Macrophage Gene Expression in Adipose Tissue is Associated with Insulin Sensitivity and Serum Lipid Levels Independent of Obesity

Objective: Obesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage infiltration directly influences human metabolism is unclear. The aim of this study was to investigate if there are obesity‐independent links betwee...

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Published inObesity (Silver Spring, Md.) Vol. 21; no. 12; pp. E571 - E576
Main Authors Ahlin, S., Sjöholm, K., Jacobson, P., Andersson‐Assarsson, J.C., Walley, A., Tordjman, J., Poitou, C., Prifti, E., Jansson, P.‐A., Borén, J., Sjöström, L., Froguel, P., Bergman, R.N., Carlsson, L.M.S., Olsson, B., Svensson, P.‐A.
Format Journal Article
LanguageEnglish
Published United States Blackwell Publishing Ltd 01.12.2013
Subjects
Adipose Tissue - metabolism
Body fat
Body Mass Index
C-Peptide - blood
Case-Control Studies
Cholesterol, HDL - blood
Diabetes Mellitus, Type 2 - blood
Diabetes Mellitus, Type 2 - genetics
Endocrinology and Diabetes
Endokrinologi och diabetes
Female
Gene Expression
Genetic Markers
Humans
Insulin
Insulin - blood
Insulin resistance
Insulin Resistance - genetics
Macrophages - metabolism
Male
Metabolic disorders
Obesity
Obesity - blood
Obesity - genetics
Oligonucleotide Array Sequence Analysis
Rodents
Studies
Triglycerides - blood
Sweden
Online AccessGet full text
ISSN1930-7381
1930-739X
1930-739X
DOI10.1002/oby.20443

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Abstract Objective: Obesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage infiltration directly influences human metabolism is unclear. The aim of this study was to investigate if there are obesity‐independent links between adipose tissue macrophages and metabolic disturbances. Design and Methods: Expression of macrophage markers in adipose tissue was analyzed by DNA microarrays in the SOS Sib Pair study and in patients with type 2 diabetes and a BMI‐matched healthy control group. Results: The expression of macrophage markers in adipose tissue was increased in obesity and associated with several metabolic and anthropometric measurements. After adjustment for BMI, the expression remained associated with insulin sensitivity, serum levels of insulin, C‐peptide, high density lipoprotein cholesterol (HDL‐cholesterol) and triglycerides. In addition, the expression of most macrophage markers was significantly increased in patients with type 2 diabetes compared to the control group. Conclusion: Our study shows that infiltration of macrophages in human adipose tissue, estimated by the expression of macrophage markers, is increased in subjects with obesity and diabetes and associated with insulin sensitivity and serum lipid levels independent of BMI. This indicates that adipose tissue macrophages may contribute to the development of insulin resistance and dyslipidemia.
AbstractList Objective: Obesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage infiltration directly influences human metabolism is unclear. The aim of this study was to investigate if there are obesity-independent links between adipose tissue macrophages and metabolic disturbances. Design and Methods: Expression of macrophage markers in adipose tissue was analyzed by DNA microarrays in the SOS Sib Pair study and in patients with type 2 diabetes and a BMI-matched healthy control group. Results: The expression of macrophage markers in adipose tissue was increased in obesity and associated with several metabolic and anthropometric measurements. After adjustment for BMI, the expression remained associated with insulin sensitivity, serum levels of insulin, C-peptide, high density lipoprotein cholesterol (HDL-cholesterol) and triglycerides. In addition, the expression of most macrophage markers was significantly increased in patients with type 2 diabetes compared to the control group. Conclusion: Our study shows that infiltration of macrophages in human adipose tissue, estimated by the expression of macrophage markers, is increased in subjects with obesity and diabetes and associated with insulin sensitivity and serum lipid levels independent of BMI. This indicates that adipose tissue macrophages may contribute to the development of insulin resistance and dyslipidemia.
Obesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage infiltration directly influences human metabolism is unclear. The aim of this study was to investigate if there are obesity-independent links between adipose tissue macrophages and metabolic disturbances.OBJECTIVEObesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage infiltration directly influences human metabolism is unclear. The aim of this study was to investigate if there are obesity-independent links between adipose tissue macrophages and metabolic disturbances.Expression of macrophage markers in adipose tissue was analyzed by DNA microarrays in the SOS Sib Pair study and in patients with type 2 diabetes and a BMI-matched healthy control group.DESIGN AND METHODSExpression of macrophage markers in adipose tissue was analyzed by DNA microarrays in the SOS Sib Pair study and in patients with type 2 diabetes and a BMI-matched healthy control group.The expression of macrophage markers in adipose tissue was increased in obesity and associated with several metabolic and anthropometric measurements. After adjustment for BMI, the expression remained associated with insulin sensitivity, serum levels of insulin, C-peptide, high density lipoprotein cholesterol (HDL-cholesterol) and triglycerides. In addition, the expression of most macrophage markers was significantly increased in patients with type 2 diabetes compared to the control group.RESULTSThe expression of macrophage markers in adipose tissue was increased in obesity and associated with several metabolic and anthropometric measurements. After adjustment for BMI, the expression remained associated with insulin sensitivity, serum levels of insulin, C-peptide, high density lipoprotein cholesterol (HDL-cholesterol) and triglycerides. In addition, the expression of most macrophage markers was significantly increased in patients with type 2 diabetes compared to the control group.Our study shows that infiltration of macrophages in human adipose tissue, estimated by the expression of macrophage markers, is increased in subjects with obesity and diabetes and associated with insulin sensitivity and serum lipid levels independent of BMI. This indicates that adipose tissue macrophages may contribute to the development of insulin resistance and dyslipidemia.CONCLUSIONOur study shows that infiltration of macrophages in human adipose tissue, estimated by the expression of macrophage markers, is increased in subjects with obesity and diabetes and associated with insulin sensitivity and serum lipid levels independent of BMI. This indicates that adipose tissue macrophages may contribute to the development of insulin resistance and dyslipidemia.
Obesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage infiltration directly influences human metabolism is unclear. The aim of this study was to investigate if there are obesity-independent links between adipose tissue macrophages and metabolic disturbances. Expression of macrophage markers in adipose tissue was analyzed by DNA microarrays in the SOS Sib Pair study and in patients with type 2 diabetes and a BMI-matched healthy control group. The expression of macrophage markers in adipose tissue was increased in obesity and associated with several metabolic and anthropometric measurements. After adjustment for BMI, the expression remained associated with insulin sensitivity, serum levels of insulin, C-peptide, high density lipoprotein cholesterol (HDL-cholesterol) and triglycerides. In addition, the expression of most macrophage markers was significantly increased in patients with type 2 diabetes compared to the control group. Our study shows that infiltration of macrophages in human adipose tissue, estimated by the expression of macrophage markers, is increased in subjects with obesity and diabetes and associated with insulin sensitivity and serum lipid levels independent of BMI. This indicates that adipose tissue macrophages may contribute to the development of insulin resistance and dyslipidemia.
Obesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage infiltration directly influences human metabolism is unclear. The aim of this study was to investigate if there are obesity-independent links between adipose tissue macrophages and metabolic disturbances. Expression of macrophage markers in adipose tissue was analyzed by DNA microarrays in the SOS Sib Pair study and in patients with type 2 diabetes and a BMI-matched healthy control group. The expression of macrophage markers in adipose tissue was increased in obesity and associated with several metabolic and anthropometric measurements. After adjustment for BMI, the expression remained associated with insulin sensitivity, serum levels of insulin, C-peptide, high density lipoprotein cholesterol (HDL-cholesterol) and triglycerides. In addition, the expression of most macrophage markers was significantly increased in patients with type 2 diabetes compared to the control group. Our study shows that infiltration of macrophages in human adipose tissue, estimated by the expression of macrophage markers, is increased in subjects with obesity and diabetes and associated with insulin sensitivity and serum lipid levels independent of BMI. This indicates that adipose tissue macrophages may contribute to the development of insulin resistance and dyslipidemia.
Objective: Obesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage infiltration directly influences human metabolism is unclear. The aim of this study was to investigate if there are obesity‐independent links between adipose tissue macrophages and metabolic disturbances. Design and Methods: Expression of macrophage markers in adipose tissue was analyzed by DNA microarrays in the SOS Sib Pair study and in patients with type 2 diabetes and a BMI‐matched healthy control group. Results: The expression of macrophage markers in adipose tissue was increased in obesity and associated with several metabolic and anthropometric measurements. After adjustment for BMI, the expression remained associated with insulin sensitivity, serum levels of insulin, C‐peptide, high density lipoprotein cholesterol (HDL‐cholesterol) and triglycerides. In addition, the expression of most macrophage markers was significantly increased in patients with type 2 diabetes compared to the control group. Conclusion: Our study shows that infiltration of macrophages in human adipose tissue, estimated by the expression of macrophage markers, is increased in subjects with obesity and diabetes and associated with insulin sensitivity and serum lipid levels independent of BMI. This indicates that adipose tissue macrophages may contribute to the development of insulin resistance and dyslipidemia.
Objective: Obesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage infiltration directly influences human metabolism is unclear. The aim of this study was to investigate if there are obesity‐independent links between adipose tissue macrophages and metabolic disturbances. Design and Methods: Expression of macrophage markers in adipose tissue was analyzed by DNA microarrays in the SOS Sib Pair study and in patients with type 2 diabetes and a BMI‐matched healthy control group. Results: The expression of macrophage markers in adipose tissue was increased in obesity and associated with several metabolic and anthropometric measurements. After adjustment for BMI, the expression remained associated with insulin sensitivity, serum levels of insulin, C‐peptide, high density lipoprotein cholesterol (HDL‐cholesterol) and triglycerides. In addition, the expression of most macrophage markers was significantly increased in patients with type 2 diabetes compared to the control group. Conclusion: Our study shows that infiltration of macrophages in human adipose tissue, estimated by the expression of macrophage markers, is increased in subjects with obesity and diabetes and associated with insulin sensitivity and serum lipid levels independent of BMI. This indicates that adipose tissue macrophages may contribute to the development of insulin resistance and dyslipidemia.
Author Sjöholm, K.
Andersson‐Assarsson, J.C.
Prifti, E.
Jacobson, P.
Walley, A.
Borén, J.
Svensson, P.‐A.
Bergman, R.N.
Froguel, P.
Carlsson, L.M.S.
Ahlin, S.
Poitou, C.
Jansson, P.‐A.
Olsson, B.
Sjöström, L.
Tordjman, J.
AuthorAffiliation 1 Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Sahlgrenska Academy at the University of Gothenburg, 413 45 Gothenburg, Sweden
2 Department of Genomics of Common Disease, School of Public Health, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom
4 Cedars-Sinai Diabetes and Obesity Research Institute, 8700 Beverly Blvd, Thalians E104, Los Angeles, CA 90048
3 Inserm, U872, 15, rue de l’École de Medecine, 75007 Paris, F-75006 France, Universite Pierre et Marie Curie-Paris 6, Centre de Recherche des Cordeliers, UMRS 872, Paris, F-75006 France
5 Clinical Neurochemistry Laboratory, Department of Neurochemistry and Psychiatry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, 431 80 Mölndal, Sweden
AuthorAffiliation_xml – name: 2 Department of Genomics of Common Disease, School of Public Health, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, United Kingdom
– name: 1 Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Sahlgrenska Academy at the University of Gothenburg, 413 45 Gothenburg, Sweden
– name: 4 Cedars-Sinai Diabetes and Obesity Research Institute, 8700 Beverly Blvd, Thalians E104, Los Angeles, CA 90048
– name: 5 Clinical Neurochemistry Laboratory, Department of Neurochemistry and Psychiatry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, 431 80 Mölndal, Sweden
– name: 3 Inserm, U872, 15, rue de l’École de Medecine, 75007 Paris, F-75006 France, Universite Pierre et Marie Curie-Paris 6, Centre de Recherche des Cordeliers, UMRS 872, Paris, F-75006 France
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Notes B. Olsson and P.‐A. Svensson contributed equally to this work.
Disclosure: The authors declared no conflict of interest. B. Olsson and P.‐A. Svensson contributed equally to this work.
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Snippet Objective: Obesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage...
Objective: Obesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage...
Obesity is linked to both increased metabolic disturbances and increased adipose tissue macrophage infiltration. However, whether macrophage infiltration...
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SubjectTerms Adipose Tissue - metabolism
Body fat
Body Mass Index
C-Peptide - blood
Case-Control Studies
Cholesterol, HDL - blood
Diabetes Mellitus, Type 2 - blood
Diabetes Mellitus, Type 2 - genetics
Endocrinology and Diabetes
Endokrinologi och diabetes
Female
Gene Expression
Genetic Markers
Humans
Insulin
Insulin - blood
Insulin resistance
Insulin Resistance - genetics
Macrophages - metabolism
Male
Metabolic disorders
Obesity
Obesity - blood
Obesity - genetics
Oligonucleotide Array Sequence Analysis
Rodents
Studies
Triglycerides - blood
Title Macrophage Gene Expression in Adipose Tissue is Associated with Insulin Sensitivity and Serum Lipid Levels Independent of Obesity
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Foby.20443
https://www.ncbi.nlm.nih.gov/pubmed/23512687
https://www.proquest.com/docview/1675011489
https://www.proquest.com/docview/1465182498
https://pubmed.ncbi.nlm.nih.gov/PMC3763968
https://gup.ub.gu.se/publication/181112
Volume 21
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