Visceral adipose tissue specific persistence of Mycobacterium tuberculosis may be reason for the metabolic syndrome

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dc.authorid0000-0002-2741-9755
dc.authorscopusid57211151450
dc.authorwosidErol, Adnan/AAJ-9616-2020
dc.contributor.authorErol, Adnan
dc.date.accessioned2022-05-11T14:39:50Z
dc.date.available2022-05-11T14:39:50Z
dc.date.issued2008
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, İç Hastalıkları Ana Bilim Dalı
dc.description.abstractMycobacterium tuberculosis (Mtb) is highly successful intracellular pathogen. Infection is maintained in spite of acquired immunity and resists eradication by antimicrobials. Following bacillaemia, small numbers of bacteria are disseminated to the extrapulmonary organs most likely including visceral, adipose tissue by a mechanism that may involve the migration of M. tuberculosis within dendritic cells. In this lipid rich environment, Mtb can metabolize the fatty acids in a glyoxylate cycle dependent manner, and a state of chronic persistence may ensue. The persistent bacilli primarily use fatty acids as their carbon source. Expression of isocitrate lyase (ICL), gating enzyme of glyoxylate cycle, is upregulated during infection. ICL is important for survival during the persistent phase of infection. Expression of adipokines, particularly monocyte chemoattractant protein-1 (MCP-1), which is a potent proinflammatory cytokine, may be increased. MCP-1 contributes both to the recruitment of macrophages to adipose tissue and to the development of insulin resistance in humans. In addition, prolonged low Level immune stimulation induces local adipolipogenesis, increasing visceral fat. Increased delivery of free fatty acid to the Liver may stimulate the glyoxylate cycle-induced gluconeogenesis, raising hepatic glucose output. Hence, inhibition of the triggering enzyme ICL, which initiates all the pathologies related to persistent Mtb infection, may block the growth of the bacteria and may resolve the systemic metabolic complications. (C) 2008 Elsevier Ltd. All rights reserved.
dc.identifier.doi10.1016/j.mehy.2008.03.028
dc.identifier.endpage228
dc.identifier.issn0306-9877
dc.identifier.issn1532-2777
dc.identifier.issue2en_US
dc.identifier.pmid18448263
dc.identifier.scopus2-s2.0-45649083623
dc.identifier.scopusqualityQ2
dc.identifier.startpage222
dc.identifier.urihttps://doi.org/10.1016/j.mehy.2008.03.028
dc.identifier.urihttps://hdl.handle.net/20.500.11776/8758
dc.identifier.volume71
dc.identifier.wosWOS:000258013800010
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorErol, Adnan
dc.language.isoen
dc.publisherChurchill Livingstone
dc.relation.ispartofMedical Hypotheses
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectCell-Envelope Lipids
dc.subjectInsulin-Resistance
dc.subjectDendritic Cells
dc.subjectPrevalence
dc.subjectMcp-1
dc.subjectMitochondrial
dc.subjectAdipocytes
dc.subjectSecretion
dc.subjectGene
dc.titleVisceral adipose tissue specific persistence of Mycobacterium tuberculosis may be reason for the metabolic syndrome
dc.typeArticle

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