Lecture 5 — Glycogen storage & mobilization

Glycogen role (storage of glucose) — Comprises glucose units stored as glycogen (mainly in liver and muscle) to buffer energy and maintain blood glucose. Glycogen synthase vs glycogen phosphorylase (opposing functions) — Liver/muscle balance glycogenesis (build) vs glycogenolysis (breakdown) to match nutrient and energy status. Liver glycogen: blood glucose support — In hepatocytes, glycogenolysis helps maintain systemic glucose availability between meals. Muscle glycogen: local fuel for exercise — In skeletal muscle, glycogen breakdown supplies ATP/CHO intermediates for contraction and local energy needs. Insulin signaling: promotes glycogenesis — Insulin favors glycogen storage by promoting pathways leading to glycogen synthase activation and reducing glucose output from liver. Glucagon/epinephrine signaling: promotes glycogenolysis — In liver (and also muscle under stress for catecholamine effects), glucagon/epinephrine promotes glycogen breakdown to raise glucose availability. Glycogenolysis overview (phosphorylase-driven cleavage) — Breaks glycogen into glucose units (high-level concept: phosphorylation-enabled release) to generate free glucose-1-phosphate for metabolism. Glycogen branching structure & mobilization — Branching increases glycogen solubility and creates many non-reducing ends for faster mobilization of glucose units. Terminal glucose handling (free glucose vs phosphate) — Liver converts glycogen-derived units toward free glucose export, whereas muscle primarily channels glycogen-derived carbon to local metabolism. Allosteric control concept (energy/redox status) — Glycogen mobilization is tuned to energy state (e.g., demand of ATP vs availability of energy equivalents), shifting net direction toward fueling when needed. Cyclic AMP (cAMP) control concept (hormone relay) — Hormones (notably glucagon/epinephrine) use cAMP-linked signaling to drive glycogen phosphorylase toward an “on” state in liver. Ca²⁺ link in muscle (exercise activation concept) — In muscle, Ca²⁺ during contraction supports activation of glycogen breakdown to match immediate energy demand. Net outcome: match storage to feeding vs fasting — Feeding favors storage (glycogenesis), fasting/exercise favors mobilization (glycogenolysis) to maintain energy and glucose homeostasis. Clinical relevance (dysregulation impacts glucose/energy) — Abnormal control of glycogen storage/mobilization can impair blood glucose regulation (liver) or exercise tolerance/energy supply (muscle).