Visceral adipose tissue specific persistence of Mycobacterium tuberculosis may be reason for the metabolic syndrome
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Dosyalar
Tarih
2008
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Churchill Livingstone
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
Mycobacterium 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.
Açıklama
Anahtar Kelimeler
Cell-Envelope Lipids, Insulin-Resistance, Dendritic Cells, Prevalence, Mcp-1, Mitochondrial, Adipocytes, Secretion, Gene
Kaynak
Medical Hypotheses
WoS Q Değeri
Q3
Scopus Q Değeri
Q2
Cilt
71
Sayı
2
