PMID- 18448263
OWN - NLM
STAT- MEDLINE
DCOM- 20080919
LR  - 20171116
IS  - 0306-9877 (Print)
IS  - 0306-9877 (Linking)
VI  - 71
IP  - 2
DP  - 2008 Aug
TI  - Visceral adipose tissue specific persistence of Mycobacterium tuberculosis may be 
      reason for the metabolic syndrome.
PG  - 222-8
LID - 10.1016/j.mehy.2008.03.028 [doi]
AB  - 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.
FAU - Erol, Adnan
AU  - Erol A
AD  - Namik Kemal University, Faculty of Medicine, Department of Internal Medicine, 
      Namik Kemal Caddesi 14, Tekirdag, Turkey. adnanerol@nku.edu.tr
LA  - eng
PT  - Journal Article
DEP - 20080429
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Glyoxylates)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Adipose Tissue/*microbiology
MH  - Chemokine CCL2/metabolism
MH  - Dendritic Cells/metabolism
MH  - Glucose/metabolism
MH  - Glyoxylates/metabolism
MH  - Humans
MH  - Immune System
MH  - Inflammation
MH  - Insulin Resistance
MH  - Liver/metabolism
MH  - Macrophages/metabolism
MH  - Metabolic Syndrome/complications/diagnosis/*microbiology
MH  - Models, Biological
MH  - Mycobacterium tuberculosis/*metabolism
MH  - Tuberculosis/*complications/microbiology
EDAT- 2008/05/02 09:00
MHDA- 2008/09/20 09:00
CRDT- 2008/05/02 09:00
PHST- 2008/02/05 00:00 [received]
PHST- 2008/03/05 00:00 [revised]
PHST- 2008/03/13 00:00 [accepted]
PHST- 2008/05/02 09:00 [pubmed]
PHST- 2008/09/20 09:00 [medline]
PHST- 2008/05/02 09:00 [entrez]
AID - S0306-9877(08)00138-2 [pii]
AID - 10.1016/j.mehy.2008.03.028 [doi]
PST - ppublish
SO  - Med Hypotheses. 2008 Aug;71(2):222-8. doi: 10.1016/j.mehy.2008.03.028. Epub 2008 
      Apr 29.