Mechanisms of Macrophage Polarization in Insulin Signaling and Sensitivity

Type-2 diabetes (T2D) is a disease of two etiologies: metabolic and inflammatory. At the cross-section of these etiologies lays the phenomenon of metabolic inflammation. Whilst metabolic inflammation is characterized as systemic, a common starting point is the tissue-resident macrophage, who's...

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Published inFrontiers in endocrinology (Lausanne) Vol. 11; p. 62
Main Authors Orliaguet, Lucie, Dalmas, Elise, Drareni, Karima, Venteclef, Nicolas, Alzaid, Fawaz
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers 19.02.2020
Frontiers Media S.A
Subjects
adipose tissue
Animals
Diabetes Mellitus, Type 2 - immunology
Diabetes Mellitus, Type 2 - physiopathology
Endocrinology
Homeostasis
Human health and pathology
Humans
inflammation
Insulin - metabolism
Insulin Resistance
Life Sciences
liver
macrophage
Macrophage Activation - immunology
pancreas
Signal Transduction
type-2 diabetes
immunometabolism
inflammation
liver
type-2 diabetes
pancreas
adipose tissue
macrophage
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Abstract Type-2 diabetes (T2D) is a disease of two etiologies: metabolic and inflammatory. At the cross-section of these etiologies lays the phenomenon of metabolic inflammation. Whilst metabolic inflammation is characterized as systemic, a common starting point is the tissue-resident macrophage, who's successful physiological or aberrant pathological adaptation to its microenvironment determines disease course and severity. This review will highlight the key mechanisms in macrophage polarization, inflammatory and non-inflammatory signaling that dictates the development and progression of insulin resistance and T2D. We first describe the known homeostatic functions of tissue macrophages in insulin secreting and major insulin sensitive tissues. Importantly we highlight the known mechanisms of aberrant macrophage activation in these tissues and the ways in which this leads to impairment of insulin sensitivity/secretion and the development of T2D. We next describe the cellular mechanisms that are known to dictate macrophage polarization. We review recent progress in macrophage bio-energetics, an emerging field of research that places cellular metabolism at the center of immune-effector function. Importantly, following the advent of the metabolically-activated macrophage, we cover the known transcriptional and epigenetic factors that canonically and non-canonically dictate macrophage differentiation and inflammatory polarization. In closing perspectives, we discuss emerging research themes and highlight novel non-inflammatory or non-immune roles that tissue macrophages have in maintaining microenvironmental and systemic homeostasis.
AbstractList Type-2 diabetes (T2D) is a disease of two etiologies: metabolic and inflammatory. At the cross-section of these etiologies lays the phenomenon of metabolic inflammation. Whilst metabolic inflammation is characterized as systemic, a common starting point is the tissue-resident macrophage, who's successful physiological or aberrant pathological adaptation to its microenvironment determines disease course and severity. This review will highlight the key mechanisms in macrophage polarization, inflammatory and non-inflammatory signaling that dictates the development and progression of insulin resistance and T2D. We first describe the known homeostatic functions of tissue macrophages in insulin secreting and major insulin sensitive tissues. Importantly we highlight the known mechanisms of aberrant macrophage activation in these tissues and the ways in which this leads to impairment of insulin sensitivity/secretion and the development of T2D. We next describe the cellular mechanisms that are known to dictate macrophage polarization. We review recent progress in macrophage bio-energetics, an emerging field of research that places cellular metabolism at the center of immune-effector function. Importantly, following the advent of the metabolically-activated macrophage, we cover the known transcriptional and epigenetic factors that canonically and non-canonically dictate macrophage differentiation and inflammatory polarization. In closing perspectives, we discuss emerging research themes and highlight novel non-inflammatory or non-immune roles that tissue macrophages have in maintaining microenvironmental and systemic homeostasis.
Type-2 diabetes (T2D) is a disease of two etiologies: metabolic and inflammatory. At the cross-section of these etiologies lays the phenomenon of metabolic inflammation. Whilst metabolic inflammation is characterized as systemic, a common starting point is the tissue-resident macrophage, who's successful physiological or aberrant pathological adaptation to its microenvironment determines disease course and severity. This review will highlight the key mechanisms in macrophage polarization, inflammatory and non-inflammatory signaling that dictates the development and progression of insulin resistance and T2D. We first describe the known homeostatic functions of tissue macrophages in insulin secreting and major insulin sensitive tissues. Importantly we highlight the known mechanisms of aberrant macrophage activation in these tissues and the ways in which this leads to impairment of insulin sensitivity/secretion and the development of T2D. We next describe the cellular mechanisms that are known to dictate macrophage polarization. We review recent progress in macrophage bio-energetics, an emerging field of research that places cellular metabolism at the center of immune-effector function. Importantly, following the advent of the metabolically-activated macrophage, we cover the known transcriptional and epigenetic factors that canonically and non-canonically dictate macrophage differentiation and inflammatory polarization. In closing perspectives, we discuss emerging research themes and highlight novel non-inflammatory or non-immune roles that tissue macrophages have in maintaining microenvironmental and systemic homeostasis.Type-2 diabetes (T2D) is a disease of two etiologies: metabolic and inflammatory. At the cross-section of these etiologies lays the phenomenon of metabolic inflammation. Whilst metabolic inflammation is characterized as systemic, a common starting point is the tissue-resident macrophage, who's successful physiological or aberrant pathological adaptation to its microenvironment determines disease course and severity. This review will highlight the key mechanisms in macrophage polarization, inflammatory and non-inflammatory signaling that dictates the development and progression of insulin resistance and T2D. We first describe the known homeostatic functions of tissue macrophages in insulin secreting and major insulin sensitive tissues. Importantly we highlight the known mechanisms of aberrant macrophage activation in these tissues and the ways in which this leads to impairment of insulin sensitivity/secretion and the development of T2D. We next describe the cellular mechanisms that are known to dictate macrophage polarization. We review recent progress in macrophage bio-energetics, an emerging field of research that places cellular metabolism at the center of immune-effector function. Importantly, following the advent of the metabolically-activated macrophage, we cover the known transcriptional and epigenetic factors that canonically and non-canonically dictate macrophage differentiation and inflammatory polarization. In closing perspectives, we discuss emerging research themes and highlight novel non-inflammatory or non-immune roles that tissue macrophages have in maintaining microenvironmental and systemic homeostasis.
Author Alzaid, Fawaz
Orliaguet, Lucie
Drareni, Karima
Venteclef, Nicolas
Dalmas, Elise
AuthorAffiliation 2 Institute for Diabetes, Obesity and Metabolism, University of Pennsylvania , Philadelphia, PA , United States
1 Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, USPC, Université Paris Descartes, Université Paris Diderot , Paris , France
AuthorAffiliation_xml – name: 2 Institute for Diabetes, Obesity and Metabolism, University of Pennsylvania , Philadelphia, PA , United States
– name: 1 Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, USPC, Université Paris Descartes, Université Paris Diderot , Paris , France
Author_xml – sequence: 1
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  surname: Orliaguet
  fullname: Orliaguet, Lucie
– sequence: 2
  givenname: Elise
  surname: Dalmas
  fullname: Dalmas, Elise
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  surname: Drareni
  fullname: Drareni, Karima
– sequence: 4
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  surname: Venteclef
  fullname: Venteclef, Nicolas
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  surname: Alzaid
  fullname: Alzaid, Fawaz
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32140136$$D View this record in MEDLINE/PubMed
https://hal.sorbonne-universite.fr/hal-02537182$$DView record in HAL
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Keywords immunometabolism
inflammation
liver
type-2 diabetes
pancreas
adipose tissue
macrophage
Language English
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This article was submitted to Diabetes: Molecular Mechanisms, a section of the journal Frontiers in Endocrinology
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Snippet Type-2 diabetes (T2D) is a disease of two etiologies: metabolic and inflammatory. At the cross-section of these etiologies lays the phenomenon of metabolic...
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SubjectTerms adipose tissue
Animals
Diabetes Mellitus, Type 2 - immunology
Diabetes Mellitus, Type 2 - physiopathology
Endocrinology
Homeostasis
Human health and pathology
Humans
inflammation
Insulin - metabolism
Insulin Resistance
Life Sciences
liver
macrophage
Macrophage Activation - immunology
pancreas
Signal Transduction
type-2 diabetes
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Title Mechanisms of Macrophage Polarization in Insulin Signaling and Sensitivity
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