Feeding versus fasting

Feeding versus fasting

In General:

Feeding process	Fasting process
2 to 4 hours after ingestion of normal meal.	1)      Results from no food ingested after feeding period. 2)      Results from inability to obtain food. 3)      Clinical situations such as trauma, surgery, cancer or burns.
Plasma glucose, amino acids, TAG increases	decreases
Insulin secretion increases glucagon secretion decreases	Insulin decreases Glucagon and epinephrine increases
Anabolism (TAG, glycogen, protein synthesis increases)	Catabolism (degradation of TAG, glycogen and protein increases)

Fasting process has 2 priorities: a) to maintain glucose level for brain and RBCs, b) mobilize fatty acids from adipose tissue and release ketone bodies from liver.

Some basic concepts relating to carbohydrates metabolism:

Glycolysis is a process in which glucose is converted into lactate or pyruvate.

Gluconeogenesis is process in which lactate or pyruvate is converted into glucose.

Glycogenolysis is process in which glycogen is converted into glucose.

Glycogenesis is process in which glucose is converted into glycogen.

VLDL stands for very-low-density lipoprotein

In Liver:

a)      Carbohydrate metabolism:

Feeding process	Fasting process
Glucose uptake by liver through GLUT-2 (insulin independent) by liver increases. So, it is phosphorylated into liver to be trapped and is converted into glycogen or used in degradation of glucose.	Glycogen degradation increases. (Glycogenolysis) for hours Glucose synthesis increases. (Gluconeogenesis) for days.
Phosphorylation of glucose increases
Glycogenesis increases (formation of glycogen)	decreases
Glycolysis increases (degradation of glucose)	decreases
Gluconeogenesis and Glycogenolysis decrease. (Formation of glucose)	Formation of glucose increases.

b)      Fat metabolism:

Feeding process	Fasting process
Fatty acids synthesis increases	Fatty acid oxidation increases (lipolysis)
TAG synthesis increases	Ketone bodies are formed to be fuel for brain and peripheral tissue

  

c)       Protein metabolism

Feeding process

Protein synthesis increases to replenish any proteins that are degraded in fasting process.

Increase amino acid degradation.

In adipose tissue:

a)      Carbohydrate metabolism:

Feeding process	Fasting process
Glucose transport through GLUT-4 (insulin dependent) increases	Glucose transport decreases Insulin decreases
Glycolysis increases as glucose is converted into DHAP that produces glycerol 3-phosphate through glycerol 3-phosphate dehydrogenase which will produce TAG So, TAG synthesis increases

b)      Fat metabolism:

Feeding process	Fasting process
FAs are stored in adipose tissue and provided by exogenous TAG from diet that sent out by intestine or endogenous TAG in VLDL that sent out by liver.	Degradation of fat increases (lipolysis). Release of fatty acids increases.  Uptake of fatty acids decreases.

In Resting skeletal muscle:

a)      Carbohydrate metabolism:

Feeding process	Fasting process
Glucose transport by GLUT-4 (insulin dependent).	switching from glucose to FAs.
Glycogen synthesis increases. (Glycogenesis).	Insulin decreases so glucose transport decreases.
	So, glucose from hepatic gluconeogenesis is unavailable for muscles and adipose tissue.

b)      Protein metabolism:

Feeding process	Fasting process
Protein synthesis increases	During the first few days, breakdown of protein increases to provide amino acids for gluconeogenesis.
uptake of branched chain amino acids increases	During weeks of fasting, muscle proteolysis decreases (Degradation of amino acid decreases) so ketone bodies synthesis increases to provide brain with energy.

c)       Fat metabolism:

Feeding process	Fasting process
Fatty acids are used as second energy resource for muscles after glucose.	During first 2 weeks, muscle uses FA from adipose tissue and ketone bodies from liver. After 3 weeks, muscle uses only FA and spares ketone bodies for brain.

In Brain:

Brain uses glucose through GLUT-1 of BBB which is insulin independent to oxidize 140 g/day

If the blood glucose falls below 40 mg/100 ml, function is impaired.

Brain lacks storage of FAs and glucose depending on their ratio in blood.

Brain uses glucose through GLUT-1 (insulin independent)

Glucose uptake by liver through GLUT-2 (insulin independent)

In adipose tissue and In Resting skeletal muscle Glucose transport through GLUT-4 (insulin dependent)

The Physiology of Fasting

Your body is switching into fat-burning mode now—glycogen is significantly depleted, so you’ll produce and use ketone bodies for energy. Through the breakdown of fat (a process called lipolysis), fat cells in the body release free fatty acids. PPAR-alpha (a regulator of fat metabolism in the liver), which is necessary for ketogenesis, is activated and ensures those fatty acids are used.

Fatty acids travel to the liver where they are transformed into ketone bodies through the process of beta-oxidation. When we say “ketone bodies,” we’re referring to three distinct types of molecules: acetone, acetoacetate, and beta-hydroxybutyrate, or BHB for short. Your body can use both acetoacetate and BHB for energy production. Blood ketone meters, which you may have seen people use while fasting or on a ketogenic diet, measure BHB levels in the blood. BHB levels can vary based on the individual, but within 24–72 hours of fasting, you’re likely to see BHB levels rise to somewhere between 0.5–2 mM; the range for nutritional ketosis.

At this point, ketones become your primary fuel, but your brain still needs a bit of glucose to function. With none to be found in your blood, and your glycogen stores completely tapped, your body makes glucose from non-carbohydrate sources like fat, ketones, and amino acids through a process called gluconeogenesis. Yes, your body can actually make sugar out of protein and fat. During this phase of fasting, you produce about 80 grams of glucose per day using this process, most of which is used by the brain. The rest of the body can rely almost exclusively on ketone bodies.

links and sources:

https://www.zerofasting.com/the-physiology-of-fasting/

Guyton Textbook of Medical Physiology 11th ed..pdf

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