Physiology · Temperature, exercise and metabolism

Fed and fasting states: the hormonal switch !

Regulation
Exam priority: high

After a meal insulin stores energy; when fasting, glucagon pulls it from stores so the brain never runs short of glucose.

Updated 2026-11-01

Also called: Absorptive and post-absorptive states, Insulin/glucagon ratio

See it in 3D: Liver · Pancreas

What it is

The body alternates between storing (fed or absorptive state) and mobilizing (post-absorptive and fasting). The switch is the insulin/glucagon ratio in portal blood, acting mainly on liver, muscle and fat. The fixed goal is a blood glucose of ≈70–100 mg/dL for the brain and red cells.

How it works, step by step

A meal raises portal glucose and amino acids; incretins (GLP-1, GIP) amplify insulin secretion.
Insulin activates glycogen synthase and lipogenesis in the liver and inserts GLUT4 in muscle and fat cells.
In fat it activates lipoprotein lipase and brakes hormone-sensitive lipase: fat is stored.
Hours later insulin falls and glucagon rises; via cAMP/PKA the liver breaks down glycogen and releases glucose.
Low insulin releases lipolysis: fatty acids fuel muscle and, by β-oxidation, the liver.
Excess hepatic acetyl-CoA forms ketone bodies, which the brain begins to use after several days of fasting.

Who does what in each state

Tissue	Fed (insulin)	Fasting (glucagon, catecholamines)
Liver	Stores glycogen, makes triglycerides	Releases glucose, gluconeogenesis, ketones
Muscle	Takes up glucose (GLUT4), builds protein	Burns fatty acids and ketones; exports alanine
Adipose tissue	Stores triglycerides	Lipolysis: fatty acids and glycerol
Brain	Glucose	Glucose; after days, ketones
Red blood cells	Glucose (glycolysis)	Always glucose (no mitochondria)

Clinical notes

Diabetic ketoacidosis: absent insulin with high glucagon: hyperglycemia, ketones and high anion gap acidosis.
Fasting hypoglycemia in children or people who drink heavily: ethanol blocks gluconeogenesis once glycogen is gone.
Cortisol, epinephrine and growth hormone also oppose insulin (counter-regulatory hormones).

Test yourself

Think of the answer, then tap the question to see it.

Why doesn't muscle glycogen help correct fasting hypoglycemia?

Muscle lacks glucose-6-phosphatase, so glucose-6-phosphate cannot leave as free glucose; it is used in the muscle's own glycolysis.

Which substrates does the liver use for gluconeogenesis after 24 h of fasting?

Lactate (Cori cycle), alanine and other amino acids from muscle, and glycerol from lipolysis. Even-chain fatty acids give no net glucose.

Why does lack of insulin, not just hyperglycemia, cause ketoacidosis?

Without insulin lipolysis is unchecked and glucagon routes fatty acids into hepatic β-oxidation; surplus acetyl-CoA forms keto-acids.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Biochemistry

In Pharmacology

Insulins

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 24.5 Metabolic States of the Body (OpenStax (Rice University), 2022); 24.3 Lipid Metabolism (OpenStax (Rice University), 2022); Diabetic ketoacidosis: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Low blood sugar: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 79). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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