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A Novel In Vitro Live-imaging Assay of Astrocyte-mediated Phagocytosis Using pH Indicator-conjugated Synaptosomes

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Adipocyte metabolic state regulates glial phagocytic function.

Mroj Alassaf¹, Akhila Rajan¹

¹Basic Sciences Division, Fred Hutch, Seattle, WA-98109. The USA.

Biorxiv : the Preprint Server for Biology

|October 10, 2024

Summary

Obesity disrupts the adipocyte-brain axis, impairing glial cells' ability to clear neural debris. This study identifies a novel lipoprotein signaling pathway linking metabolic disorders to neurodegeneration.

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Area of Science:

Neuroscience
Metabolic Disorders
Cell Biology

Background:

Obesity and type 2 diabetes are risk factors for neurodegenerative disorders.
The adipocyte-brain axis, involving signaling molecules from fat cells, is vital for brain function but its role in neurodegeneration is unclear.
Glial cells clear neural debris, a process essential for brain health.

Purpose of the Study:

To investigate how adipocyte metabolism influences glial phagocytic activity in the brain.
To identify molecular mechanisms linking metabolic disorders to impaired glial function and neurodegeneration.

Main Methods:

Utilized adult *Drosophila* (fruit fly) models.
Examined the effects of a prolonged obesogenic diet on adipocyte metabolism and glial phagocytosis.
Employed genetic manipulations to alter adipocyte lipid and mitochondrial metabolism.
Investigated the role of *Apolpp* (apolipoprotein B) and Lipoprotein Receptor 1 (LpR1) in glial phagocytosis.

Main Results:

An obesogenic diet increased adipocyte fatty acid oxidation and ketogenesis.
Diet-induced metabolic changes in adipocytes reduced the expression of the phagocytic receptor Draper in glial cells.
Adipocyte-derived *Apolpp* was identified as a key signal regulating glial phagocytosis.
Lipoprotein Receptor 1 (LpR1) on glia is essential for clearing neuronal debris.

Conclusions:

Adipocyte metabolism significantly impacts glial phagocytic function through lipoprotein signaling.
This pathway links metabolic disorders, such as obesity, to impaired neural debris clearance and potentially neurodegeneration.
Findings reveal a novel mechanism connecting the adipocyte-brain axis to brain health and disease.