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Updated: Sep 4, 2025

Extracellular Glucose Depletion as an Indirect Measure of Glucose Uptake in Cells and Tissues Ex Vivo
Published on: April 6, 2022
Fabkin and glucose homeostasis.
Piyas Gargari1, Pradip Mukhopadhyay1, Banshi Saboo2
1Department of Endocrinology, Institute of Post Graduate Medical Education & Research, Kolkata, India.
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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