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Biochem

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2 views3 pages

Biochem

Uploaded by

Elia Giudici
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Describe how glycogen synthesis is regulated and controlled

Glycogen synthesis ensure the proper storage of glucose for energy needs.

Regulation occurs primarily through the activity of glycogen synthase (enzyme)

Role of Glycogen Synthase

catalyses the addition of glucose units from UDP-glucose to a growing glycogen chain

Active (dephosphorylated) form: Glycogen synthase a

Inactive (phosphorylated) form: Glycogen synthase b

Regulation by Phosphorylation

Glycogen synthase controlled by phosphorylation-dephosphorylation cycles:

Phosphorylation (via protein kinases): Decreases activity

Dephosphorylation (via protein phosphatase): Increases activity

Hormonal Regulation

Insulin

Activate protein phosphatase-1 (PP1), which dephosphorylates and activates glycogen


synthase

Inhibiting glycogen synthase kinase-3, preventing glycogen synthase phosphorylation

Increases glucose uptake by activating GLUT4 transporters in muscle and adipose tissues

Glucagon

Inhibits glycogen synthesis in the liver by activating protein kinase A (PKA), leading to the
phosphorylation and inactivation of glycogen synthase

Promotes glycogen breakdown via activation of glycogen phosphorylase

Epinephrine

similarly to glucagon but affects both liver and muscle cells.

PKA activation, which inhibits glycogen synthesis and enhances glycogenolysis

Allosteric Regulation

Glycogen synthase sensitive to cellular glucose levels:

Glucose-6-phosphate (G6P): Activates glycogen synthase by acting as an allosteric activator,


even when the enzyme is phosphorylated

Ensures glycogen synthesis occurs only when glucose availability is high


Energy Status of the Cell

High-energy molecules like ATP and glucose-6-phosphate promote glycogen


synthesis, while low-energy signals favour glycogen breakdown

Describe the energy effects of the Krebs cycle

Krebs cycle (citric acid cycle), central metabolic pathway in aerobic respiration

generate high-energy electron carriers and ATP equivalents by oxidizing acetyl-CoA (from
carbohydrates, fats, and proteins) energy effects :

Generation of High-Energy Electron Carriers

molecules essential for driving the electron transport chain (ETC) and oxidative
phosphorylation:

NADH:

- 3 NADH molecules are generated per cycle (one each in the isocitrate dehydrogenase,
α-ketoglutarate dehydrogenase, and malate dehydrogenase reactions)

Each NADH contributes ~2.5 ATP during oxidative phosphorylation

FADH₂:

- 1 FADH₂ molecule is produced per cycle (via succinate dehydrogenase).


- Each FADH₂ contributes ~1.5 ATP during oxidative phosphorylationDirect ATP

Equivalent (GTP) Production

- Substrate-level phosphorylation occurs at the succinyl-CoA synthetase step,


producing 1 GTP (readily converted to ATP) contributes directly to cellular energy
availability

Net Energy Yield

For each molecule of acetyl-CoA that enters the Krebs cycle:

3 NADH → 3 × 2.5 ATP = 7.5 ATP

1 FADH₂ → 1 × 1.5 ATP = 1.5 ATP

1 GTP → 1 ATP

Total energy yield per cycle: 10 ATP per acetyl-CoA

molecule of glucose generate 2 molecules of acetyl-CoA (via glycolysis and pyruvate


oxidation): Total yield from the Krebs cycle per glucose: 20 ATP

Krebs cycle provides metabolic intermediates (e.g., α-ketoglutarate, oxaloacetate) for


biosynthetic processes.
Efficiency and Role in Aerobic Respiration

• The Krebs cycle does not directly consume oxygen but relies on the regeneration of
NAD⁺ and FAD in the ETC, which requires oxygen.

• Without oxygen, the Krebs cycle halts because NADH and FADH₂ cannot be oxidized,
leading to an energy bottleneck.

oxidative phosphorylation

process of ATP production that occurs in the inner mitochondrial membrane, coupling
electron transport to ATP synthesis.

Electron Transport Chain (ETC) and ATP synthesis via ATP synthase

Electron Transport Chain (ETC)

• series of protein complexes (I-IV) and mobile carriers (coenzyme Q and cytochrome c)

• Electrons from NADH and FADH₂ (produced during glycolysis, pyruvate oxidation, and
the Krebs cycle) are transferred through the ETC to oxygen (O₂), the final electron
acceptor, forming H2O

• Proton Pumping:

o Complex I: Accepts electrons from NADH, pumps 4 protons.

o Complex II: Accepts electrons from FADH₂, does not pump protons.

o Complex III: Transfers electrons to cytochrome c, pumps 4 protons.

o Complex IV: Transfers electrons to O₂, pumps 2 protons.

The ETC creates a proton gradient (proton-motive force) by pumping protons (H⁺) into the
intermembrane space.

ATP Synthesis (ATP Synthase)

• Protons flow back into the matrix through ATP synthase (Complex V)

• This flow drives the phosphorylation of ADP + Pi → ATP

• Each NADH generates ~2.5 ATP, and each FADH₂ generates ~1.5 ATP.

Energy Yield From one glucose molecule:

• NADH: 10 molecules → ~25 ATP

• FADH₂: 2 molecules → ~3 ATP

• Total: ~28 ATP (from oxidative phosphorylation alone).

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