Endotoxemia chuyển hóa kích hoạt bệnh béo phì và kháng insulin

Diabetes - Tập 56 Số 7 - Trang 1761-1772 - 2007
Patrice D. Cani1,2, Jacques Amar3, Miguel A. Iglesias1, Marjorie Poggi4, Claude Knauf1, Delphine Bastelica4, Audrey M. Neyrinck2, Francesca Fava5, Kieran Tuohy5, Chantal Chabo1, Aurélie Waget1, Evelyne Delmée2, Béatrice Cousin6, Thierry Sulpice7, B Chamontin3, Jean Ferrières3, Jean‐François Tanti8, Glenn R. Gibson5, Louis Casteilla6, Nathalie M. Delzenne2, Marie‐Christine Alessi4, Rémy Burcelin1
1Institute of Molecular Medicine, I2MR Toulouse, France
2Unité Pharmacokinetics, Metabolism, Nutrition, and Toxicology-73/69, Université catholique de Louvain, Brussels, Belgium
3Institut National de la Santé et de la Recherche Médicale (INSERM) 558, Toulouse, France
4INSERM U 626, Marseille, France
5Food Microbial Sciences Unit, Department of Food Biosciences, University of Reading, Reading, U.K
6Unité Mixte de Recherche 5241, Centre National de la Recherche Scientifique, Université Paul Sabatier, Toulouse, France
7Physiogenex S.A.S., Labège Innopole, France
8INSERM U 568, Nice, France

Tóm tắt

Bệnh tiểu đường và béo phì là hai bệnh trao đổi chất đặc trưng bởi kháng insulin và viêm mức độ thấp. Khi tìm kiếm yếu tố viêm dẫn đến khởi phát kháng insulin, béo phì và tiểu đường, chúng tôi đã xác định được lipopolysaccharide (LPS) từ vi khuẩn là yếu tố gây khởi phát. Chúng tôi phát hiện rằng tình trạng nội độc tố bình thường tăng hoặc giảm trong trạng thái ăn no hoặc nhịn ăn, theo cơ sở dinh dưỡng và một chế độ ăn giàu chất béo kéo dài 4 tuần đã làm tăng nồng độ LPS trong huyết tương từ hai đến ba lần, ngưỡng mà chúng tôi đã định nghĩa là nội độc tố chuyển hóa. Quan trọng là, chế độ ăn giàu chất béo làm tăng tỷ lệ vi khuẩn chứa LPS trong ruột. Khi nội độc tố chuyển hóa được gây ra trong 4 tuần ở chuột thông qua việc truyền LPS liên tục dưới da, đường huyết và insulin lúc đói cùng với sự tăng cân toàn thân, gan và mô mỡ tăng lên ở mức tương tự như ở chuột ăn chế độ giàu chất béo. Ngoài ra, các tế bào dương tính F4/80 trong mô mỡ và các chỉ số viêm nhiễm, lượng triglyceride trong gan cũng tăng. Hơn nữa, tình trạng kháng insulin ở gan, nhưng không phải toàn thân, được phát hiện ở chuột truyền LPS. Chuột đột biến CD14 chống lại phần lớn các đặc điểm do LPS và chế độ ăn giàu chất béo gây ra của các bệnh chuyển hóa. Phát hiện mới này chứng minh rằng nội độc tố chuyển hóa làm rối loạn mức độ viêm và kích hoạt tăng cân và tiểu đường. Chúng tôi kết luận rằng hệ thống LPS/CD14 điều chỉnh độ nhạy insulin và khởi đầu bệnh tiểu đường và béo phì. Giảm nồng độ LPS trong huyết tương có thể là chiến lược mạnh để kiểm soát các bệnh chuyển hóa.

Từ khóa

#bệnh tiểu đường #béo phì #kháng insulin #lipopolysaccharide #nội độc tố chuyển hóa #hệ thống LPS/CD14 #viêm mức độ thấp #bệnh chuyển hóa

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