Mars1946
BANNED
- Messages
- 29
- Type of diabetes
- Type 2
- Treatment type
- Insulin
PARADOX about treatment of T2DM with Insulin and Metformin
The disposal of glucose after meals depends on the ability of insulin to increase peripheral glucose uptake and to simultaneously decrease endogenous glucose production. Although studies have suggested that the kidney can contribute up to 25% of endogenous glucose production. The defect in T2DM is primarily in defective regulation of glucose production from the liver. Two routes of glucose production from the liver are glycogenolysis of stored glycagon and gluconeogenesis from two and three-carbon substrates derived primarily from skeletal muscle.
Hepatic insulin resistance plays an important role in the hyperglycemia of T2DM and the impaired suppression of hepatic glucose output appears to be quantitatively similar to, or even larger than, the defect in stimulation of peripheral glucose disposal. There is a direct relationship between increased hepatic glucose output and fasting hyperglycemia.
Insulin mediated suppression of hepatic glucose output is impaired at both low and high plasma insulin levels in T2DM; hepatic glucose production is elevated early in the course of the disease, but may be normal in lean, relatively insulin sensitive type 2 diabetics.
Treatment of patients with Metformin, which suppresses hepatic glucose production, results in improved glucose tolerance.
My opinion is the best treatment of T2DM is with Insulin and Metformin.
This treatment is equivalent to the Tertiary Prophylactic Therapy.
The purpose of this treatment is to achieve a stage of EUGLYCEMIA.
The disposal of glucose after meals depends on the ability of insulin to increase peripheral glucose uptake and to simultaneously decrease endogenous glucose production. Although studies have suggested that the kidney can contribute up to 25% of endogenous glucose production. The defect in T2DM is primarily in defective regulation of glucose production from the liver. Two routes of glucose production from the liver are glycogenolysis of stored glycagon and gluconeogenesis from two and three-carbon substrates derived primarily from skeletal muscle.
Hepatic insulin resistance plays an important role in the hyperglycemia of T2DM and the impaired suppression of hepatic glucose output appears to be quantitatively similar to, or even larger than, the defect in stimulation of peripheral glucose disposal. There is a direct relationship between increased hepatic glucose output and fasting hyperglycemia.
Insulin mediated suppression of hepatic glucose output is impaired at both low and high plasma insulin levels in T2DM; hepatic glucose production is elevated early in the course of the disease, but may be normal in lean, relatively insulin sensitive type 2 diabetics.
Treatment of patients with Metformin, which suppresses hepatic glucose production, results in improved glucose tolerance.
My opinion is the best treatment of T2DM is with Insulin and Metformin.
This treatment is equivalent to the Tertiary Prophylactic Therapy.
The purpose of this treatment is to achieve a stage of EUGLYCEMIA.
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