Physiological norms and dynamics
In the human body, the concentration of glucose in arterial blood between meals remains stable at 3.3–5.5 mmol/L (or 80–100 mg/dL). This is the so-called basal level.
When a person consumes a carbohydrate-rich meal, a physiological state develops: alimentary hyperglycosemia. Sugar concentration begins to rise, reaching its maximum in approximately 30–60 minutes. At the peak of this postprandial period, values may reach 7–8 mmol/L (120–140 mg/dL). A healthy body takes about two hours to completely level out this spike and return indicators to the initial basal norm.
The entire cycle can be divided into several key phases:
- Absorptive period (digestive period): the time of active nutrient absorption.
- Postabsorptive period: the time when nutrients from the intestine are no longer entering, and the body switches to using internal reserves.
- Fasting period: sets in during prolonged absence of food.
Biochemistry of the absorptive period
Immediately after a carbohydrate meal, the circulatory picture changes dramatically. In the hepatic portal vein, where blood drains from the intestine, glucose concentration increases enormously — up to 10–20 mmol/L (180–360 mg/dL). In response, the pancreas secretes insulin, while glucagon secretion is suppressed. Consequently, the insulin-glucagon ratio sharply increases.
Processes in the liver The liver takes the initial carbohydrate hit. Insulin triggers the following reactions here:
- The glucokinase reaction, which captures free glucose, is accelerated.
- Phosphoprotein phosphatase enzymes are activated, cleaving phosphate residues from key proteins.
- As a result of dephosphorylation, glycogen synthase transitions to an active state, while glycogen phosphorylase transitions to an inactive state (is inhibited).
Outcome for the liver: the generated glucose-6-phosphate is massively channeled into glycolysis pathways (for energy production) and glycogenesis (for storage as glycogen).
Processes in muscles and adipose tissue These tissues are insulin-dependent. Elevated insulin levels signal special carrier proteins, GLUT-4. They translocate from the intracellular cytosol directly into the plasma membrane. This opens the "doors" for glucose — it rapidly leaves the bloodstream and enters the cells. In muscle tissue, as in the liver, insulin additionally stimulates glycogen synthesis. Due to active glucose uptake by these three tissues (liver, muscles, and fat), blood glucose concentration normalizes in about 2 hours.
Regulation in the postabsorptive period and during fasting
Once food has been digested and assimilated, glucose levels begin to drop smoothly. Along with it, the insulin-glucagon ratio also falls — now glucagon takes the stage.
The main task of this period is to prevent hypoglycemia. To maintain normoglycemia, the body uses two main mechanisms:
- Glycogenolysis — breakdown of liver glycogen stores.
- Gluconeogenesis — generation of new glucose from non-carbohydrate precursors (amino acids, lactate, glycerol).
Temporal dynamics of sugar sources:
- If you have not eaten for about 12 hours, hepatic glycogen remains the main energy supplier. Glucagon activates the enzyme glycogen phosphorylase, leading to the mobilization of carbohydrate reserves.
- If fasting continues for 24 hours (a full day), hepatic glycogen stores are depleted to zero. From this moment on, the sole mechanism rescuing the body from falling blood sugar levels becomes gluconeogenesis.
Briefly: answers to topical questions
Which hormones, besides glucagon, are involved in maintaining glucose levels during the postabsorptive period and fasting?
During the postabsorptive period and fasting, glucose levels are maintained by counter-regulatory hormones, which are insulin antagonists.
These include:
- Adrenaline — stimulates glycogenolysis, gluconeogenesis, and lipolysis.
- Cortisol — triggers gluconeogenesis, lipolysis, and protein breakdown.
- Growth hormone (GH) — secreted in response to decreased glucose levels during fasting.
- Iodothyronines — thyroid hormones involved in regulating energy substrate metabolism.
How to remember the effects of insulin on enzymes: Insulin is the hormone of "satiety and construction". Therefore, under its action, Glycogen SYNTHASE (which synthesizes) becomes Active, while Glycogen PHOSPHORYLASE (which breaks down) goes on vacation (is inactive).
Class and exam questions
How long after a carbohydrate meal does glucose concentration peak?
The maximum concentration (7–8 mmol/L) in arterial blood is observed 30–60 minutes after a meal.
What is the glucose concentration in the portal vein after a meal?
In the hepatic portal vein, sugar levels may briefly rise to 10–20 mmol/L (180–360 mg/dL).
Where does the body get glucose 24 hours after the last meal?
After 24 hours of fasting, hepatic glycogen stores are completely depleted. Gluconeogenesis remains the sole source of glucose for maintaining normoglycemia.
What is the role of GLUT-4 transporters?
Under the action of insulin, GLUT-4 proteins translocate from the cytosol to the membranes of muscle and adipose tissue cells, allowing glucose to rapidly enter the cell from the bloodstream.
What else to study on this topic
- Mechanism of action of the insulin-glucagon ratio
- Structure and isoforms of GLUT family transporters
- Cascade of enzyme phosphorylation and dephosphorylation
- Detailed reactions of gluconeogenesis
- Differences in glycogen metabolism between the liver and muscles
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