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> Why can’t the TCA cycle provide organic carbon for biosynthesis?
> How do plants get around it?
> What’s the overall path to get to this, starting from lipids?
> TCA cycle fully oxidizes AcCoA → 2 CO2 lost → no net organic carbon gained.
> Divert AcCoA into glyoxylate cycle (bypasses CO2‑releasing steps).
> Overall: lipids → β‑oxidation → acetyl‑CoA → glyoxylate cycle → organic carbon for roots & stems.
In the plant’s growth, when is the glyoxylate shunt generally used, and when does it stop using it? State reasons for both start and stop.
> Used when seedlings w/o stems and roots b/c limited CO2 exposure.
> Stops when grown and exposed to CO2 → switches to TCA cycle instead of glyoxylate shunt.
Why do cells polymerize glucose instead of storing it as monomers?
> Free Glc = many small solute particles → draws in H2O → risk of cell bursting.
> Solution: polymerize into glycogen/starch → one large molecule instead of thousands of small ones.
> Result: each particle has a tiny osmotic effect.
How is glycogen structured?
Main chain: Glc units linked by α‑1,4 glycosidic bonds.
Branches: every ~10 residues, branch formed by α‑1,6 glycosidic bonds.
Why must glycogen phosphorylase (GPase) and glycogen synthase (GSase) not be active at the same time?
> GPase breaks glycogen → G1P
> GSase: consumes G1P to make glycogen
> Net waste of UTP and energy w/ no productive outcome.
Regulation ensures catabolism and anabolism never run together.
How does insulin regulate glycogen synthesis, and where is it produced?
> Pancreas has endocrine & exocrine parts.
> Endocrine has islets of Langerhans (clusters of hormone‑secreting cells) = one of them are β‑cells.
> β‑cells secrete insulin when blood Glc high.
> Insulin tells cells to take up Glc and store it as glycogen/fat → promotes GSase activity.
How does glucagon regulate glycogen breakdown?
> Islets of Langerhans = α‑cells = secrete glucagon when blood Glc low.
> Glucagon tells cells to break down glycogen, fats, and protein, and run gluconeogenesis.
Where is epinephrine secreted from and what does it rely on?
> Secreted from adrenal medulla = part of adrenal glands = on top of kidneys.
> Heavily relies on small glycogen stores for fight-or-flight response (short-term compared to glucagon).
How does epinepherine regulate glycogen breakdown?
> Epi binds to β‑adrenergic receptor → activates adenylate cyclase.
> Adenylate cyclase (AC) uses ATP → cAMP.
> cAMP binds to protein kinase (PK).
> PK phosphorylates & activates subcellular components.
How do AC and PDE control cAMP levels?
> When AC on → cAMP produced faster than PDE can bdown → cAMP levels rise.
> When AC off → PDE still working slowly in the background → cAMP levels drop.