ArticleScientific reports2013
Hypothalamic neuronal toll-like receptor 2 protects against age-induced obesity.
Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- Toll signaling controls stem cell proliferation in intestinal regeneration and tumorigenesis.EMBO reports · 2026Article
- The Role of Cytokines in the Development and Functioning of the Hypothalamic-Pituitary-Gonadal Axis in Mammals in Normal and Pathological Conditions.International journal of molecular sciences · 2025Review
- Review
- The Role of TLRs in Obesity and Its Related Metabolic Disorders.International journal of molecular sciences · 2025Review
- From Immunity to Neurogenesis: Toll-like Receptors as Versatile Regulators in the Nervous System.International journal of molecular sciences · 2024Review
- Impact of high-fat diet on cognitive behavior and central and systemic inflammation with aging and sex differences in mice.Brain, behavior, and immunity · 2024Article
- Role of pattern recognition receptors and microbiota-derived ligands in obesity.Frontiers in microbiomes · 2024Review
- Toll-like receptors in pathogenesis of neurodegenerative diseases and their therapeutic potential.Immunity, inflammation and disease · 2023Review
- Opposing Actions of TLR2 and TLR4 in Adipocyte Differentiation and Mature-Onset Obesity.International journal of molecular sciences · 2022Article
- Dietary fat: a potent microglial influencer.Trends in endocrinology and metabolism: TEM · 2022Review
- Hypothalamic inflammation in metabolic disorders and aging.Cellular and molecular life sciences : CMLS · 2021Review
- Innate immunity at the crossroads of healthy brain maturation and neurodevelopmental disorders.Nature reviews. Immunology · 2021Review
- Lipoteichoic acid, a cell wall component of Gram-positive bacteria, induces sleep and fever and suppresses feeding.Brain, behavior, and immunity · 2021Article
- Beyond defense: regulation of neuronal morphogenesis and brain functions via Toll-like receptors.Journal of biomedical science · 2019Review
- Diet induced obesity is independent of metabolic endotoxemia and TLR4 signalling, but markedly increases hypothalamic expression of the acute phase protein, SerpinA3N.Scientific reports · 2018Article
- Toll-like receptor 2 deficiency hyperactivates the FoxO1 transcription factor and induces aging-associated cardiac dysfunction in mice.The Journal of biological chemistry · 2018Article
- Toll-Like Receptor 2 Signaling and Current Approaches for Therapeutic Modulation in Synucleinopathies.Frontiers in pharmacology · 2018Review
- TLR2 agonism reverses chemotherapy-induced neutropenia inBlood advances · 2017Article
- POMC Neurons: From Birth to Death.Annual review of physiology · 2017Review
- Toll-like receptor 2 is increased in neurons in Parkinson's disease brain and may contribute to alpha-synuclein pathology.Acta neuropathologica · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) are traditionally associated with immune-mediated host defense. Here, we ascribe a novel extra-immune, hypothalamic-associated function to TLR2, a TLR-family member known to recognize lipid components, in the protection against obesity. We found that TLR2-deficient mice exhibited mature-onset obesity and susceptibility to high-fat diet (HFD)-induced weight gain, via modulation of food intake. Age-related obesity was still evident in chimeric mice, carrying comparable TLR2(+) immune cells, suggesting a non-hematopoietic-related involvement of this receptor. TLR2 was up-regulated with age or HFD in pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus, a brain area participating in central-metabolic regulation, possibly modulating the hypothalamic-anorexigenic peptide, α-melanocyte-stimulating hormone (α-MSH). Direct activation of TLR2 in a hypothalamic-neuronal cell-line via its known ligands, further supports its capacity to mediate non-immune related metabolic regulation. Thus, our findings identify TLR2 expressed by hypothalamic neurons as a potential novel regulator of age-related weight gain and energy expenditure.
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Registered trials
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.