EVER WONDER WHAT HAPPENS TO FOOD AFTER WE EAT IT?

After digested nutrients enter the blood via absorption in the small intestine (mechanisms not covered in article) in the form of amino acids, glucose and triglycerides (carried in chylomicrons) oxidation of glucose for ATP (cellular energy) production occurs in most body cells, while any excess “fuel” molecules are stored in hepatocytes (liver cells), adipocytes (fat cells) and skeletal muscle fibers for future use between meals. This process is known as the absorptive state (mechanisms beyond scope of article). How then is energy maintained or more specifically how is blood glucose stabilized long after a meal (4 hours) after all absorption of nutrients is almost completed in the small intestine?

Blood glucose homeostasis is extremely important for the body’s cells and especially important for the nervous system and red blood cells.
This is known as Postabsorptive state, and the following mechanisms help prevent hypoglycemia (ie., blood glucose below 3.9 – 6.1 mmol/liter) in otherwise healthy individuals. During this postabsorptive state glucose is both conserved and produced to maintain normal blood glucose levels. For example, the liver cells (Hepatocytes) produce glucose and release molecules into the bloodstream. In contrast, other body cells switch from glucose to alternate fuels for the production of cellular energy (ATP) for glucose conservation.
Mechanistically, the major postabsorptive reactions that produce glucose and glucose conservation are indicated below (see diagram, not included are the hormonal regulators ie., “ant-insulin” hormones if interested further, please refer to chart below. These hormones aid in the increase/conservation of glucose/ATP)

1)Breakdown of liver glycogen. During fasting, a major source of blood glucose is liver glycogen, which can provide about a 4-hour supply of glucose. Liver glycogen is continually being formed and broken down as needed.

2)Lipolysis. Glycerol, produced by breakdown of triglycerides in adipose tissue, is also used to form glucose.

3)Gluconeogenesis. Using lactic acid. During exercise, skeletal muscle tissue breaks down stored glycogen (see step 9 ) and produces some ATP anaerobically via glycolysis. Some of the pyruvic acid that results is converted to acetyl CoA, and some is converted to lactic acid, which diffuses into the blood. In the liver, lactic acid can be used for gluconeogenesis, and the resulting glucose is released into the blood.

4)Gluconeogenesis. Using amino acids. Modest breakdown of proteins in skeletal muscle and other tissues releases large amounts of amino acids, which then can be converted to glucose by gluconeogenesis in the liver.

Despite all of these ways the body produces glucose, blood glucose level cannot be maintained for very long without further metabolic changes. Thus, a major adjustment must be made during the postabsorptive state to produce ATP while conserving glucose. The following reactions produce ATP without using glucose:

5)Oxidation of fatty acids. The fatty acids released by lipolysis of triglycerides cannot be used for glucose production because acetyl CoA cannot be readily converted to pyruvic acid. But most cells can oxidize the fatty acids directly, feed them into the Krebs cycle as acetyl CoA, and produce ATP through the electron transport chain.

6)Oxidation of lactic acid. Cardiac muscle can produce ATP aerobically from lactic acid.

7)Oxidation of amino acids. In hepatocytes, amino acids may be oxidized directly to produce ATP.

8)Oxidation of ketone bodies. Hepatocytes also convert fatty acids to ketone bodies, which can be used by the heart, kidneys, and other tissues for ATP production.

9)Breakdown of muscle glycogen. Skeletal muscle cells break down glycogen to glucose 6-phosphate, which undergoes glycolysis and provides ATP for muscle contraction.

Source: Tortora, G. J., & Derrickson, B. H. (2014). Principles of anatomy and physiology. Milton, Qld: John Wiley & Sons Australia (all information and diagrams)