Defects in insulin secretion and action in the pathogenesis of type 2 diabetes mellitus

Area of Science:

• Endocrinology
• Metabolic Diseases
• Molecular Biology

Background:

• Type 2 diabetes mellitus (T2DM) is defined by impaired insulin action and secretion.
• Insulin resistance is an early feature, but beta-cell dysfunction ultimately triggers T2DM onset.
• Understanding these defects is crucial for effective T2DM management.

Purpose of the Study:

• To review recent advancements in the molecular mechanisms underlying insulin resistance.
• To explore the latest findings on beta-cell dysfunction in T2DM.
• To discuss the roles of novel factors in T2DM pathogenesis.

Main Methods:

• Literature review focusing on recent molecular and cellular studies.
• Analysis of research on mitochondrial function, enteroinsular axis, and endoplasmic reticulum stress.
• Examination of studies on adipose tissue and adipocytokines.
• Review of candidate genes and transcription factors.

Main Results:

• Mitochondrial dysfunction contributes significantly to insulin resistance and beta-cell failure.
• Dysregulation of the enteroinsular axis impacts insulin secretion and glucose homeostasis.
• Endoplasmic reticulum stress exacerbates beta-cell dysfunction.
• Adipose tissue secretes adipocytokines influencing metabolic regulation.
• Candidate genes and transcription factors play roles in insulin signaling and secretion.

Conclusions:

• Molecular insights into insulin resistance and beta-cell dysfunction are rapidly evolving.
• Mitochondrial health, enteroinsular axis regulation, and ER stress are critical therapeutic targets.
• Adipose tissue and genetic factors offer further avenues for T2DM research and treatment.