Bariatric Surgery-induced High-density Lipoprotein Functionality Enhancement Is Associated With Reduced Inflammation.


Journal

The Journal of clinical endocrinology and metabolism
ISSN: 1945-7197
Titre abrégé: J Clin Endocrinol Metab
Pays: United States
ID NLM: 0375362

Informations de publication

Date de publication:
14 07 2022
Historique:
received: 12 10 2021
pubmed: 1 6 2022
medline: 19 7 2022
entrez: 31 5 2022
Statut: ppublish

Résumé

Emerging evidence suggests an association between impaired high-density lipoprotein (HDL) functionality and cardiovascular disease (CVD). HDL is essential for reverse cholesterol transport (RCT) and reduces inflammation and oxidative stress principally via paraoxonase-1 (PON1). RCT depends on HDL's capacity to accept cholesterol (cholesterol efflux capacity [CEC]) and active transport through ATP-binding cassette (ABC) A1, G1, and scavenger receptor-B1 (SR-B1). We have studied the impact of Roux-en-Y gastric bypass (RYGB) in morbidly obese subjects on RCT and HDL functionality. Biomarkers associated with increased CVD risk including tumour necrosis factor-α (TNF-α), high-sensitivity C-reactive protein (hsCRP), myeloperoxidase mass (MPO), PON1 activity, and CEC in vitro were measured in 44 patients before and 6 and 12 months after RYGB. Overweight but otherwise healthy (mean body mass index [BMI] 28 kg/m2) subjects acted as controls. Twelve participants also underwent gluteal subcutaneous adipose tissue biopsies before and 6 months after RYGB for targeted gene expression (ABCA1, ABCG1, SR-B1, TNF-α) and histological analysis (adipocyte size, macrophage density, TNF-α immunostaining). Significant (P < 0.05) improvements in BMI, HDL-cholesterol, hsCRP, TNF-α, MPO mass, PON1 activity, and CEC in vitro were observed after RYGB. ABCG1 (fold-change, 2.24; P = 0.005) and ABCA1 gene expression increased significantly (fold-change, 1.34; P = 0.05). Gluteal fat adipocyte size (P < 0.0001), macrophage density (P = 0.0067), and TNF-α immunostaining (P = 0.0425) were reduced after RYBG and ABCG1 expression correlated inversely with TNF-α immunostaining (r = -0.71; P = 0.03). RYGB enhances HDL functionality in association with a reduction in adipose tissue and systemic inflammation.

Sections du résumé

BACKGROUND
Emerging evidence suggests an association between impaired high-density lipoprotein (HDL) functionality and cardiovascular disease (CVD). HDL is essential for reverse cholesterol transport (RCT) and reduces inflammation and oxidative stress principally via paraoxonase-1 (PON1). RCT depends on HDL's capacity to accept cholesterol (cholesterol efflux capacity [CEC]) and active transport through ATP-binding cassette (ABC) A1, G1, and scavenger receptor-B1 (SR-B1). We have studied the impact of Roux-en-Y gastric bypass (RYGB) in morbidly obese subjects on RCT and HDL functionality.
METHODS
Biomarkers associated with increased CVD risk including tumour necrosis factor-α (TNF-α), high-sensitivity C-reactive protein (hsCRP), myeloperoxidase mass (MPO), PON1 activity, and CEC in vitro were measured in 44 patients before and 6 and 12 months after RYGB. Overweight but otherwise healthy (mean body mass index [BMI] 28 kg/m2) subjects acted as controls. Twelve participants also underwent gluteal subcutaneous adipose tissue biopsies before and 6 months after RYGB for targeted gene expression (ABCA1, ABCG1, SR-B1, TNF-α) and histological analysis (adipocyte size, macrophage density, TNF-α immunostaining).
RESULTS
Significant (P < 0.05) improvements in BMI, HDL-cholesterol, hsCRP, TNF-α, MPO mass, PON1 activity, and CEC in vitro were observed after RYGB. ABCG1 (fold-change, 2.24; P = 0.005) and ABCA1 gene expression increased significantly (fold-change, 1.34; P = 0.05). Gluteal fat adipocyte size (P < 0.0001), macrophage density (P = 0.0067), and TNF-α immunostaining (P = 0.0425) were reduced after RYBG and ABCG1 expression correlated inversely with TNF-α immunostaining (r = -0.71; P = 0.03).
CONCLUSION
RYGB enhances HDL functionality in association with a reduction in adipose tissue and systemic inflammation.

Identifiants

pubmed: 35639942
pii: 6594151
doi: 10.1210/clinem/dgac244
doi:

Substances chimiques

ATP Binding Cassette Transporter 1 0
Lipoproteins, HDL 0
Tumor Necrosis Factor-alpha 0
C-Reactive Protein 9007-41-4
Cholesterol 97C5T2UQ7J
Aryldialkylphosphatase EC 3.1.8.1
PON1 protein, human EC 3.1.8.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2182-2194

Informations de copyright

© The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Auteurs

Safwaan Adam (S)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.
The Christie Hospital NHS Foundation Trust, Manchester M20 4BX, United Kingdom.

Jan H Ho (JH)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.
Cardiovascular Trials Unit, Manchester University NHS Foundation Trust, Manchester M13 9WL, United Kingdom.

Yifen Liu (Y)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.

Tarza Siahmansur (T)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.

Kirk Siddals (K)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.

Zohaib Iqbal (Z)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.
Cardiovascular Trials Unit, Manchester University NHS Foundation Trust, Manchester M13 9WL, United Kingdom.

Shazli Azmi (S)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.
Cardiovascular Trials Unit, Manchester University NHS Foundation Trust, Manchester M13 9WL, United Kingdom.

Siba Senapati (S)

Department of Surgery, Salford Royal NHS Foundation Trust, Salford M6 8HD, United Kingdom.

John New (J)

Department of Diabetes, Endocrinology and Obesity Medicine, Salford Royal NHS Foundation Trust, Salford M6 8HD, United Kingdom.

Maria Jeziorska (M)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.

Basil J Ammori (BJ)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.
Department of Diabetes, Endocrinology and Obesity Medicine, Salford Royal NHS Foundation Trust, Salford M6 8HD, United Kingdom.

Akheel A Syed (AA)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.
Department of Diabetes, Endocrinology and Obesity Medicine, Salford Royal NHS Foundation Trust, Salford M6 8HD, United Kingdom.

Rachelle Donn (R)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.

Rayaz A Malik (RA)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.
Weill-Cornell Medicine-Qatar, Doha 24144, Qatar.

Paul N Durrington (PN)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.

Handrean Soran (H)

Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9WU, United Kingdom.
Cardiovascular Trials Unit, Manchester University NHS Foundation Trust, Manchester M13 9WL, United Kingdom.

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Classifications MeSH