Abstract

The aim of this article is to evaluate the impact of postprandial hyperglycemia in patients with type 2 diabetes mellitus (T2DM). Postprandial hyperglycemia is a major determinant in overall glycemic control. Diabetic mellitus is an endocrine disorder steadily increasing worldwide, particularly in the developing countries like India. Diabetic patients are at high risk of cardiovascular events and mealtime plasma glucose fluctuations are important cardiovascular risk factors in type 2 diabetic patients. Diabetes is also one of the most important risk factors for chronic kidney disease. For diabetic patients with chronic kidney disease (CKD), the risk of cardiovascular disease is even higher. CKD can impair the ability of the kidneys to metabolize drugs and as a consequence a dose adjustment or an extended dose interval is usually needed in CKD patients in order to keep an optimal safety/efficacy profile. Oral hypoglycemic agents like glinides and alpha glucosidase inhibitors do not require dose adjustments and hence can be used safely in patients with CKD. Oral treatment with Repaglinide has proven beneficial effect on cardiovascular risk factors. It is therefore very important to use pharmacological tools allowing keeping post-meal glucose oscillations within narrow range. Regimens that target both fasting and post meal glycemia are needed to achieve optimal glucose control to prevent microvascular and macrovascular complications.

Highlights

  • [2] type 2 diabetes mellitus (T2DM) is a disorder characterized by insulin resistance and a progressive decline in pancreatic β-cell function associated with increasing hyperglycaemia

  • The early and late postlunch glucose values are predictive for poor diabetes control, indicating that PPHG is a major determinant in overall glycaemic control. [4]

  • (1) Both postprandial hyperglycaemia and hypertriglyceridaemia are accompanied by oxidative stress, which in turn causes endothelial dysfunction and eventually atherosclerosis (2) acute increases in glucose stimulate superoxide production at the mitochondrial level in endothelial cells, which in turn leads to endothelial dysfunction and atherosclerosis (3) rapid increases in glucose and lipid levels after ingestion of a meal are likely to trigger carbonyl stress which, either independently or by potentiation of oxidative stress, contributes to the development of both microvascular and macrovascular complications. [4]

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Summary

Introduction

Chronic illness requiring continuous medical care with multifactorial risk reduction strategies beyond glycemic control. [1] As per International diabetes federation (IDF) data, in 2035 India will stand 2nd in the world with a total of 109.0 million people suffering from diabetes. [2] T2DM is a disorder characterized by insulin resistance and a progressive decline in pancreatic β-cell function associated with increasing hyperglycaemia. The UK Prospective Diabetes Study (UKPDS) indicated that by the time T2DM is diagnosed, individuals have already lost up to 50% of their β-cell function. Values are in the non-diabetic range, whereas elevated fasting plasma glucose (FPG) concentrations are not independently associated with increased cardiovascular disease (CVD) risk. The objective of this review article was to enlighten about the significant contribution of PPHG to be a major determinant in increased HbA1c. Apprising the use of drugs (Glinides, Alpha glucosidase inhibitors etc.) which can contribute in reducing HbA1c in individuals by targeting PPHG and without any dose reduction for those with renal impairment can prove to be a new armamentarium of treating diabetes in majority population. The early and late postlunch glucose values are predictive for poor diabetes control, indicating that PPHG is a major determinant in overall glycaemic control. 1139 men and women with newly diagnosed type 2 diabetes 93 men and 82 women with type 2 diabetes not previously drug-treated

Key findings
Cardiovascular Impact of Oral Hypoglycemic Agents
Factors Related to Drug Pharmacokinetics in Ckd Population
Renal Safety of Antihyperglycemic Agents in CKD
Discussion
Findings
Conclusions
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