ArticleEBioMedicine2019
mTORC2/Akt activation in adipocytes is required for adipose tissue inflammation in tuberculosis.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Pseudorabies virus pUL40 drives inflammatory signaling through competitive hijacking of EphA2 from the Akt-EphA2 interaction.Veterinary research · 2026Article
- From fat storage to immune hubs: the emerging role of adipocytes in coordinating the immune response to infection.The FEBS journal · 2025Review
- Tuberculosis and Increased Incidence of Cardiovascular Disease: Cohort Study Using United States and United Kingdom Health Records.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2025Article
- Altered hepatic metabolic landscape and insulin sensitivity in response to pulmonary tuberculosis.PLoS pathogens · 2024Article
- Diabetes and tuberculosis: An emerging dual threat to healthcare.World journal of diabetes · 2024Article
- Prior tuberculosis, radiographic lung abnormalities and prevalent diabetes in rural South Africa.BMC infectious diseases · 2024Article
- Longitudinal trends in glycated hemoglobin during and after tuberculosis treatment.Diabetes research and clinical practice · 2023Article
- Adipose Tissue Remodeling in Pathophysiology.Annual review of pathology · 2023Review
- The cause-effect relation of tuberculosis on incidence of diabetes mellitus.Frontiers in cellular and infection microbiology · 2023Review
- Beyond energy balance regulation: The underestimated role of adipose tissues in host defense against pathogens.Frontiers in immunology · 2023Review
- The Immune Response in Adipocytes and Their Susceptibility to Infection: A Possible Relationship with Infectobesity.International journal of molecular sciences · 2022Review
- Increased Risk of Incident Diabetes Among Individuals With Latent Tuberculosis Infection.Diabetes care · 2022Article
- Sp1 transcription factor represses transcription of phosphatase and tensin homolog to aggravate lung injury in mice with type 2 diabetes mellitus-pulmonary tuberculosis.Bioengineered · 2022Article
- Screening of latent tuberculosis infection among patients with diabetes mellitus from a high-burden area in Brazil.Frontiers in clinical diabetes and healthcare · 2022Article
- MicroRNAs as immune regulators and biomarkers in tuberculosis.Frontiers in immunology · 2022Review
- Latent tuberculosis infection among patients with and without type-2 diabetes mellitus: results from a hospital case-control study in Atlanta.BMC research notes · 2021Article
- Loss of Rictor in tubular cells exaggerates lipopolysaccharide induced renal inflammation and acute kidney injury via Yap/Taz-NF-κB axis.Cell death discovery · 2020Article
- Inflammatory Signaling and Brown Fat Activity.Frontiers in endocrinology · 2020Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 4 countries.
Funding
Abstract
backgroundMycobacterium tuberculosis has co-evolved with the human host, adapting to exploit the immune system for persistence and transmission. While immunity to tuberculosis (TB) has been intensively studied in the lung and lymphoid system, little is known about the participation of adipose tissues and non-immune cells in the host-pathogen interaction during this systemic disease.
methodsC57BL/6J mice were aerosol infected with M. tuberculosis Erdman and presence of the bacteria and the fitness of the white and brown adipose tissues, liver and skeletal muscle were studied compared to uninfected mice.
findingsM. tuberculosis infection in mice stimulated immune cell infiltration in visceral, and brown adipose tissue. Despite the absence of detectable bacterial dissemination to fat tissues, adipocytes produced localized pro-inflammatory signals that disrupted adipocyte lipid metabolism, resulting in adipocyte hypertrophy. Paradoxically, this resulted in increased insulin sensitivity and systemic glucose tolerance. Adipose tissue inflammation and enhanced glucose tolerance also developed in obese mice after aerosol M. tuberculosis infection. We found that infection induced adipose tissue Akt signaling, while inhibition of the Akt activator mTORC2 in adipocytes reversed TB-associated adipose tissue inflammation and cell hypertrophy.
interpretationOur study reveals a systemic response to aerosol M. tuberculosis infection that regulates adipose tissue lipid homeostasis through mTORC2/Akt signaling in adipocytes. Adipose tissue inflammation in TB is not simply a passive infiltration with leukocytes but requires the mechanistic participation of adipocyte signals.
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