PMID- 24694333
OWN - NLM
STAT- MEDLINE
DCOM- 20140929
LR  - 20140709
IS  - 1945-7197 (Electronic)
IS  - 0021-972X (Linking)
VI  - 99
IP  - 7
DP  - 2014 Jul
TI  - Changes in lipoprotein kinetics associated with type 2 diabetes affect the 
      distribution of lipopolysaccharides among lipoproteins.
PG  - E1245-53
LID - 10.1210/jc.2013-3463 [doi]
AB  - CONTEXT: Lipopolysaccharides (LPSs) are inflammatory components of the outer 
      membrane of Gram-negative bacteria and, in plasma, are mostly associated with 
      lipoproteins. This association is thought to promote their catabolism while 
      reducing their proinflammatory effects. OBJECTIVES: Our aim was to determine the 
      impact of lipoprotein kinetics on plasma LPS distribution and how it may affect 
      patients with type 2 diabetes mellitus (T2DM). DESIGN: We performed a kinetic 
      study in 30 individuals (16 T2DM patients, 14 controls) and analyzed the impact 
      of changes in lipoprotein kinetics on LPS distribution among lipoproteins. 
      RESULTS: Plasma LPS levels in T2DM patients were not different from those in 
      controls, but LPS distribution in the two groups was different. Patients with 
      T2DM had higher LPS-very low-density lipoprotein (VLDL; 31% +/- 7% vs 22% +/- 11%, P 
      = .002), LPS-high-density lipoprotein (HDL; 29% +/- 9% vs 19% +/- 10%, P = .015), 
      free (nonlipoprotein bound) LPS (10% +/- 4% vs 7% +/- 4%, P = .043) and lower 
      LPS-low-density lipoprotein (LDL; 30% +/- 13% vs 52% +/- 16%, P = .001). In 
      multivariable analysis, VLDL-LPS was associated with HDL-LPS (P < .0001); LDL-LPS 
      was associated with VLDL-LPS (P = .004), and VLDL apolipoprotein (apo) B100 
      catabolism (P = .002); HDL-LPS was associated with free LPS (P < .0001) and 
      VLDL-LPS (P = .033); free LPS was associated with HDL-LPS (P < .0001). In a 
      patient featuring a dramatic decrease in VLDL catabolism due to apoA-V mutation, 
      LDL-LPS was severely decreased (0.044 EU/mL vs 0.788 EU/mL in controls). The 
      difference between T2DM patients and controls for LDL-LPS fraction was no longer 
      significant after controlling for VLDL apoB100 total fractional catabolic rate. 
      CONCLUSIONS: Our data suggest that in humans, free LPS transfers first to HDL and 
      then to VLDL, whereas the LPS-bound LDL fraction is mainly derived from VLDL 
      catabolism; the latter may hence represent a LPS catabolic pathway. T2DM patients 
      show lower LDL-LPS secondary to reduced VLDL catabolism, which may represent an 
      impaired catabolic pathway.
FAU - Verges, Bruno
AU  - Verges B
AD  - Department of Endocrinology-Diabetology (B.V.), University-Hospital, and INSERM 
      CRI 866 (B.V., L.D., L.L.), Medicine University, 21000 Dijon, France; INSERM 
      Unite 1048 (C.V., C.G., C.P., R.B.), Institut de Recherche sur les Maladies 
      Metaboliques et Cardiovasculaires de Rangueil (I2MC), 31432 Toulouse, France; and 
      VAIOMER SAS (K.B., M.C.), 31670 Labege, France.
FAU - Duvillard, Laurence
AU  - Duvillard L
FAU - Lagrost, Laurent
AU  - Lagrost L
FAU - Vachoux, Christelle
AU  - Vachoux C
FAU - Garret, Celine
AU  - Garret C
FAU - Bouyer, Karine
AU  - Bouyer K
FAU - Courtney, Michael
AU  - Courtney M
FAU - Pomie, Celine
AU  - Pomie C
FAU - Burcelin, Remy
AU  - Burcelin R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140402
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Lipoproteins)
RN  - 0 (Lipoproteins, HDL)
RN  - 0 (Lipoproteins, VLDL)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Case-Control Studies
MH  - Diabetes Mellitus, Type 2/*blood
MH  - Female
MH  - Humans
MH  - Kinetics
MH  - Lipopolysaccharides/*blood/chemistry
MH  - Lipoproteins/*blood/chemistry
MH  - Lipoproteins, HDL/blood/chemistry
MH  - Lipoproteins, VLDL/blood/chemistry
MH  - Male
MH  - Middle Aged
MH  - Young Adult
EDAT- 2014/04/04 06:00
MHDA- 2014/09/30 06:00
CRDT- 2014/04/04 06:00
PHST- 2014/04/04 06:00 [entrez]
PHST- 2014/04/04 06:00 [pubmed]
PHST- 2014/09/30 06:00 [medline]
AID - 10.1210/jc.2013-3463 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 2014 Jul;99(7):E1245-53. doi: 10.1210/jc.2013-3463. Epub 
      2014 Apr 2.