Fabkin and glucose homeostasis

Piyas Gargari1, Pradip Mukhopadhyay1, Banshi Saboo2

  • 1Department of Endocrinology, Institute of Post Graduate Medical Education & Research, Kolkata, India.

Abstract

Insights

Fabkin, a complex involving Fatty Acid Binding Protein 4 (FABP4), Adenosine Kinase (ADK), and Nucleoside Diphosphate Kinase (NDPK), impairs insulin secretion and contributes to glucose homeostasis disruption. This complex plays a significant role in type 2 diabetes pathogenesis.

Area of Science:

  • Endocrinology
  • Metabolic Research
  • Molecular Biology

Background:

  • The precise role of Fatty Acid Binding Protein 4 (FABP4) in type 2 diabetes mellitus (T2DM) pathogenesis remains unclear.
  • FABP4, an intracellular lipid chaperone, is secreted by adipocytes and macrophages and is linked to insulin resistance.
  • The Fabkin complex, comprising FABP4, Adenosine Kinase (ADK), and Nucleoside Diphosphate Kinase (NDPK), is proposed to elucidate T2DM pathogenesis.

Purpose of the Study:

  • To summarize the role of the Fabkin complex in regulating glucose homeostasis.
  • To investigate the mechanisms by which Fabkin influences insulin secretion and metabolic balance.

Main Methods:

  • A review of published manuscripts discussing the effects of FABP4 and Fabkin on glucose homeostasis.
  • Analysis of the molecular interactions and signaling pathways involved in Fabkin complex formation and function.

Main Results:

  • Fabkin formation is driven by high-affinity interactions between FABP4, ADK, and NDPK.
  • The complex modulates Glucose-Stimulated Insulin Signaling (GSIS) by altering the extracellular ADP/ATP ratio via P2Y1 receptors, leading to impaired insulin secretion.
  • Fabkin also regulates intracellular calcium dynamics and induces Endoplasmic Reticulum (ER) stress.

Conclusions:

  • Fabkin may integrate energy balance with metabolic organ functions.
  • The Fabkin complex plays a significant role in glucose homeostasis and T2DM pathogenesis.

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