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Related Concept Videos

Type II Diabetes II: Pathophysiology01:24

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.
Diabetes Mellitus: Type 2 and Gestational01:22

Diabetes Mellitus: Type 2 and Gestational

Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
Carbohydrate Metabolism01:36

Carbohydrate Metabolism

Carbohydrates are polymers composed of molecules containing atoms of carbon, hydrogen and oxygen. One gram of carbohydrate can provide four kilo-calories of energy, which makes it the most efficient instant energy source.
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Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis01:25

Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis

Type 2 diabetes mellitus develops gradually and is often asymptomatic in early stages.Clinical ManifestationsWhen symptoms appear, they include fatigue, blurred vision, pruritus, delayed wound healing, and recurrent infections, particularly candidal infections. Peripheral neuropathy may present as numbness or tingling in the extremities. Classic hyperglycemia symptoms—polyuria, polydipsia, and polyphagia—are less common. Most patients are overweight and frequently have associated hypertension...

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Related Experiment Video

Updated: Jun 24, 2026

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)
08:13

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

Published on: January 7, 2018

The second-meal phenomenon in type 2 diabetes.

Ana Jovanovic1, Jean Gerrard, Roy Taylor

  • 1Diabetes Research Group and Newcastle Magnetic Resonance Centre, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK.

Diabetes Care
|April 16, 2009
PubMed
Summary

Eating breakfast significantly reduces the post-lunch glucose spike in type 2 diabetes, demonstrating a preserved second-meal effect. This finding suggests therapeutic potential for non-glucose insulin secretagogues.

Related Experiment Videos

Last Updated: Jun 24, 2026

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)
08:13

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

Published on: January 7, 2018

Area of Science:

  • Metabolic research
  • Diabetes mellitus studies

Background:

  • The second-meal effect, where eating breakfast lowers post-lunch glucose rise, is known in healthy individuals.
  • Its presence in type 2 diabetes requires investigation.

Purpose of the Study:

  • To evaluate the second-meal effect in individuals with type 2 diabetes.
  • To explore the impact of pre-meal arginine on post-lunch glucose levels.

Main Methods:

  • Compared post-lunch metabolic changes in 8 obese type 2 diabetic subjects over 3 conditions: breakfast eaten, no breakfast, and no breakfast with pre-meal intravenous arginine.
  • Measured plasma glucose and free fatty acid concentrations.

Main Results:

  • Significantly lower post-lunch plasma glucose rise when breakfast was consumed (P < 0.0001).
  • Arginine administration before lunch reduced the post-lunch glucose rise by nearly half.
  • Plasma free fatty acid levels at lunchtime correlated directly with the post-lunch glucose rise (r = 0.67, P = 0.0005).

Conclusions:

  • The second-meal effect is maintained in type 2 diabetes.
  • Pre-meal administration of a non-glucose insulin secretagogue, like arginine, can halve postprandial glucose elevation.
  • These findings indicate potential therapeutic applications for managing type 2 diabetes.