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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.
Type I Diabetes II: Pathophysiology01:26

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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...
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Diabetes: Management and Pharmacotherapy

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Oral Hypoglycemic Agents: Biguanides and Glitazones

Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood glucose levels...
Pathophysiology of Diabetes01:20

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Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
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[Antipsychotics and diabetes: pathophysiology and current recommendations].

Myriam Déban Kuflom1, Marc Rajakoski1, Vasiliki Galani2

  • 1Service d'endocrinologie, diabétologie et métabolisme, Département de médecine, Hôpitaux universitaires de Genève, 1211 Genève 14.

Revue Medicale Suisse
|May 29, 2026
PubMed
Summary

Antipsychotic medications for psychotic disorders raise diabetes and metabolic syndrome risks, increasing cardiovascular issues. Clozapine and olanzapine pose the highest risks, necessitating improved monitoring and early intervention.

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A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
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Last Updated: May 31, 2026

Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
07:30

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Published on: May 10, 2018

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
10:03

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory

Published on: February 28, 2013

Area of Science:

  • Pharmacology
  • Endocrinology
  • Cardiology

Background:

  • Antipsychotic drugs are crucial for treating psychotic disorders.
  • These medications are associated with increased risks of diabetes and metabolic syndrome.
  • This elevates cardiovascular morbidity and mortality rates.

Purpose of the Study:

  • To review the risks of metabolic complications associated with antipsychotic drug use.
  • To discuss the mechanisms underlying these metabolic effects.
  • To emphasize the need for improved monitoring and management strategies.

Main Methods:

  • Literature review of studies on antipsychotic drugs and metabolic side effects.
  • Analysis of mechanisms involving central and peripheral pathways.
  • Evaluation of current guidelines and implementation challenges.

Main Results:

  • Risk of diabetes and metabolic syndrome varies among antipsychotic agents.
  • Clozapine and olanzapine exhibit the highest liability for metabolic complications.
  • Mechanisms include hypothalamic and peripheral actions, leading to insulin resistance and hormonal dysregulation, sometimes independent of weight gain.

Conclusions:

  • Metabolic monitoring for patients on antipsychotics is inadequately implemented.
  • Systematic screening and early preventive strategies are vital.
  • Reducing metabolic complications is essential to lower cardiovascular risks in this population.