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Related Concept Videos

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 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...
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...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
Diabetes Mellitus: Overview and Type I Subtype01:22

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...

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Related Experiment Video

Updated: Jun 27, 2026

Generation of High Quality Chromatin Immunoprecipitation DNA Template for High-throughput Sequencing (ChIP-seq)
09:52

Generation of High Quality Chromatin Immunoprecipitation DNA Template for High-throughput Sequencing (ChIP-seq)

Published on: April 19, 2013

Polymorphisms within the novel type 2 diabetes risk locus MTNR1B determine beta-cell function.

Harald Staiger1, Fausto Machicao, Silke A Schäfer

  • 1Division of Endocrinology, Diabetology, Angiology, Nephrology, and Clinical Chemistry, Department of Internal Medicine, University Hospital Tübingen, Tübingen, Germany.

Plos One
|December 18, 2008
PubMed
Summary
This summary is machine-generated.

Genetic variations in the MTNR1B gene influence fasting glucose levels and insulin secretion, impacting type 2 diabetes risk. These MTNR1B variants affect beta-cell function, a key mechanism in diabetes development.

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Last Updated: Jun 27, 2026

Generation of High Quality Chromatin Immunoprecipitation DNA Template for High-throughput Sequencing (ChIP-seq)
09:52

Generation of High Quality Chromatin Immunoprecipitation DNA Template for High-throughput Sequencing (ChIP-seq)

Published on: April 19, 2013

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds
12:32

High-resolution Respirometry to Measure Mitochondrial Function of Intact Beta Cells in the Presence of Natural Compounds

Published on: January 23, 2018

Area of Science:

  • Genetics
  • Metabolic Disease
  • Endocrinology

Background:

  • MTNR1B is a newly identified gene associated with type 2 diabetes risk and fasting glucose levels.
  • Previous studies suggest MTNR1B plays a role in glucose metabolism.

Purpose of the Study:

  • To investigate the association between common genetic variations in the MTNR1B gene and obesity, impaired insulin secretion, and insulin resistance in individuals at high risk for type 2 diabetes.

Main Methods:

  • Genotyping of 1,578 non-diabetic subjects for five MTNR1B single nucleotide polymorphisms (SNPs).
  • Metabolic characterization including oral glucose tolerance tests (OGTT), hyperinsulinemic-euglycemic clamps, and intravenous glucose tolerance tests (IVGTT).

Main Results:

  • No significant association was found between MTNR1B SNPs and obesity measures.
  • SNPs rs10830962, rs4753426, and rs10830963 were linked to higher fasting glucose and reduced insulin secretion.
  • SNP rs3781638 showed association with lower fasting glucose, increased insulin secretion, and improved insulin sensitivity.

Conclusions:

  • Common genetic variations within MTNR1B significantly influence glucose-stimulated insulin secretion and plasma glucose concentrations.
  • The impact of MTNR1B variants on beta-cell function is a likely mechanism contributing to increased type 2 diabetes risk.