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Diabetes Mellitus: Overview and Type I Subtype

Diabetes Mellitus: Overview and Type I Subtype

Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
Type 1 diabetes is an autoimmune disease in which the immune system mistakenly attacks and destroys the insulin-producing beta cells in the pancreas. As a result, the body is unable to produce sufficient insulin, and individuals with...

Diabetes: Symptoms, Diagnosis, and Complications

Diabetes: Symptoms, Diagnosis, and Complications

For most patients, experiencing several weeks of polyuria, polydipsia, fatigue, and significant weight loss may indicate the presence of diabetes. Furthermore, adults displaying the phenotypic appearance of type 2 diabetes (particularly those who are obese and not initially insulin-requiring), may have islet cell autoantibodies, suggesting autoimmune-mediated β cell destruction and a diagnosis of latent autoimmune diabetes of adults (LADA). The categorization of glucose homeostasis is based on...

Diabetes Mellitus: Introduction

Diabetes Mellitus: Introduction

Diabetes mellitus consists of chronic metabolic disorders characterized by persistent hyperglycemia. This elevated blood glucose results from defects in insulin secretion, impaired insulin action, or both. Insulin, produced by pancreatic β-cells, is essential for maintaining glucose homeostasis by facilitating cellular glucose uptake for energy or storage. Disruptions in insulin production or function lead to glucose accumulation in the bloodstream, causing the clinical features and long-term...

Type I Diabetes III: Clinical Manifestations

Type I Diabetes III: Clinical Manifestations

Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...

Type II Diabetes II: Pathophysiology

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.

Hyperglycemia

Hyperglycemia

Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...

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Updated: Jul 10, 2026

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test

Published on: November 13, 2016

Impaired glucose tolerance as a disease.

¹Amylin Pharmaceuticals, San Diego, CA 92121, USA.

The American Journal of Cardiology

|September 29, 2001

Summary

Current diabetes diagnosis methods are insensitive. Post-oral glucose tolerance test (OGTT) measurements better predict risk, highlighting the need for interventions in prediabetes to reduce cardiovascular disease.

Area of Science:

Endocrinology
Metabolic Disorders
Cardiovascular Health

Background:

Current diabetes diagnostic criteria using fasting plasma glucose (FPG) lack sensitivity and predictive power for microvascular complications.
The post-oral glucose tolerance test (OGTT) phase is more sensitive for risk prediction and reflects the postprandial state associated with elevated microvascular risk.
Dysglycemia, or impaired glucose tolerance, can precede diabetes and is linked to macrovascular disease development at lower glucose levels than microvascular disease.

Purpose of the Study:

To review factors contributing to dysglycemia, such as insulin resistance and obesity.
To explore strategies for reducing cardiovascular risk in individuals with dysglycemia or prediabetes.
To highlight the importance of the post-OGTT period for risk assessment.

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Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

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Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test

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Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

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Published on: January 7, 2018

Main Methods:

Literature review of factors causing dysglycemia.
Analysis of interventions targeting cardiovascular risk in prediabetic populations.
Evaluation of the predictive value of post-OGTT glucose levels.

Main Results:

Fasting plasma glucose criteria are suboptimal for diabetes diagnosis and risk prediction.
Post-OGTT glucose levels offer superior prediction of microvascular risk.
Dysglycemia is associated with graded increases in macrovascular risk.

Conclusions:

Prediabetes and dysglycemia represent significant cardiovascular risk.
Interventions including diet modification, blood pressure control, statins, and insulin-sensitizing agents may mitigate risk.
Rethinking diagnostic criteria and focusing on post-OGTT measures is crucial for managing prediabetes.