Passive osmosis through specialized water channels

Secondary active transport via a sodium-glucose cotransporter 

Simple diffusion directly through the phospholipid bilayer 

Primary active transport using a dedicated ATP-pump 

To protect vital protein stores, the body "spares" glucose in the post-absorptive state by inducing most tissues to switch from glucose to fatty acid and ketone utilization. 

During the absorptive state, glucose is "spared" by converting it into urea, which can be stored in the liver for energy during chronic starvation.

The body "spares" glucose by increasing the theoretical maximum yield of ATP from glycolysis, allowing cells to survive on less fuel during the post-absorptive state.

"Glucose sparing" is a metabolic adjustment that occurs during the fed state to ensure that excess dietary glucose is delivered exclusively to the adipose tissues. 

Plasma insulin levels fall, leading to net catabolism of energy stores, while increased glucagon levels stimulate hepatic glycogenolysis and gluconeogenesis.

Plasma insulin levels rise to promote the breakdown of triglycerides, while glucagon levels fall to inhibit hepatic glucose uptake. 

Both insulin and glucagon levels rise simultaneously to ensure that most body cells continue using glucose as their primary fuel source. 

Glucagon levels fall to trigger the synthesis of ketones, while insulin levels rise to stimulate the "glucose sparing" effect for the brain.

Alpha-keto acids

Fatty acids

Ketones 

Satiation is the result of processes that terminate a meal and limit meal size, while satiety is the feeling of fullness that persists after eating. 

Satiation refers to the metabolic sparing of glucose, while satiety refers to the anabolism of triglycerides.

Satiation persists long after a meal to suppress further consumption, while satiety occurs only during ingestion. 

Satiation is the psychological desire to eat, while satiety is the biological drive. 

Plasma levels of glucose increase while the secretion of glucagon decreases.

Plasma levels of fatty acids and ketone bodies increase significantly.

Protein catabolism increases while fatty acid oxidation decreases.

reducing insulin resistance

reducing the release of satiety hormones

increasing blood glucose levels more quickly

increasing free fatty acids

Low-Density Lipoproteins (LDL) 

Very Low-Density Lipoproteins (VLDL) 

High-Density Lipoproteins (HDL)

Chylomicrons

The liver converts ketone bodies into fatty acids 4-5 hours after a meal.

Ketones are the only source of energy for the brain during fasted-state metabolism.

Beta oxidation of fatty acids forms acidic ketone in the post-absorptive state. 

Plasma levels of ketones significantly decline during prolonged starvation.

The physiological actions of glucagon primarily occur in the brain.

The net result of glucagon action is glucose synthesis from glycogen.

Glucagon stimulates glycogenolysis but inhibits ketone synthesis.

Glucagon stimulates gluconeogenesis but inhibits glucose release.