Increased gluconeogenesis

Introduction For those who suffer from chronic hunger and excessive fatigue, hunger feels a significant reduction in inhibition. As liver glycogen is significantly reduced, blood sugar is lowered, insulin secretion is reduced, glucagon secretion is increased, so that catabolism is enhanced, and gluconeogenesis is promoted to ensure the supply of glucose, first of all, the needs of the brain. Throughout the hunger process, the body's physiological protection is very prominent, that is, to strengthen the decomposition of minor parts such as muscles, to ensure the nutritional needs of the brain and the central nervous system and the vital organs.

Cause

Cause:

In the case of chronic hunger and excessive fatigue, the secretion of glucagon increases, which enhances catabolism and promotes gluconeogenesis. Glucagon has a strong role in promoting glycogenolysis and gluconeogenesis, resulting in a significant increase in blood sugar. Glucagon activates hepatocyte phosphorylase through the cAMP-PK system to accelerate glycogenolysis. The gluconeogenesis is enhanced by the fact that the hormone accelerates the entry of amino acids into the liver cells and activates the enzyme system involved in the gluconeogenesis process.

When the liver or kidney is gluconeogenic with pyruvic acid as a raw material, the seven-step reaction in gluconeogenesis is a reverse reaction in glycolysis, which has the same enzyme catalysis. However, there are three steps in glycolysis, which are irreversible reactions. These three-step reactions must be bypassed during gluconeogenesis at the expense of more energy expenditure.

These three steps are all strongly exothermic, they are:

1. Glucose is catalyzed by hexokinase to produce glucose 6 G=-33.5kJ/mol

2, 6-phosphate fructose catalyzed by phosphofructokinase to produce 1,6-diphosphate fructose G=-22.2kJ/mol

3. Phosphoenol-type pyruvate produces pyruvate by pyruvate kinase G=-16.7kJ/mol

These three steps will be bypassed like this:

1. Glucose 6 phosphatase catalyzes the production of glucose by glucose 6 phosphate.

2. Fructose 1,6 diphosphatase catalyzes the fructose 1,6 diphosphate to produce fructose 6 phosphate.

3. Pyruvate enters the mitochondria with the help of a monocarboxylic acid transport enzyme. Under the catalysis of pyruvate carboxylase, one molecule of ATP is consumed to form oxaloacetate. Oxaloacetic acid does not pass through the mitochondrial membrane. In the malate-aspartate cycle, oxaloacetate passes through the mitochondrial membrane and becomes phosphoenolpyruvate with the help of phosphoenolpyruvate carboxylase. The reaction consumes one molecule of GTP.

an examination

Related inspection

Glucagon serum glucagon (PG) blood pyruvate

The hunger process is metabolized under hormone regulation such as decreased insulin and increased glucagon:

1 Muscle breakdown strengthens, and most of the released amino acids are converted to alanine and glutamine.

2 gluconeogenesis enhanced. Alanine is regulated by glucagon in the liver, significantly accelerating gluconeogenesis. Muscle-forming glutamine is taken up by the intestinal mucosa, converted to alanine, and enters the liver through the portal vein, which is another source of gluconeogenesis. It can be seen that the gluconeogenesis during the starvation process is mainly carried out in the liver (about 80% of the xenobiotics, and the remaining 20% in the renal cortex).

3 fat decomposition accelerated, plasma glycerol and fatty acid content increased, the result is still gluconeogenesis. Because glycerol can directly produce sugar, and fatty acid can provide gluconeogenesis energy, and can also produce acetyl-CoA to promote the gluconeogenesis of amino acids, pyruvic acid, lactic acid and the like. About 1/4 of the fatty acids decomposed by fat are converted into ketone bodies in the liver, so plasma ketone bodies can be increased hundreds of times when starved. Fatty acids and ketone bodies are the source of energy for the heart muscle, kidney cortex and skeletal muscle, and some ketone bodies can also be used by the brain.

4 tissue utilization of glucose reduction, due to tissue oxidation and the use of fatty acids and ketone bodies to strengthen, the physiological significance is to reduce the source of restricted glucose, and turn to the use of fat in the fat, because the body reserves the fat according to the isothermal price, far More than the reserve of glycogen. It can be seen that when hunger is enhanced by gluconeogenesis, the use of glucose is reduced, which is conducive to maintaining blood sugar levels, which is extremely beneficial for maintaining the functions of the brain and central nervous system.

Differential diagnosis

Insulin regulation of glucose metabolism:

Insulin promotes the uptake and utilization of glucose by tissues and cells, accelerates the synthesis of glucose into glycogen, stores it in the liver and muscle, inhibits gluconeogenesis, promotes the conversion of glucose into fatty acids, and stores it in adipose tissue, resulting in a decrease in blood sugar levels. When insulin is deficient, the blood sugar level rises. If it exceeds the renal sugar threshold, sugar will appear in the urine, causing diabetes.

Glucagon is a hormone that promotes catabolism. Glucagon has a strong role in promoting glycogenolysis and gluconeogenesis, which causes a significant increase in blood glucose. A 1 mol/L hormone can rapidly decompose 3 x 106 mol/L of glucose from glycogen. Glucagon activates hepatocyte phosphorylase through the cAMP-PK system to accelerate glycogenolysis. The gluconeogenesis is enhanced by the fact that the hormone accelerates the entry of amino acids into the liver cells and activates the enzyme system involved in the gluconeogenesis process. Glucagon also activates lipase, which promotes fat breakdown, while at the same time enhancing fatty acid oxidation and increasing ketone body formation.

The metabolic characteristics of the hunger process under the regulation of hormones such as insulin reduction and glucagon increase are:

1 Muscle breakdown strengthens, and most of the released amino acids are converted to alanine and glutamine.

2 gluconeogenesis enhanced. Alanine is regulated by glucagon in the liver, significantly accelerating gluconeogenesis. Muscle-forming glutamine is taken up by the intestinal mucosa, converted to alanine, and enters the liver through the portal vein, which is another source of gluconeogenesis. It can be seen that the gluconeogenesis during the starvation process is mainly carried out in the liver (about 80% of the xenobiotics, and the remaining 20% in the renal cortex).

3 fat decomposition accelerated, plasma glycerol and fatty acid content increased, the result is still gluconeogenesis. Because glycerol can directly produce sugar, and fatty acid can provide gluconeogenesis energy, and can also produce acetyl-CoA to promote the gluconeogenesis of amino acids, pyruvic acid, lactic acid and the like. About 1/4 of the fatty acids decomposed by fat are converted into ketone bodies in the liver, so plasma ketone bodies can be increased hundreds of times when starved. Fatty acids and ketone bodies are the source of energy for the heart muscle, kidney cortex and skeletal muscle, and some ketone bodies can also be used by the brain.

4 tissue utilization of glucose reduction, due to tissue oxidation and the use of fatty acids and ketone bodies to strengthen, the physiological significance is to reduce the source of restricted glucose, and turn to the use of fat in the fat, because the body reserves the fat according to the isothermal price, far More than the reserve of glycogen. It can be seen that when hunger is enhanced by gluconeogenesis, the use of glucose is reduced, which is conducive to maintaining blood sugar levels, which is extremely beneficial for maintaining the functions of the brain and central nervous system.

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