Glucose metabolism and hyperglycemia

Dario Giugliano, Antonio Ceriello, Katherine Esposito

Research output: Contribution to journalArticle

131 Citations (Scopus)

Abstract

Islet dysfunction and peripheral insulin resistance are both present in type 2 diabetes and are both necessary for the development of hyperglycemia. In both type 1 and type 2 diabetes, large, prospective clinical studies have shown a strong relation between time-averaged mean values of glycemia, measured as glycated hemoglobin (HbA1c), and vascular diabetic complications. These studies are the basis for the American Diabetes Association's current recommended treatment goal that HbA1c should be 1c concentration is considered the gold standard for assessing long-term glycemia; however, it does not reveal any information on the extent or frequency of blood glucose excursions, but provides an overall mean value only. Postprandial hyperglycemia occurs frequently in patients with diabetes receiving active treatment and can occur even when metabolic control is apparently good. Interventional studies indicate that reducing postmeal glucose excursions is as important as controlling fasting plasma glucose in persons with diabetes and impaired glucose tolerance. Evidence exists for a causal relation between postmeal glucose increases and microvascular and macrovascular outcomes; therefore, it is not surprising that treatment with different compounds that have specific effects on postprandial glucose regulation is accompanied by a significant improvement of many pathways supposed to be involved in diabetic complications, including oxidative stress, endothelial dysfunction, inflammation, and nuclear factor-κB activation. The goal of therapy should be to achieve glycemic status as near to normal as safely possible in all 3 components of glycemic control: HbA1c, fasting glucose, and postmeal glucose peak.

Original languageEnglish
JournalAmerican Journal of Clinical Nutrition
Volume87
Issue number1
Publication statusPublished - Jan 1 2008

Fingerprint

hyperglycemia
Hyperglycemia
glycohemoglobin
Glucose
glucose
metabolism
blood glucose
diabetes
noninsulin-dependent diabetes mellitus
Type 2 Diabetes Mellitus
fasting
Fasting
Diabetic Angiopathies
glycemic control
Glucose Intolerance
Glycosylated Hemoglobin A
glucose tolerance
Diabetes Complications
Therapeutics
Type 1 Diabetes Mellitus

Keywords

  • Cardiovascular disease risk
  • Fasting hyperglycemia
  • Glycated hemoglobin
  • Lifestyle
  • Postprandial hyperglycemia
  • Type 2 diabetes

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

Glucose metabolism and hyperglycemia. / Giugliano, Dario; Ceriello, Antonio; Esposito, Katherine.

In: American Journal of Clinical Nutrition, Vol. 87, No. 1, 01.01.2008.

Research output: Contribution to journalArticle

Giugliano, Dario ; Ceriello, Antonio ; Esposito, Katherine. / Glucose metabolism and hyperglycemia. In: American Journal of Clinical Nutrition. 2008 ; Vol. 87, No. 1.
@article{49fa2d081e4049cb9501a795e9d0151b,
title = "Glucose metabolism and hyperglycemia",
abstract = "Islet dysfunction and peripheral insulin resistance are both present in type 2 diabetes and are both necessary for the development of hyperglycemia. In both type 1 and type 2 diabetes, large, prospective clinical studies have shown a strong relation between time-averaged mean values of glycemia, measured as glycated hemoglobin (HbA1c), and vascular diabetic complications. These studies are the basis for the American Diabetes Association's current recommended treatment goal that HbA1c should be 1c concentration is considered the gold standard for assessing long-term glycemia; however, it does not reveal any information on the extent or frequency of blood glucose excursions, but provides an overall mean value only. Postprandial hyperglycemia occurs frequently in patients with diabetes receiving active treatment and can occur even when metabolic control is apparently good. Interventional studies indicate that reducing postmeal glucose excursions is as important as controlling fasting plasma glucose in persons with diabetes and impaired glucose tolerance. Evidence exists for a causal relation between postmeal glucose increases and microvascular and macrovascular outcomes; therefore, it is not surprising that treatment with different compounds that have specific effects on postprandial glucose regulation is accompanied by a significant improvement of many pathways supposed to be involved in diabetic complications, including oxidative stress, endothelial dysfunction, inflammation, and nuclear factor-κB activation. The goal of therapy should be to achieve glycemic status as near to normal as safely possible in all 3 components of glycemic control: HbA1c, fasting glucose, and postmeal glucose peak.",
keywords = "Cardiovascular disease risk, Fasting hyperglycemia, Glycated hemoglobin, Lifestyle, Postprandial hyperglycemia, Type 2 diabetes",
author = "Dario Giugliano and Antonio Ceriello and Katherine Esposito",
year = "2008",
month = "1",
day = "1",
language = "English",
volume = "87",
journal = "American Journal of Clinical Nutrition",
issn = "0002-9165",
publisher = "American Society for Nutrition",
number = "1",

}

TY - JOUR

T1 - Glucose metabolism and hyperglycemia

AU - Giugliano, Dario

AU - Ceriello, Antonio

AU - Esposito, Katherine

PY - 2008/1/1

Y1 - 2008/1/1

N2 - Islet dysfunction and peripheral insulin resistance are both present in type 2 diabetes and are both necessary for the development of hyperglycemia. In both type 1 and type 2 diabetes, large, prospective clinical studies have shown a strong relation between time-averaged mean values of glycemia, measured as glycated hemoglobin (HbA1c), and vascular diabetic complications. These studies are the basis for the American Diabetes Association's current recommended treatment goal that HbA1c should be 1c concentration is considered the gold standard for assessing long-term glycemia; however, it does not reveal any information on the extent or frequency of blood glucose excursions, but provides an overall mean value only. Postprandial hyperglycemia occurs frequently in patients with diabetes receiving active treatment and can occur even when metabolic control is apparently good. Interventional studies indicate that reducing postmeal glucose excursions is as important as controlling fasting plasma glucose in persons with diabetes and impaired glucose tolerance. Evidence exists for a causal relation between postmeal glucose increases and microvascular and macrovascular outcomes; therefore, it is not surprising that treatment with different compounds that have specific effects on postprandial glucose regulation is accompanied by a significant improvement of many pathways supposed to be involved in diabetic complications, including oxidative stress, endothelial dysfunction, inflammation, and nuclear factor-κB activation. The goal of therapy should be to achieve glycemic status as near to normal as safely possible in all 3 components of glycemic control: HbA1c, fasting glucose, and postmeal glucose peak.

AB - Islet dysfunction and peripheral insulin resistance are both present in type 2 diabetes and are both necessary for the development of hyperglycemia. In both type 1 and type 2 diabetes, large, prospective clinical studies have shown a strong relation between time-averaged mean values of glycemia, measured as glycated hemoglobin (HbA1c), and vascular diabetic complications. These studies are the basis for the American Diabetes Association's current recommended treatment goal that HbA1c should be 1c concentration is considered the gold standard for assessing long-term glycemia; however, it does not reveal any information on the extent or frequency of blood glucose excursions, but provides an overall mean value only. Postprandial hyperglycemia occurs frequently in patients with diabetes receiving active treatment and can occur even when metabolic control is apparently good. Interventional studies indicate that reducing postmeal glucose excursions is as important as controlling fasting plasma glucose in persons with diabetes and impaired glucose tolerance. Evidence exists for a causal relation between postmeal glucose increases and microvascular and macrovascular outcomes; therefore, it is not surprising that treatment with different compounds that have specific effects on postprandial glucose regulation is accompanied by a significant improvement of many pathways supposed to be involved in diabetic complications, including oxidative stress, endothelial dysfunction, inflammation, and nuclear factor-κB activation. The goal of therapy should be to achieve glycemic status as near to normal as safely possible in all 3 components of glycemic control: HbA1c, fasting glucose, and postmeal glucose peak.

KW - Cardiovascular disease risk

KW - Fasting hyperglycemia

KW - Glycated hemoglobin

KW - Lifestyle

KW - Postprandial hyperglycemia

KW - Type 2 diabetes

UR - http://www.scopus.com/inward/record.url?scp=38149010468&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=38149010468&partnerID=8YFLogxK

M3 - Article

C2 - 18175761

AN - SCOPUS:38149010468

VL - 87

JO - American Journal of Clinical Nutrition

JF - American Journal of Clinical Nutrition

SN - 0002-9165

IS - 1

ER -