Anabolic Catabolic state (3)
Metabolic Homeostasis: Anabolic/Catabolic State
Page 1: Introduction
LIFE1029: Genes, Molecules & Cells
Focus on Metabolic Homeostasis and understanding the balance between Anabolic and Catabolic states.
Page 2: Metabolic Pathways
Key intermediates: 6-P gluconate, Ribulose 5-P, Glucose, Fructose, etc.
Framework of glycolysis and other pathways leading to energy production and storage.
Importance of reactions: Glycogenesis (storage of glucose), Glycolysis (energy production).
Page 3: Objectives
Understand the interconnected nature of metabolism.
Grasp the function of hormones insulin and glucagon in regulating metabolic states.
Learn about metabolic processes in the liver during fed and fasting states.
Page 4: Metabolic Requirements
Maintain metabolic homeostasis by:
Synthesis of necessary compounds not provided by diet.
Detoxification and waste disposal.
Four basic types of metabolic pathways:
Fuel oxidative pathways.
Fuel storage & mobilization pathways.
Biosynthetic pathways.
Detoxification/waste disposal pathways.
Anabolic pathways: build larger molecules (e.g., glycogen).
Catabolic pathways: break down molecules for energy.
Page 5: Balance of Metabolism
Maintain balance between:
Intake of macronutrients (fats, proteins, carbohydrates).
Oxidation rates and synthesis needs.
Different tissues specialize in various metabolic functions:
Liver, adipose tissue, muscle, brain.
Page 6: Glucose Regulation
Tissues requiring glucose include the brain, red blood cells, and exercising muscles.
Optimal blood glucose levels: 80 to 100 mg/dL (~5 mM).
Negative effects of hypoglycemia (< 60 mg/dL) on brain function and health.
Page 7: Mechanisms of Integration
Balance achieved through:
Blood nutrient levels.
Hormonal control.
Central Nervous System signaling.
Page 8: Major Hormones
Insulin: Increases glucose uptake and use, helps with protein synthesis, decreases glucose output.
Glucagon: Stimulates glucose production, increases glycogenolysis and gluconeogenesis.
Epinephrine/Norepinephrine: Mobilize energy during stress.
Page 9: Insulin Function
Insulin synthesized as proinsulin, released from β-cells when glucose levels exceed 80 mg/dL.
Promotes glucose utilization and storage as glycogen and fat.
Page 10: Glucagon Action
Released from α-cells of pancreas in response to low glucose.
Promotes glucose/energy production, especially through glycogen breakdown.
Page 11: Intracellular Signaling
Hormonal action leads to cellular signaling changes that modify enzyme activity and gene expression.
Insulin signaling involves autophosphorylation and cascade activation of downstream effects.
Page 12: The Absorptive State
Following meals, increased insulin levels create an anabolic state for nutrient storage.
Tissues actively uptake glucose, with the liver focusing on nutrient absorption.
Page 13: Carbohydrate Metabolism
Increased glucose uptake by hepatocytes through insulin-dependent transporters.
Glycogen synthesis activated by insulin through dephosphorylation of specific enzymes.
Page 14-15: Continued Carbohydrate and Fat Metabolism
Increased glycolytic enzyme activity in response to insulin level changes.
The liver is vital for fatty acid synthesis, aided by acetyl CoA and NADPH.
Page 16: Amino Acid Metabolism
Amino acids not used for protein synthesis are either exported for use or degraded.
Page 17: Intertissue Metabolism
Excess dietary intake leads to conversion to triacylglycerols for storage.
Integration of carbohydrate, protein, and fat metabolism across tissues.
Page 18: The Fasting State
Transition into a catabolic state after the absorptive period, with decreased insulin and increased glucagon.
Focus on maintaining glucose levels and mobilizing stored nutrients for energy.
Page 19-20: Enzyme Regulation in the Fasting State
Enzymes active during the absorptive state are inactivated.
Key processes include glycogenolysis, lipolysis, and proteolysis to maintain glucose levels.
Page 21-22: Gluconeogenesis and Fatty Acid Oxidation
The liver synthesizes glucose and ketone bodies when in a fasted state; focus on gluconeogenesis from various substrates.
Fatty acids serve as a primary energy source through oxidation.
Page 23: Intertissue Integration
Priority management route for glucose-dependent and non-dependent tissues during fasting, with hormone regulation balancing energy stores and nutrient release.
Page 24: Hypercatabolic States
Can occur during severe stress or injury, leading to a catabolic state characterized by increased fuel use and muscle degradation.
Role of cortisol in response to stress and nutrient mobilization.
Page 25: Summary of Metabolic States
Metabolic homeostasis relies on hormonal action and availability of substrates to modulate enzyme activity.
Anabolic pathways dominate in fed states; catabolic pathways activate when nutrients are absent.
Page 26: References
Core readings from key biochemical texts about metabolic pathways and hormonal actions.
Page 27: Feed/Fast Cycle Summary
The transition between fed and fasted states leads to different cellular responses and metabolic priorities for energy production and storage.