Evidence map›Paper›PMID 27122369›Full record

ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2016

Fatty acid-induced astrocyte ketone production and the control of food intake.

Christelle Le Foll, Barry E Levin

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. A 3D Astrocyte Microenvironment Model Enables Rapid CaAdvanced healthcare materials · 2026
    Article
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  6. Review
  7. Review
  8. Review
  9. Review
  10. Observational
  11. The role of astrocyte metabolic reprogramming in ischemic stroke (Review).International journal of molecular medicine · 2025
    Review
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  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Christelle Le FollInstitute of Veterinary Physiology, University of Zurich, Zurich, Switzerland; and.
Barry E LevinDepartment of Neurology, Rutgers, New Jersey Medical School, Newark, New Jersey.
Rutgers, The State University of New Jersey · USUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity and Type 2 diabetes are major worldwide public health issues today. A relationship between total fat intake and obesity has been found. In addition, the mechanisms of long-term and excessive high-fat diet (HFD) intake in the development of obesity still need to be elucidated. The ventromedial hypothalamus (VMH) is a major site involved in the regulation of glucose and energy homeostasis where "metabolic sensing neurons" integrate metabolic signals from the periphery. Among these signals, fatty acids (FA) modulate the activity of VMH neurons using the FA translocator/CD36, which plays a critical role in the regulation of energy and glucose homeostasis. During low-fat diet (LFD) intake, FA are oxidized by VMH astrocytes to fuel their ongoing metabolic needs. However, HFD intake causes VMH astrocytes to use FA to generate ketone bodies. We postulate that these astrocyte-derived ketone bodies are exported to neurons where they produce excess ATP and reactive oxygen species, which override CD36-mediated FA sensing and act as a signal to decrease short-term food intake. On a HFD, VMH astrocyte-produced ketones reduce elevated caloric intake to LFD levels after 3 days in rats genetically predisposed to resist (DR) diet-induced obesity (DIO), but not leptin-resistant DIO rats. This suggests that, while VMH ketone production on a HFD can contribute to protection from obesity, the inherent leptin resistance overrides this inhibitory action of ketone bodies on food intake. Thus, astrocytes and neurons form a tight metabolic unit that is able to monitor circulating nutrients to alter food intake and energy homeostasis.

Indexed as

AppetiteAppetite RegulationAstrocytesDiet, High-FatEatingFatty AcidsKetone BodiesModels, BiologicalNeuronsVentromedial Hypothalamic NucleusFatty AcidsKetone Bodiesastrocytesfeedinghypothalamusketone bodiesmetabolic sensing

Identifiers

PMID27122369
PMCPMC4935491
OpenAlexW2343633074

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.