Ketonuria

Introduction Low blood sugar levels in severely starved or untreated diabetics lead to increased gluconeogenesis, fatty acid oxidation accelerates the production of large amounts of acetyl-CoA, and gluconeogenesis causes oxaloacetate to be depleted, while the latter is acetyl-CoA entering the citric acid cycle. Necessary, whereby acetyl-CoA is directed to the direction of the ketone body. A large number of ketone bodies appear in the blood and urine. Once the diagnosis is clear, active treatment should be given as soon as possible, mainly diet therapy. The younger the treatment begins, the better the effect.

Cause

When the insulin is severely deficient, the oxaloacetate is reduced. Therefore, a large amount of acetyl-CoA cannot be sufficiently oxidized to form a large amount of ketone bodies, and if it exceeds its oxidative utilization ability, it can accumulate into hyperketonemia and ketonuria.

In diabetic patients, exogenous and endogenous triglyceride removal is attenuated due to insulin deficiency, and triglycerides in the blood are often increased. In addition, when insulin is insufficient, the tricarboxylic acid cycle and the pentose phosphate pathway are weakened, the gluconeogenesis is strengthened, and acetyl-CoA is accumulated. Therefore, acetyl-CoA increases cholesterol synthesis, thereby forming hypercholesterolemia accompanied by hypertriglyceridemia. And high free fatty acidemia, collectively called hyperlipidemia, and combined with protein and apolipoprotein to form hyperlipoproteinemia. Hyperlipidemia and hyperlipoproteinemia in diabetic patients have an important relationship with arteriosclerosis and vascular complications.

an examination

Related inspection

Urine ferric chloride test blood test urine microscopy

When the insulin is severely deficient, 1 because the glycolysis is significantly weakened, the raw material x-phosphoglycerol required for the synthesis of fat is reduced. 2 As the pentose phosphate pathway is weakened, the hydrogen donor required for the synthesis of fat and the production of reduced coenzyme are reduced, resulting in a decrease in fat synthesis. 3 A large amount of fat mobilizes and decomposes into x-glycerophosphate and free fatty acids. A large amount of fatty acids are -oxidized in hepatocytes to produce a large amount of acetyl-CoA.

Under normal circumstances, most of acetyl-CoA is combined with oxaloacetate to oxidize to produce energy and carbon dioxide and water through a cycle of tricarboxylic acid, and a small portion is condensed into a ketone body. However, when the insulin is severely deficient, the oxaloacetate is reduced. Therefore, a large amount of acetyl-CoA cannot fully enter the tricarboxylic acid cycle to form a large amount of ketone bodies. If it exceeds its oxidative utilization ability, it can accumulate into hyperketonemia and ketoneuria. Ketoacidosis can occur, and even coma.

Differential diagnosis

When the insulin is severely deficient, 1 because the glycolysis is significantly weakened, the raw material x-phosphoglycerol required for the synthesis of fat is reduced. 2 As the pentose phosphate pathway is weakened, the hydrogen donor required for the synthesis of fat and the production of reduced coenzyme are reduced, resulting in a decrease in fat synthesis. 3 A large amount of fat mobilizes and decomposes into x-glycerophosphate and free fatty acids. A large amount of fatty acids are -oxidized in hepatocytes to produce a large amount of acetyl-CoA. Under normal circumstances, most of acetyl-CoA is combined with oxaloacetate to oxidize to produce energy and carbon dioxide and water through a cycle of tricarboxylic acid, and a small portion is condensed into a ketone body. However, when the insulin is severely deficient, the oxaloacetate is reduced. Therefore, a large amount of acetyl-CoA cannot fully enter the tricarboxylic acid cycle to form a large amount of ketone bodies. If it exceeds its oxidative utilization ability, it can accumulate into hyperketonemia and ketoneuria. Ketoacidosis can occur, and even coma.

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