, forms a Lysin Schiff Base in mechanism)

Ex. DHAP + erthyrose 4-phosphate →sedoheptulose 1,7-bisphosphate

Pentose Phosphate Pathway

source of NADPH needed for biosynthetic pathways, involves two phase: phase 1 of oxidative generation of NADPH that converts G6P+2NADP^(+)+H20→ Ru5P+2NADPH+CO2 via G6PD. Phase 2 is nonoxidative interconversion of sugars

Modes of PPP

1) R5P needed over NADPH

2) R5P and NADPH both needed; balanced

3) NADPH needed over R5P

4) ATP and pyruvate needed; energy

Glutathione

antioxidant made up of glutamate, cysteine, and glycine. reduced form reduces reactive oxygen species (ROS) into less harmful species and requires NADPH. With G6PD deficiency, ROS would build up in the body

GSSG + NADPH + H+ ←→ 2GSH + NADP+ via glutathione reductase

2GSH+ROOH →GSSG + H2O +ROH via glutathione peroxidase

Glycogen

less osmotically active (than glucose) and highly balanced polymer that can break down into glucose for energy. structure is made up of ~12 layers of glucose monomers with a core glycogenin protein every 12 monomers

Glycogen Phosphorylysis

allows for glycogen degradation via glycogen phosphorylase for a sequential removal of glucosyl residues from the nonreducing end

glycogen (n) + P_i ←→ G1P + glycogen (n-1)

Pyridoxal Phosphate (PLP)

required by phosphorylase as a cofactor, a vitamin B6 pyridoxine with a Schiff base to Lysine and an electron sink

Transferase

enzyme used to shift 3 glucosyl residues from one outer branch to another in the glycogen mobilization scheme

alpha-1,6-glucosidase

enzyme that hydrolyzes the branch linkage bond in the glycogen mobilization scheme

phosphorylase a

usually in R state, usually active, phosphorylated, liver form of enzyme, in equilibria with phosphorylase b

binding of glucose shifts enzyme from R to T state and inactivates the enzyme causing glycogen to be immobilized with abundant glucose

phosphorylase b

usually in T state,usually inactivate, dephosphorylated, skeletal muscle form of enzyme, in equilibria with phosphorylase a

allosterically regulated by ATP, AMP, and G6P

where high [AMP] shifts enzyme from T to R state and high [ATP/G6P] stabilizes the T state

Type I Muscle Fibers

slow-twitch, endurance, uses cell respiration, long-term energy

Type IIa Muscle Fibers

intermediate between I and IIb, slightly trainable

Type IIb Muscle Fibers

fast-twitch, power-burst, uses glycogen metabolism, short-term energy

phosphorylase kinase

regulates the interconversion of phosphorylase from a to b and is initiated by hormones and activated by calcium

inactive → (Ca2+) partially active → (PKA) fully active → b to a via 2 ATP

Epinephrine

binds G-protein coupled receptors (7TM) that signals glycogen mobilization and is produced from the adrenal medulla and binds to the beta-adrenergic receptor in the muscle

Inhibits glycogen synthesis

Glucagon

binds G-protein coupled receptors (7TM) that signals glycogen mobilization and is produced from the alpha-pancreatic cells and binds to the glucagon receptor in the liver

Inhibits glycogen synthesis

G-protein coupled receptor binding event by epinephrine + glucagon

1. hormone binds to specific receptors for target cells which activates Gs

2. GTP-bound subunit Gs activates adenylate cyclase which converts ATP to cAMP

3. cAMP activates PKA

4. PKA phosphorylates phosphorylase kinase which activates glycogen phosphorylase for glycogen breakdown

Signal Transduction in the Liver

binding to the 7TM receptor initiates the phosphoinositide cascades that induces Ca2+ release which leads to phosphorylase kinase activation

Hormone End Signaling

can be ended by a decrease in hormone concentration, dephosphorylation, GTP hydrolysis of the G protein, and hydrolyzing cAMP into AMP

Glycogen Synthesis

utilizes uridine diphosphate (UDP-)glucose as an activates glucose donor to elongate glycogen. Hydrolysis of PPi drives the synthesis of UDP-glucose via the reaction of G1P and UTP

Glycogen Synthase

allows for the polymerization of the alpha-1,4 linear linkages with the addition of glucose from UDP-glucose

Branching Enzyme

transfers a block of 7 alpha-1,4 linked glucosyl residues to form the branch point

Glycogen Synthase a

usually in T state, active, dephosphorylated and controlled by hormones

Glycogen Synthase b

usually in R state, inactive, phosphorylated and is an allosteric regulator
activated via G6P which stabilizes the R state

Glycogen Synthase Kinase

phosphorylates glycogen synthase and is controlled by insulin and also phosphorylates PKA

Protein Phosphatase I (PPI)

reverses the regulatory effects of kinases on glycogen metabolism by dephosphorylated proteins to decrease the rate of glycogen breakdown and inactivates phosphorylase a and the kinase and will convert glycogen synthase b to a and accelerates glycoen synthesis

Insulin

stimulates glycogen synthesis by inactivating glycogen synthase kinase and leading to glycogen synthase a formation

von Gierke disease

distended abdomen caused by liver enlargement and decreased blood glucose between meals because of a lack of G6Pase

Pompe Disease

glycogen engorged lysosomes that occurs when lysosomeslack an alpha-1,4-glucosidase

Cori Disease

mild enlargement of liver due to increased glycogen of the short outer branches from a defective alpha-1,6 glucosidase (debranching enzyme)

Triacylglycerol

primary storage of fatty acids that serves as a major energy reservoir stored in the adipose tissue and some muscles

Adipose tissue

composed of subcutaneous and visceral fat and are composed on adipocytes that store fat which can be accumulated in TAG

Pancreatic Lipases

enable absorption of fatty acids when TAG is degraded into DAG, then MAG and free fats

Glycocholate

amphipathic molecules coated with bile salts that allows for lipid digestion by lipase

Micelles and Chylomicrons

allow for the absorption of fats from the diet as fats are transferred across membranes

Fatty Acid Processing for Fuel

1. Mobilization: lipids move through TAG degradation, release from adipose tissue, and transport to energy-requiring tissues via albumin

2. Activation/Transport: of the fatty acids into mitochondria for degradation, begins with activation oF FA as an adenylate by acyl CoA synthetase, transport occurs via acyl carnitine

3. Breakdown into acetyl CoA: degradation of fatty acids into acetyl CoA to be processed in TCA via beta-oxidation by FAD, hydration, a second beta-oxidation by NAD+ and cleavage by thiolysis. Fatty acids are degraded 2C at a time from the thioester end of acyl CoA

Hormone Control of Lipases

Glucagon and Epinephrine activate the cascade for lipolysis while ATGL, HS Lipase, and MAG lipase allow for mobilization of fat energy stores