Microglial UCP2 mediates inflammation and obesity induced by high-fat feeding

Kim, Jung Dae; Yoon, Nal Ae; Jin, Sungho; Diano, Sabrina

doi:10.1016/j.cmet.2019.08.010

Cited by 240Neuroinflammation and Neurodegeneration MechanismsRegulation of Appetite and ObesityAdipokines, Inflammation, and Metabolic Diseases

Microglial UCP2 mediates inflammation and obesity induced by high-fat feeding

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Kim, Jung Dae, Yoon, Nal Ae, Jin, Sungho, Diano, Sabrina·2019·Cell Metabolism

DOI 10.1016/j.cmet.2019.08.010PMC PMC7251564

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Abstract

Microglia play a crucial role in immune responses, including inflammation. Diet-induced obesity (DIO) triggers microglia activation and hypothalamic inflammation as early as 3 days after high-fat diet (HFD) exposure, before changes in body weight occur. The intracellular mechanism(s) responsible for HFD-induced microglia activation is ill defined. Here, we show that in vivo, HFD induced a rapid and transient increase in uncoupling protein 2 (Ucp2) mRNA expression together with changes in mitochondrial dynamics. Selective microglial deletion of Ucp2 prevented changes in mitochondrial dynamics and function, microglia activation, and hypothalamic inflammation. In association with these, male and female mice were protected from HFD-induced obesity, showing decreased feeding and increased energy expenditure that were associated with changes in the synaptic input organization and activation of the anorexigenic hypothalamic POMC neurons and astrogliosis. Together, our data point to a fuel-availability-driven mitochondrial mechanism as a major player of microglia activation in the central regulation of DIO.

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Both increased and decreased microglial inflammatory activity within the mediobasal hypothalamus can disrupt leptin/melanocortin related neuronal signaling, a pathway central to the regulation of energy balance.
“Recent studies have shown that both increased and decreased microglial inflammatory activity within the mediobasal hypothalamus can disrupt leptin/melanocortin related neuronal signaling, a pathway that is central to the regulation of energy balance (Gao et al., 2017; Valdearcos et al., 2017; Kim et al., 2019).”
From Deletion of the Alzheimer’s disease risk gene Abi3 locus results in obesity and systemic metabolic disruption in mice (2022) · cites this paper as Kim et al., 2019
The Discussion links high-fat-diet-induced microglial activation and inflammatory signaling to hypothalamic metabolic dysfunction. But the Results section on POMC neuronal activation reports that mice lacking microglial UCP2 had greater POMC activation and retained leptin responsiveness under high-fat feeding. The paper therefore supports disruption associated with increased microglial activity, not the claim that decreased activity also disrupts this signaling. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Reducing dietary induced microgliosis can mitigate weight gain.
“Further, it has been demonstrated that reducing this dietary induced microgliosis can mitigate weight gain (Andre et al., 2017; Valdearcos et al., 2017; Kim et al., 2019).”
From Deletion of the Alzheimer’s disease risk gene Abi3 locus results in obesity and systemic metabolic disruption in mice (2022) · cites this paper as Kim et al., 2019
Reversing neuroinflammation via targeted genetic, pharmacological, or dietary approaches that rescue behavioral anomalies supports a causal role of neuroinflammation in obesity-induced neuropathophysiology.
“Reversing neuroinflammation via targeted genetic [96,97], pharmacological [98,99], or dietary [49,100] approaches that rescue behavioral anomalies offers convincing support for a causal role of neuroinflammation in obesity-induced neuropathophysiology.”
From The menace of obesity to depression and anxiety prevalence (2022) · cites this paper as [96]

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Authors: Kim, J. D., Yoon, N. A., Jin, S., & Diano, S.
Affiliations: Yale University (US)
Corresponding author: Diano, Sabrina
ORCID: Kim, Jung Dae
Yoon, Nal Ae
Jin, Sungho
Diano, Sabrina
Venue: Cell Metabolism
Publisher: Elsevier BV
Published: 2019-11
Volume: 30
Issue: 5
Pages: 952-962.e5
ISSN: 1550-4131 (ISSN-L)
DOI: 10.1016/j.cmet.2019.08.010
PMC: PMC7251564
OpenAlex: W2971465822
Cited by: 240
References: 42
Citations by year: 2026: 23 · 2025: 37 · 2024: 47 · 2023: 34 · 2022: 37 · 2021: 34 · 2020: 25 · 2019: 3
FWCI: 10.90
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 370 d)
Locations: Cell Metabolism (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Yale University
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords: microglia, UCP2, diet-induced obesity, high-fat diet, hypothalamic inflammation, microglial activation, mitochondrial dynamics, mitochondrial function, energy expenditure, feeding behavior, POMC neurons, astrocyte activation, sex differences, fuel availability
MeSH terms: Uncoupling Protein 2, Animals, Body Weight, Energy Metabolism, Female, Hypothalamus, Inflammation, Male, Mitochondria, Neurons, Obesity, RNA, Messenger, Microglia, Mice, Knockout, Mice, Gene Knockout Techniques, Diet, High-Fat

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Microglial UCP2 mediates inflammation and obesity induced by high-fat feeding

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