Cellular-Level Integration
Start with the big picture
Low insulin and increased glucagon, epinephrine, and cortisol promote a catabolic state. The liver shifts away from glycolysis and fatty acid synthesis toward glucose production, fatty acid oxidation, and ketogenesis. Adipose lipolysis releases fatty acids for oxidation and glycerol for gluconeogenesis; lactate and alanine also provide glucose precursors. As fasting continues, ketones become an important fuel for the brain, helping reduce its dependence on glucose and the demand for muscle protein breakdown. Some tissues remain dependent on glucose, while the kidney contributes to gluconeogenesis during prolonged fasting. At the cellular level, AMPK favors catabolic pathways and autophagy, while changes in protein metabolism and thyroid hormones help conserve resources.
What you'll learn
- Describe the hormonal shift from anabolic to catabolic metabolism during fasting.
- Identify major gluconeogenic substrates and their tissue sources.
- Explain how hepatic fatty acid oxidation supports ketone production.
- Compare fuel use across the brain, muscle, kidney, and obligate glucose-using tissues.
- Summarize the roles of AMPK, autophagy, and protein metabolism in starvation.
Continue your study
Work through the complete notes and reinforce the topic with the study tools available in the full lesson.
