Hormonal Regulation of Metabolism & Starvation Metabolism (Quick Notes)
- Define homeostasis
- Maintenance of stable internal conditions (e.g., blood glucose) despite external changes.
- Role of the pancreas in blood glucose regulation
- Hormones: insulin (from beta cells) and glucagon (from alpha cells).
- Insulin lowers blood glucose; glucagon raises blood glucose.
- Negative feedback: insulin/glucagon coordinate to keep glucose within a narrow range.
- Enzyme regulation in glycogen metabolism
- Insulin promotes glucose uptake and glycogen synthesis via signaling that activates glycogen synthesis pathways (phosphorylation cascades).
- Glucagon and adrenaline activate enzymes involved in glycogen breakdown (glycogenolysis) via signal amplification.
- Role of phosphorylation in activating/deactivating enzymes
- Phosphorylation changes enzyme conformation and activity; it can activate, inhibit, or alter localization.
- Phosphorylation cascades underlie hormonal control of metabolism.
- Insulin’s role in glycogen metabolism
- Insulin binding activates glycogen synthase (glycogen synthesis).
- Insulin inhibits glycogen phosphorylase (reduces glycogen breakdown).
- Glycogen synthesis and breakdown are not simultaneous due to coordinated control.
- Hormonal response to low blood glucose (glucagon & epinephrine)
- When glucose is low, pancreas releases glucagon; adrenal glands release adrenaline (epinephrine).
- Glucagon signals liver to break down glycogen (glycogenolysis) and promote gluconeogenesis.
- Epinephrine also stimulates glycogen breakdown in liver and muscle for rapid glucose availability.
- Hormone regulation of metabolic pathways (liver, muscle, adipose)
- Insulin: promotes glycogen synthesis and glucose uptake; supports glycolysis; promotes fat storage in adipose tissue.
- Glucagon: promotes glycogenolysis and gluconeogenesis; supports mobilization of glucose; can promote lipolysis in adipose tissue.
- Adrenaline (epinephrine): promotes glycogenolysis and rapid glucose availability; supports lipolysis.
- Key outcomes and concepts
- Negative feedback maintains blood glucose within normal range for stable energy (brain relies on glucose).
- Hormonal regulation integrates with metabolic pathways to shift between storage (fed state) and mobilization (fasted/starved state).
- Quick review prompts
- What triggers insulin release and what are its primary metabolic effects?
- How does glucagon respond to hypoglycemia? What pathways are activated?
- How does phosphorylation regulate glycogen synthase vs. glycogen phosphorylase?
- Learning objectives (summary)
- Explain physiological stages of starvation and associated metabolic adaptations.
- Describe gluconeogenesis, lipolysis, and ketogenesis.
- Discuss hormonal regulation during starvation.
- Relate organ-specific metabolic roles during prolonged fasting.
- Physiological adaptation to prolonged starvation (stages)
1) Glycogenolysis supplies energy for the first ~24 hours.
2) As glycogen is depleted, gluconeogenesis maintains blood glucose from non-carbohydrate sources (amino acids, lactate, glycerol).
3) Prolonged starvation shifts to lipolysis, mobilizing fat stores into fatty acids and glycerol.
4) Liver converts fatty acids to ketone bodies (ketogenesis) to provide brain and other tissues with an alternative fuel, sparing protein. - Fuel reserves and organ-specific roles
- Body stores: glycogen (short-term carbohydrates), triglycerides (long-term fats), mobilizable proteins.
- Brain relies on glucose but can use ketones during extended starvation.
- Liver coordinates fatty acid and amino acid catabolism and gluconeogenesis/ketogenesis; adipose tissue provides fatty acids; heart primarily uses fatty acids; muscle uses glycogen and fatty acids.
- Why fatty acids rise in plasma during starvation
- Increased lipolysis in adipose tissue and liver glycogen depletion reduce carbohydrate fuel stores, raising circulating fatty acids.
- Ketones and glucose during starvation
- Ketone bodies derived from acetyl-CoA provide an alternative brain fuel when glucose is scarce.
- Ketosis vs ketoacidosis
- Ketosis: controlled elevation of ketone bodies (typically 0.5–3 mmol/L); generally safe.
- Ketoacidosis: excessive ketone production causing blood acidity (blood ketone > ~10 mmol/L) and requires treatment.
- Gluconeogenesis and ketogenesis in survival
- Gluconeogenesis sustains circulating glucose from non-carbohydrate sources.
- Ketogenesis provides brain-friendly fuel, reducing muscle proteolysis during extended fasting.
- Energy management during starvation (concepts to recall)
- The body prioritizes fuel delivery to critical organs (brain, heart) by shifting from glycogenolysis to gluconeogenesis and then to lipolysis/ketogenesis.
- Proteins are used as a last resort to supply gluconeogenic precursors.
- Quick wrap-up prompts
- What are the four stages of metabolic adaptation to starvation?
- What roles do gluconeogenesis and ketogenesis play in prolonged fasting?
- How do hormones regulate the shift from fed to starved state, and which organs drive these changes?
- Visual/reference notes
- Ketone production and its brain-fuel role; differentiation between ketosis and ketoacidosis.
- General idea of how organs contribute to energy balance during starvation.
Quick terms to remember
- Homeostasis, glycogenesis, glycogenolysis, gluconeogenesis, ketogenesis, lipolysis
- Insulin, glucagon, epinephrine (adrenaline)
- Glycogen synthase, glycogen phosphorylase
- Ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone)
- Negative feedback loop in glucose regulation
- Starvation stages: glycogenolysis → gluconeogenesis → lipolysis → ketogenesis