ArticleThe Journal of biological chemistry2009
Deletion of tumor necrosis factor-alpha receptor 1 (TNFR1) protects against diet-induced obesity by means of increased thermogenesis.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 70 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
70 citing papers in PubMed, 146 citations in OpenAlex.
- Linear ubiquitination prevents lipodystrophy and obesity-associated metabolic syndrome.Science advances · 2025Article
- Exploring TNFR1: from discovery to targeted therapy development.Journal of translational medicine · 2025Review
- Genetic variation in satiety signaling and hypothalamic inflammation: merging fields for the study of obesity.The Journal of nutritional biochemistry · 2022Review
- Etanercept Prevents Endothelial Dysfunction in Cafeteria Diet-Fed Rats.International journal of environmental research and public health · 2022Article
- Diet-Induced Obesity Mice Execute Pulmonary Cell Apoptosis via Death Receptor and ER-Stress Pathways afterOxidative medicine and cellular longevity · 2020Article
- Obesity-related cognitive impairment: The role of endothelial dysfunction.Neurobiology of disease · 2019Review
- Dual-specificity phosphatases regulate mitogen-activated protein kinase signaling in adipocytes in response to inflammatory stress.Cellular signalling · 2019Article
- Transcriptomic and microRNA analyses of gene networks regulated by eicosapentaenoic acid in brown adipose tissue of diet-induced obese mice.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Article
- The involvement of 4-1BB/4-1BBL signaling in glial cell-mediated hypothalamic inflammation in obesity.FEBS open bio · 2018Article
- Environmental Pollutants Effect on Brown Adipose Tissue.Frontiers in physiology · 2018Review
- Relationship Between Obesity, Alzheimer's Disease, and Parkinson's Disease: an Astrocentric View.Molecular neurobiology · 2017Review
- DUSP5 functions as a feedback regulator of TNFα-induced ERK1/2 dephosphorylation and inflammatory gene expression in adipocytes.Scientific reports · 2017Article
- Inactivation of TNF/LT locus alters mouse metabolic response to concentrated ambient PMToxicology · 2017Article
- The cellular and molecular bases of leptin and ghrelin resistance in obesity.Nature reviews. Endocrinology · 2017Review
- Cinnamon induces browning in subcutaneous adipocytes.Scientific reports · 2017Article
- POMC Neurons: From Birth to Death.Annual review of physiology · 2017Review
- Resolvin RvD2 reduces hypothalamic inflammation and rescues mice from diet-induced obesity.Journal of neuroinflammation · 2017Article
- Hypothalamic inflammation in obesity and metabolic disease.The Journal of clinical investigation · 2017Review
- Leptin Resistance and the Neuro-Adipose Connection.Frontiers in endocrinology · 2017Article
- The Leptin Receptor Complex: Heavier Than Expected?Frontiers in endocrinology · 2017Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2016-12-23Duplication of/in Image · Error in Image · Euphemisms for Duplication ·
- Retracted
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In diet-induced obesity, hypothalamic and systemic inflammatory factors trigger intracellular mechanisms that lead to resistance to the main adipostatic hormones, leptin and insulin. Tumor necrosis factor-alpha (TNF-alpha) is one of the main inflammatory factors produced during this process and its mechanistic role as an inducer of leptin and insulin resistance has been widely investigated. Most of TNF-alpha inflammatory signals are delivered by TNF receptor 1 (R1); however, the role played by this receptor in the context of obesity-associated inflammation is not completely known. Here, we show that TNFR1 knock-out (TNFR1 KO) mice are protected from diet-induced obesity due to increased thermogenesis. Under standard rodent chow or a high-fat diet, TNFR1 KO gain significantly less body mass despite increased caloric intake. Visceral adiposity and mean adipocyte diameter are reduced and blood concentrations of insulin and leptin are lower. Protection from hypothalamic leptin resistance is evidenced by increased leptin-induced suppression of food intake and preserved activation of leptin signal transduction through JAK2, STAT3, and FOXO1. Under the high-fat diet, TNFR1 KO mice present a significantly increased expression of the thermogenesis-related neurotransmitter, TRH. Further evidence of increased thermogenesis includes increased O(2) consumption in respirometry measurements, increased expressions of UCP1 and UCP3 in brown adipose tissue and skeletal muscle, respectively, and increased O(2) consumption by isolated skeletal muscle fiber mitochondria. This demonstrates that TNF-alpha signaling through TNFR1 is an important mechanism involved in obesity-associated defective thermogenesis.
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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.