| Management |
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| Post-Prandial Hyperglycemia |
Ashok Kumar DasDirector, Professor & Head of Medicine, JIPMER
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| Introduction |
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| It is widely believed that blood sugar levels should be maintained as close to normal as possible in a diabetic from the times of Dr. Ellison P. Joslin, maintenance of glycemia has been advocated to prevent the morbidity and mortality associated with diabetes. |
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| However, this primary goal of treatment has been very difficult to achieve in clinical practice. Among the numerous obstacles faced, post-prandial hyperglycemia is the important problem. |
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| A lot of recent research is being focused on this vexing
problem. This is due to the fact that most large-scale trials including the
Diabetes Control and Complications Trial (DCCT)1 have found that the morbidity
and complications associated with diabetes are reduced with strict blood sugar
control. Also of interest is the fact that many patients with controlled fasting
blood glucose levels have raised post-prandial blood glucose levels2. |
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| This review seeks to highlight some of the key issues in the pathogenesis, clinical implications and treatment of post-prandial hyperglycemia. |
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| Definition |
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| Impaired glucose tolerance is diagnosed when the 2-hour blood sugar value following a fasting oral glucose local of 75 gms is between 140 mg/dl and 200 mg/dl, according to the WHO criteria. Diabetes mellitus is present when the 2-hour value is more than 200 mg/dl. |
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| According to the standard goals of therapy, the 2-hour blood sugar value should be less than 200 mg/dl. According to the goals of intensive therapy, the 2-hour blood sugar value should be between 70 and 140 mg/dl. |
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| Values greater than these in a diabetic patient attest to the presence of postprandial hyperglycemia. |
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| Glucose Homeostasis in Post-Prandial State: |
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| After the ingestion of a meal or a glucose load, the plasma glucose concentration achieved depends on the amount of the ingested glucose appearing in the peripheral circulation (which is inversely proportional to the first-pass splanchnic glucose extraction), on the degree of suppression of endogenous glucose production, and on the disposal rate of glucose in the peripheral tissues3. |
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| The role of insulin in the post-prandial state has been subject to a lot of research. Insulin controls the suppression of hepatic glucose production and stimulation of glucose disposal in the insulin-dependent tissues (mainly the skeletal muscles). |
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| Sacca Let al4 and De Fronzo et al4 have also found evidence to link insulin along with hyperglycemia, in the stimulation glucose uptake. Conson A et al3 on an analysis, opined that insulin suppression of hepatic glucose production is much more significant physiologically as compared to its effect an stimulation of splanchnic glucose uptake. |
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| The relative importance of the different issues in the handling of a glucose load also needs to be considered. The double-isotope technique, where a subject is fed glucose labeled with an isotope orally and also infused with glucose labeled with another isotope, has been used to investigate glucose metabolism4,7,8. The results of studies indicate that the splanchnic bed and the liver are primarily involved in glucose homeostasis in the post-prandial state. |
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| Pathogenesis and Pathophysiology |
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| The important determinants of Post Prandial Hyperglycemia (PPHG) include |
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- Increased glucose influx from the gut
- Altered insulin secretion from pancreas
- Increased glucose production from liver
- Reduced uptake of glucose by liver
- Reduced uptake of glucose by muscle and adipose tissue
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| The controversy over the primary defect in diabetes and impaired glucose tolerance (IGT) still rages. Is it a defect in insulin secretion, or is it a defect of insulin action? Varying findings in different populations have only confounded the issue. |
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| Defective carbohydrate metabolism is central to the pathogenesis of IGT and NIDDM. Plasma glucose concentrations are determined by a fine balance between glucose entry and removal from circulation. |
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| In non-diabetic individuals, an oral glucose load triggers a rapid insulin secretory response. Insulin suppresses hepatic glucose release and stimulates peripheral glucose uptake, thereby limiting the post-prandial rise in plasma glucose concentration. In addition the term glucose effectiveness describes how glucose regulates its own metabolism. |
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