---
title: "MBH astrocyte lipid handling (FATP4, HMGCL) modulates weight gain on high-fat diet"
id: "biorxiv-7-astrocyte-fatty-acid-uptake-and-ketogenesis-in-the-mediobasal-hypothalamus"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-7-astrocyte-fatty-acid-uptake-and-ketogenesis-in-the-mediobasal-hypothalamus"
content_type: "clinical_feed_article"
specialty: "General"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.07.757016v1?rss=1"
published_at: "2026-10-14T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# MBH astrocyte lipid handling (FATP4, HMGCL) modulates weight gain on high-fat diet
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-7-astrocyte-fatty-acid-uptake-and-ketogenesis-in-the-mediobasal-hypothalamus
- **Specialty:** [General](https://medichelpline.com/clinical-feed/general.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.07.757016v1?rss=1)
- **Published At:** 2026-10-14T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- The mediobasal hypothalamus (**MBH**) contains neurons and glia that coordinate systemic energy balance; this study investigated MBH astrocyte lipid metabolism as a regulator of adaptation to a **high-fat diet**. - Investigators manipulated two astrocytic components: genetic depletion of fatty acid transporter **FATP4** in mice, and knockdown of ketogenesis enzyme **HMGCL** in rats; both interventions targeted MBH astrocytes specifically, as reported by the authors. - MBH astrocyte **FATP4** depletion markedly worsened HFD-induced obesity in mice, increasing body weight and fat mass. The cohort showed no increase in food intake, indicating weight gain occurred independently of caloric intake. - The FATP4-deficient mice exhibited reduced energy expenditure and impaired brown adipose tissue oxidation; the study team observed these effects as the primary drivers of the obesogenic phenotype. - MBH astrocyte **HMGCL** knockdown in rats also promoted HFD-induced weight gain. Data indicated reduced energy expenditure and a transient early hyperphagic response during initial HFD exposure contributed to the phenotype. - In primary astrocyte cultures, FATP4 disruption altered expression of genes linked to mitochondrial lipid oxidation and **ketogenesis**, consistent with impaired astrocytic lipid handling reported in vivo. - HMGCL knockdown lowered expression of monocarboxylate transporter **MCT4** in astrocytes, suggesting reduced capacity for lactate and/or ketone body release from MBH astrocytes. - The authors concluded that MBH astrocyte lipid metabolism is an active regulator of whole-body energy balance and may contribute to the pathogenesis of obesity. - The source did not report experiment-specific details such as precise knockdown methods, timing, sample sizes, or statistical values in the accessible abstract; those methodological specifics were not provided in the summary text.
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Keila Navarro i Batista 1 Institute of Veterinary Physiology, University of Zurich, Switzerland; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Keila%2BNavarro%2Bi%2BBatista%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Navarro%20i%20Batista%20K&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AKeila%2BNavarro%2Bi%2BBatista%2B) Nadine Ellersiek 1 Institute of Veterinary Physiology, University of Zurich, Switzerland; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Nadine%2BEllersiek%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Ellersiek%20N&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ANadine%2BEllersiek%2B) Patricia Kulka 1 Institute of Veterinary Physiology, University of Zurich, Switzerland; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Patricia%2BKulka%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Kulka%20P&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3APatricia%2BKulka%2B) Gaia Serra 1 Institute of Veterinary Physiology, University of Zurich, Switzerland; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Gaia%2BSerra%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Serra%20G&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AGaia%2BSerra%2B) Francesco Prisco 2 Institute of Veterinary Pathology; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Francesco%2BPrisco%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Prisco%20F&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AFrancesco%2BPrisco%2B) Christelle Le Foll 3 University of Zurich * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Christelle%2BLe%2BFoll%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Le%20Foll%20C&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AChristelle%2BLe%2BFoll%2B) * [ORCID record for Christelle Le Foll](http://orcid.org/0000-0002-6677-5488 "Open in new tab") * For correspondence: christelle.lefoll@uzh.ch * [Abstract](https://www.biorxiv.org/content/10.64898/2026.10.07.757016v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5870042/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.10.07.757016v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5870042/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.10.07.757016v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5870042/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.10.07.757016v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5870042/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.10.07.757016v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5870042/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract The mediobasal hypothalamus (MBH) constitutes a central regulator of energy homeostasis; specialized neurons in this region integrate peripheral metabolic signals to coordinate processes like food intake, energy expenditure or glucose homeostasis. While MBH neuronal dysfunction has been linked to obesity, increasing evidence indicates that astrocytes in this region are also active participants in the modulation of energy balance. MBH astrocyte ketone body signaling, in particular, has been proposed as an adaptive mechanism aimed at regulating energy homeostasis during dietary challenge. Here, we investigated the effects of MBH astrocytic lipid metabolism on the control of energy balance. We targeted distinct components of this pathway, ablating fatty acid (FA) transporter FATP4 in mice and knocking down 3-hydroxy-3-methylglutaryl-CoA lyase (HMGCL) in rats. MBH astrocyte FATP4 depletion markedly exacerbated high-fat diet (HFD)-induced obesity, increasing body weight and fat mass independently of food intake. Rather, this phenotype was driven by reduced energy expenditure and impaired brown adipose tissue oxidation. HMGCL knockdown in MBH astrocytes also promoted HFD-induced weight gain, not only through reduced energy expenditure but also through a transient hyperphagic response during early HFD exposure. In vitro studies in primary astrocyte cultures confirmed that disruption of FATP4 altered the expression of genes involved in mitochondrial lipid oxidation and ketogenesis. Similarly, HMGCL knockdown reduced the expression of monocarboxylate transporter MCT4, suggesting impaired astrocytic lactate and/or ketone body release. Together, these findings identify MBH astrocyte lipid metabolism as a critical component of the hypothalamic circuitry regulating energy balance, highlighting astrocytes as active contributors to the pathogenesis of obesity. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared Swiss National Science Foundation, 310030_207960, 213511 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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