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Changes in Lipoprotein Kinetics Associated With Type 2 Diabetes Affect the Distribution of Lipopolysaccharides Among Lipoproteins

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 de... Full description

Journal Title: The journal of clinical endocrinology and metabolism 2014, Vol.99 (7), p.E1245-E1253
Main Author: Vergès, Bruno
Other Authors: Duvillard, Laurence , Lagrost, Laurent , Vachoux, Christelle , Garret, Céline , Bouyer, Karine , Courtney, Michael , Pomié, Céline , Burcelin, Rémy
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: United States: Endocrine Society
ID: ISSN: 0021-972X
Link: https://www.ncbi.nlm.nih.gov/pubmed/24694333
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title: Changes in Lipoprotein Kinetics Associated With Type 2 Diabetes Affect the Distribution of Lipopolysaccharides Among Lipoproteins
format: Article
creator:
  • Vergès, Bruno
  • Duvillard, Laurence
  • Lagrost, Laurent
  • Vachoux, Christelle
  • Garret, Céline
  • Bouyer, Karine
  • Courtney, Michael
  • Pomié, Céline
  • Burcelin, Rémy
subjects:
  • Adolescent
  • Adult
  • Aged
  • Case-Control Studies
  • Diabetes Mellitus, Type 2 - blood
  • Female
  • Humans
  • Kinetics
  • Lipopolysaccharides - blood
  • Lipopolysaccharides - chemistry
  • Lipoproteins - blood
  • Lipoproteins - chemistry
  • Lipoproteins, HDL - blood
  • Lipoproteins, HDL - chemistry
  • Lipoproteins, VLDL - blood
  • Lipoproteins, VLDL - chemistry
  • Male
  • Middle Aged
  • Young Adult
ispartof: The journal of clinical endocrinology and metabolism, 2014, Vol.99 (7), p.E1245-E1253
description: 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.
language: eng
source:
identifier: ISSN: 0021-972X
fulltext: no_fulltext
issn:
  • 0021-972X
  • 1945-7197
url: Link


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titleChanges in Lipoprotein Kinetics Associated With Type 2 Diabetes Affect the Distribution of Lipopolysaccharides Among Lipoproteins
creatorVergès, Bruno ; Duvillard, Laurence ; Lagrost, Laurent ; Vachoux, Christelle ; Garret, Céline ; Bouyer, Karine ; Courtney, Michael ; Pomié, Céline ; Burcelin, Rémy
creatorcontribVergès, Bruno ; Duvillard, Laurence ; Lagrost, Laurent ; Vachoux, Christelle ; Garret, Céline ; Bouyer, Karine ; Courtney, Michael ; Pomié, Céline ; Burcelin, Rémy
descriptionContext: 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.
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subjectAdolescent ; Adult ; Aged ; Case-Control Studies ; Diabetes Mellitus, Type 2 - blood ; Female ; Humans ; Kinetics ; Lipopolysaccharides - blood ; Lipopolysaccharides - chemistry ; Lipoproteins - blood ; Lipoproteins - chemistry ; Lipoproteins, HDL - blood ; Lipoproteins, HDL - chemistry ; Lipoproteins, VLDL - blood ; Lipoproteins, VLDL - chemistry ; Male ; Middle Aged ; Young Adult
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7Pomié, Céline
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descriptionContext: 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.
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authorVergès, Bruno ; Duvillard, Laurence ; Lagrost, Laurent ; Vachoux, Christelle ; Garret, Céline ; Bouyer, Karine ; Courtney, Michael ; Pomié, Céline ; Burcelin, Rémy
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notesThis work was supported by the Institut National de la Santé et de la Recherche Médicale, by the Seventh Framework Program FP7 FLORINASH (to R.B.) and by a French Government grant managed by the French National Research Agency under the program, Investissements d'Avenir, with Reference ANR-11-LABX-0021 (LipSTIC Labex).
abstractContext: 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.
copUnited States
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pmid24694333
doi10.1210/jc.2013-3463
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