33 results on '"Dalmas E"'
Search Results
2. Time course of oxidative stress after major burns
- Author
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Bertin-Maghit, M., Goudable, J., Dalmas, E., Steghens, J. P., Bouchard, C., Gueugniaud, P. Y., Petit, P., and Delafosse, B.
- Published
- 2000
- Full Text
- View/download PDF
3. Soya bean tempe extracts show antibacterial activity against Bacillus cereus cells and spores
- Author
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Roubos-van den Hil, P. J., Dalmas, E., Nout, M. J.R., and Abee, T.
- Published
- 2010
- Full Text
- View/download PDF
4. CD14(dim)CD16(+) and CD14(+)CD16(+) Monocytes in Obesity and During Weight Loss Relationships With Fat Mass and Subclinical Atherosclerosis
- Author
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Poitou, C., Dalmas, E., Renovato, M., Benhamo, V., Hajduch, F., Abdennour, M., Kahn, J.-F., Veyrie, N., Rizkalla, S., Fridman, W.-H., Sautes-Fridman, C., Clement, K., and Cremer, I.
- Published
- 2011
- Full Text
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5. Inflammation du tissu adipeux au cours de l'obésité.
- Author
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Poitou, C., Dalmas, E., and Clément, K.
- Published
- 2013
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6. Spontaneous baroreflex cardiac sensitivity in end-stage liver disease: effect of liver transplantation.
- Author
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Lhuillier, F., Dalmas, E. D., Gratadour, P. M., Cividjian, A. A., Boillot, O. C., Quintin, L., and Vaile, J. P.
- Subjects
BAROREFLEXES ,LIVER diseases ,LIVER transplantation ,AUTONOMIC nervous system ,SURGERY - Abstract
Background and objective: End-stage liver disease is associated with an imbalance in the autonomic nervous system. The purpose of this study was to estimate the effect of liver transplantation on this imbalance. Method: The study involved 10 patients undergoing liver transplantation and 9 patients without liver impairment undergoing liver surgery. The spontaneous baroreflex sensitivity was measured before and 1 month after surgery for the liver surgery group; before and 1, 3, 6, 12 and 18 months after orthotopic liver transplantation. Results: The spontaneous baroreflex slope of patients with end-stage liver disease was decreased before liver transplantation compared to the liver surgery group (3.9 ± 2.5 ms mmHg
-1 vs. 9.9 ± 5.0 ms mmHg-1 , P = 0.002). The mean slope was significantly increased at 12 and 18 months compared to the pre-transplantation value (3.9 ± 2.5 ms mmHg-1 vs. 8.1 ± 6.6 ms mmHg-1 and 7.4 ± 4.8 ms mmHg-1 respectively; P = 0.042). Nevertheless, further analysis of individual data showed that only four patients exhibited a marked increase in their baroreflex slope 12 months after the liver transplantation whereas it remained decreased in the six others. Conclusions: These results confirm that the baroreflex sensitivity is depressed in end-stage liver disease in line with an autonomic nervous system imbalance. The liver transplantation reverses this disturbance only in some patients. [ABSTRACT FROM AUTHOR]- Published
- 2006
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7. Patient-ventilator interactions during partial ventilatory support: a preliminary study comparing the effects of adaptive support ventilation with synchronized intermittent mandatory ventilation plus inspiratory pressure support.
- Author
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Tassaux D, Dalmas E, Gratadour P, Jolliet P, Tassaux, Didier, Dalmas, Eric, Gratadour, Pierre, and Jolliet, Philippe
- Published
- 2002
8. mTOR inhibition suppresses salinomycin-induced ferroptosis in breast cancer stem cells by ironing out mitochondrial dysfunctions.
- Author
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Cosialls E, Pacreau E, Duruel C, Ceccacci S, Elhage R, Desterke C, Roger K, Guerrera C, Ducloux R, Souquere S, Pierron G, Nemazanyy I, Kelly M, Dalmas E, Chang Y, Goffin V, Mehrpour M, and Hamaï A
- Subjects
- Humans, Female, TOR Serine-Threonine Kinases metabolism, Iron metabolism, Neoplastic Stem Cells metabolism, Ferroptosis, Breast Neoplasms drug therapy, Breast Neoplasms metabolism
- Abstract
Ferroptosis constitutes a promising therapeutic strategy against cancer by efficiently targeting the highly tumorigenic and treatment-resistant cancer stem cells (CSCs). We previously showed that the lysosomal iron-targeting drug Salinomycin (Sal) was able to eliminate CSCs by triggering ferroptosis. Here, in a well-established breast CSCs model (human mammary epithelial HMLER CD24
low /CD44high ), we identified that pharmacological inhibition of the mechanistic target of rapamycin (mTOR), suppresses Sal-induced ferroptosis. Mechanistically, mTOR inhibition modulates iron cellular flux and thereby limits iron-mediated oxidative stress. Furthermore, integration of multi-omics data identified mitochondria as a key target of Sal action, leading to profound functional and structural alteration prevented by mTOR inhibition. On top of that, we found that Sal-induced metabolic plasticity is mainly dependent on the mTOR pathway. Overall, our findings provide experimental evidence for the mechanisms of mTOR as a crucial effector of Sal-induced ferroptosis pointing not only that metabolic reprogramming regulates ferroptosis, but also providing proof-of-concept that careful evaluation of such combination therapy (here mTOR and ferroptosis co-targeting) is required in the development of an effective treatment., (© 2023. The Author(s).)- Published
- 2023
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9. Targeting colonic macrophages improves glycemic control in high-fat diet-induced obesity.
- Author
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Rohm TV, Keller L, Bosch AJT, AlAsfoor S, Baumann Z, Thomas A, Wiedemann SJ, Steiger L, Dalmas E, Wehner J, Rachid L, Mooser C, Yilmaz B, Fernandez Trigo N, Jauch AJ, Wueest S, Konrad D, Henri S, Niess JH, Hruz P, Ganal-Vonarburg SC, Roux J, Meier DT, and Cavelti-Weder C
- Subjects
- Animals, Blood Glucose metabolism, Colon metabolism, Glycemic Control, Macrophages metabolism, Mice, Obesity etiology, Obesity metabolism, TOR Serine-Threonine Kinases metabolism, Diet, High-Fat adverse effects, Insulin Resistance
- Abstract
The obesity epidemic continues to worsen worldwide. However, the mechanisms initiating glucose dysregulation in obesity remain poorly understood. We assessed the role that colonic macrophage subpopulations play in glucose homeostasis in mice fed a high-fat diet (HFD). Concurrent with glucose intolerance, pro-inflammatory/monocyte-derived colonic macrophages increased in mice fed a HFD. A link between macrophage numbers and glycemia was established by pharmacological dose-dependent ablation of macrophages. In particular, colon-specific macrophage depletion by intrarectal clodronate liposomes improved glucose tolerance, insulin sensitivity, and insulin secretion capacity. Colonic macrophage activation upon HFD was characterized by an interferon response and a change in mitochondrial metabolism, which converged in mTOR as a common regulator. Colon-specific mTOR inhibition reduced pro-inflammatory macrophages and ameliorated insulin secretion capacity, similar to colon-specific macrophage depletion, but did not affect insulin sensitivity. Thus, pharmacological targeting of colonic macrophages could become a potential therapy in obesity to improve glycemic control., (© 2022. The Author(s).)
- Published
- 2022
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10. Islet Inflammation and β Cell Dysfunction in Type 2 Diabetes.
- Author
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Cuenco J and Dalmas E
- Subjects
- Humans, Inflammation, Insulin metabolism, Macrophages, Obesity complications, Obesity metabolism, Diabetes Mellitus, Type 2, Insulin-Secreting Cells, Islets of Langerhans metabolism
- Abstract
Pancreatic islets are the body's central rheostat that regulates glucose homeostasis through the production of different hormones, including β cell-derived insulin. During obesity-induced type 2 diabetes (T2D), islet β cells become dysfunctional and inadequate insulin secretion no longer ensures glycemic control. T2D is associated with a chronic low-grade inflammation that manifests in several metabolic organs including the pancreatic islets. Growing evidence suggests that components of the innate immune system, and especially macrophages, play a crucial role in regulating islet homeostasis. Yet, the phenotypes and functions of islet macrophages in physiology and during T2D have only started to attract attention and remain unclear. In this review, the current knowledge about islet inflammation and macrophages will be summarized in humans and rodent models. Recent findings on the cellular and molecular mechanisms involved in islet remodeling and β cell function during obesity and T2D will be discussed., (© 2022. The Author(s), under exclusive license to Springer Nature Switzerland AG.)
- Published
- 2022
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11. Understanding the heterogeneity and functions of metabolic tissue macrophages.
- Author
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Grosjean A, Venteclef N, and Dalmas E
- Subjects
- Animals, Homeostasis, Humans, Mice, Signal Transduction, Adipose Tissue metabolism, Macrophages metabolism
- Abstract
Growing evidence places tissue-resident macrophages as essential gatekeepers of metabolic organ homeostasis, including the adipose tissue and the pancreatic islets. Therein, macrophages may adopt specific phenotypes and ensure local functions. Recent advances in single cell genomic analyses provide a comprehensive map of adipose tissue macrophage subsets and their potential roles are now better apprehended. Whether they are beneficial or detrimental, macrophages overall contribute to the proper adipose tissue expansion under steady state and during obesity. By contrast, macrophages residing inside pancreatic islets, which may exert fundamental functions to fine tune insulin secretion, have only started to attract attention and their cellular heterogeneity remains to be established. The present review will focus on the latest findings exploring the phenotype and the properties of macrophages in adipose tissue and pancreatic islets, questioning early beliefs and future perspectives in the field of immunometabolism., (Copyright © 2021. Published by Elsevier Ltd.)
- Published
- 2021
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12. Monocytopenia, monocyte morphological anomalies and hyperinflammation characterise severe COVID-19 in type 2 diabetes.
- Author
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Alzaid F, Julla JB, Diedisheim M, Potier C, Potier L, Velho G, Gaborit B, Manivet P, Germain S, Vidal-Trecan T, Roussel R, Riveline JP, Dalmas E, Venteclef N, and Gautier JF
- Subjects
- Aged, COVID-19 complications, COVID-19 virology, Chemokine CCL2 genetics, Chemokine CCL2 metabolism, Diabetes Mellitus, Type 2 complications, Female, Humans, Immunophenotyping, Inflammation etiology, Interleukin-6 genetics, Interleukin-6 metabolism, Leukocytes, Mononuclear cytology, Leukocytes, Mononuclear metabolism, Lipopolysaccharide Receptors metabolism, Lymphopenia diagnosis, Male, Middle Aged, Monocytes cytology, Monocytes pathology, Risk Factors, SARS-CoV-2 isolation & purification, Severity of Illness Index, COVID-19 pathology, Diabetes Mellitus, Type 2 pathology, Monocytes physiology
- Abstract
Early in the COVID-19 pandemic, type 2 diabetes (T2D) was marked as a risk factor for severe disease and mortality. Inflammation is central to the aetiology of both conditions where variations in immune responses can mitigate or aggravate disease course. Identifying at-risk groups based on immunoinflammatory signatures is valuable in directing personalised care and developing potential targets for precision therapy. This observational study characterised immunophenotypic variation associated with COVID-19 severity in T2D. Broad-spectrum immunophenotyping quantified 15 leucocyte populations in peripheral circulation from a cohort of 45 hospitalised COVID-19 patients with and without T2D. Lymphocytopenia and specific loss of cytotoxic CD8
+ lymphocytes were associated with severe COVID-19 and requirement for intensive care in both non-diabetic and T2D patients. A morphological anomaly of increased monocyte size and monocytopenia restricted to classical CD14Hi CD16- monocytes was specifically associated with severe COVID-19 in patients with T2D requiring intensive care. Increased expression of inflammatory markers reminiscent of the type 1 interferon pathway (IL6, IL8, CCL2, INFB1) underlaid the immunophenotype associated with T2D. These immunophenotypic and hyperinflammatory changes may contribute to increased voracity of COVID-19 in T2D. These findings allow precise identification of T2D patients with severe COVID-19 as well as provide evidence that the type 1 interferon pathway may be an actionable therapeutic target for future studies., (© 2020 The Authors. Published under the terms of the CC BY 4.0 license.)- Published
- 2020
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13. Adipocyte Reprogramming by the Transcriptional Coregulator GPS2 Impacts Beta Cell Insulin Secretion.
- Author
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Drareni K, Ballaire R, Alzaid F, Goncalves A, Chollet C, Barilla S, Nguewa JL, Dias K, Lemoine S, Riveline JP, Roussel R, Dalmas E, Velho G, Treuter E, Gautier JF, and Venteclef N
- Subjects
- Adipocytes, White metabolism, Adipose Tissue metabolism, Animals, Diabetes Mellitus, Type 2 metabolism, Female, Glucose metabolism, Glucose Intolerance metabolism, Inflammation metabolism, Insulin metabolism, Insulin Resistance genetics, Insulin Secretion physiology, Intracellular Signaling Peptides and Proteins physiology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Obesity metabolism, Adipose Tissue, White metabolism, Insulin-Secreting Cells metabolism, Intracellular Signaling Peptides and Proteins metabolism
- Abstract
Glucose homeostasis is maintained through organ crosstalk that regulates secretion of insulin to keep blood glucose levels within a physiological range. In type 2 diabetes, this coordinated response is altered, leading to a deregulation of beta cell function and inadequate insulin secretion. Reprogramming of white adipose tissue has a central role in this deregulation, but the critical regulatory components remain unclear. Here, we demonstrate that expression of the transcriptional coregulator GPS2 in white adipose tissue is correlated with insulin secretion rate in humans. The causality of this relationship is confirmed using adipocyte-specific GPS2 knockout mice, in which inappropriate secretion of insulin promotes glucose intolerance. This phenotype is driven by adipose-tissue-secreted factors, which cause increased pancreatic islet inflammation and impaired beta cell function. Thus, our study suggests that, in mice and in humans, GPS2 controls the reprogramming of white adipocytes to influence pancreatic islet function and insulin secretion., Competing Interests: Declaration of Interests The authors declare no competing interests., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2020
- Full Text
- View/download PDF
14. Inhibition of IL-1beta improves Glycaemia in a Mouse Model for Gestational Diabetes.
- Author
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Schulze F, Wehner J, Kratschmar DV, Makshana V, Meier DT, Häuselmann SP, Dalmas E, Thienel C, Dror E, Wiedemann SJ, Traub S, Nordmann TM, Rachid L, De Baat A, Rohm TV, Zhao C, Odermatt A, Böni-Schnetzler M, and Donath MY
- Subjects
- Animals, Diabetes, Gestational blood, Disease Models, Animal, Female, Hormones blood, Hyperglycemia blood, Interleukin-1beta metabolism, Mice, Inbred C57BL, Pregnancy, Steroids blood, Diabetes, Gestational metabolism, Hyperglycemia complications, Hyperglycemia metabolism, Interleukin-1beta antagonists & inhibitors
- Abstract
Gestational diabetes mellitus (GDM) is one of the most common diseases associated with pregnancy, however, the underlying mechanisms remain unclear. Based on the well documented role of inflammation in type 2 diabetes, the aim was to investigate the role of inflammation in GDM. We established a mouse model for GDM on the basis of its two major risk factors, obesity and aging. In these GDM mice, we observed increased Interleukin-1β (IL-1β) expression in the uterus and the placenta along with elevated circulating IL-1β concentrations compared to normoglycemic pregnant mice. Treatment with an anti-IL-1β antibody improved glucose-tolerance of GDM mice without apparent deleterious effects for the fetus. Finally, IL-1β antagonism showed a tendency for reduced plasma corticosterone concentrations, possibly explaining the metabolic improvement. We conclude that IL-1β is a causal driver of impaired glucose tolerance in GDM.
- Published
- 2020
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15. Mechanisms of Macrophage Polarization in Insulin Signaling and Sensitivity.
- Author
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Orliaguet L, Dalmas E, Drareni K, Venteclef N, and Alzaid F
- Subjects
- Animals, Diabetes Mellitus, Type 2 immunology, Homeostasis, Humans, Signal Transduction, Diabetes Mellitus, Type 2 physiopathology, Insulin metabolism, Insulin Resistance, Macrophage Activation immunology
- 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., (Copyright © 2020 Orliaguet, Dalmas, Drareni, Venteclef and Alzaid.)
- Published
- 2020
- Full Text
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16. Role of innate immune cells in metabolism: from physiology to type 2 diabetes.
- Author
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Dalmas E
- Subjects
- Animals, Humans, Diabetes Mellitus, Type 2 immunology, Diabetes Mellitus, Type 2 metabolism, Diabetes Mellitus, Type 2 pathology, Diabetes Mellitus, Type 2 physiopathology, Immunity, Innate, Obesity immunology, Obesity metabolism, Obesity pathology, Obesity physiopathology
- Abstract
Growing evidence suggests that components of the innate immune system play a crucial role in regulating metabolic homeostasis. Macrophages were the primary immune cells to be described in both the white adipose tissue and the pancreatic islets. Therein, their functions, beneficial or detrimental, are extending under steady state and in the context of obesity-induced type 2 diabetes. Other populations, including innate lymphoid cells, are emerging as key sentinels of metabolic tissues and privileged partners of macrophages. The present review will thus explore the phenotype and the role of innate immune cells in metabolic physiology and dysfunction. Discussion will tackle pending questions and future perspectives in the field of immunometabolism.
- Published
- 2019
- Full Text
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17. Innate immune priming of insulin secretion.
- Author
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Dalmas E
- Subjects
- Animals, Homeostasis, Humans, Signal Transduction, Diabetes Mellitus, Type 1 metabolism, Immune System metabolism, Immunity, Innate, Insulin metabolism, Insulin Secretion, Islets of Langerhans immunology
- Abstract
Increasing evidence suggests a role for the immune system to finely tune metabolic homeostasis. The possibility that the immune system can likewise regulate islet endocrine function has only commenced drawing attention. Islet beta cells are the main producers of insulin and have to dynamically respond to fluctuating insulin demands of the body. While inflammation has long been considered as an important pathogenic feature of diabetes development, pioneer studies have shown that immune cells reside inside pancreatic islets under steady state and that components of the immune system can promote beta cell insulin production. The present review will thus highlight the recent research on specific immune pathways regulating beta cell function discussing the beneficial influence of innate immune cells., (Copyright © 2018 The Author. Published by Elsevier Ltd.. All rights reserved.)
- Published
- 2019
- Full Text
- View/download PDF
18. IL-33 Deals with the Gray Matter.
- Author
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Delmas C and Dalmas E
- Subjects
- Animals, Astrocytes metabolism, Brain immunology, Brain metabolism, Gray Matter immunology, Humans, Microglia immunology, Microglia metabolism, Neurogenesis, Synapses metabolism, Gray Matter metabolism, Interleukin-33 genetics, Interleukin-33 metabolism
- Abstract
The central nervous system undergoes extensive postnatal synapse remodeling that is critical for the formation of mature neural circuits. In a recent issue of Science, Vainchtein et al. (2018) describe an additional role for astrocyte-derived interleukin-33 (IL-33) in promoting synapse refinement by microglia in the developing brain., (Copyright © 2018 Elsevier Inc. All rights reserved.)
- Published
- 2018
- Full Text
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19. β Cell-Specific Deletion of the IL-1 Receptor Antagonist Impairs β Cell Proliferation and Insulin Secretion.
- Author
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Böni-Schnetzler M, Häuselmann SP, Dalmas E, Meier DT, Thienel C, Traub S, Schulze F, Steiger L, Dror E, Martin P, Herrera PL, Gabay C, and Donath MY
- Subjects
- Animals, Biomarkers metabolism, Cell Proliferation drug effects, E2F1 Transcription Factor metabolism, Glucose pharmacology, Glucose Intolerance metabolism, Glucose Intolerance pathology, Insulin-Secreting Cells drug effects, Interleukin 1 Receptor Antagonist Protein blood, Male, Mice, Inbred C57BL, Mice, Knockout, Mice, Obese, Myeloid Cells drug effects, Myeloid Cells metabolism, Obesity blood, Obesity pathology, Organ Specificity drug effects, Gene Deletion, Insulin Secretion drug effects, Insulin-Secreting Cells metabolism, Interleukin 1 Receptor Antagonist Protein metabolism
- Abstract
Interleukin-1 receptor antagonist (IL-1Ra) is elevated in the circulation during obesity and type 2 diabetes (T2D) but is decreased in islets from patients with T2D. The protective role of local IL-1Ra was investigated in pancreatic islet β cell (βIL-1Ra)-specific versus myeloid-cell (myeloIL-1Ra)-specific IL-1Ra knockout (KO) mice. Deletion of IL-1Ra in β cells, but not in myeloid cells, resulted in diminished islet IL-1Ra expression. Myeloid cells were not the main source of circulating IL-1Ra in obesity. βIL-1Ra KO mice had impaired insulin secretion, reduced β cell proliferation, and decreased expression of islet proliferation genes, along with impaired glucose tolerance. The key cell-cycle regulator E2F1 partly reversed IL-1β-mediated inhibition of potassium channel Kir6.2 expression and rescued impaired insulin secretion in IL-1Ra knockout islets. Our findings provide evidence for the importance of β cell-derived IL-1Ra for the local defense of β cells to maintain normal function and proliferation., (Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.)
- Published
- 2018
- Full Text
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20. Interleukin-33-Activated Islet-Resident Innate Lymphoid Cells Promote Insulin Secretion through Myeloid Cell Retinoic Acid Production.
- Author
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Dalmas E, Lehmann FM, Dror E, Wueest S, Thienel C, Borsigova M, Stawiski M, Traunecker E, Lucchini FC, Dapito DH, Kallert SM, Guigas B, Pattou F, Kerr-Conte J, Maechler P, Girard JP, Konrad D, Wolfrum C, Böni-Schnetzler M, Finke D, and Donath MY
- Subjects
- Animals, Humans, Inflammation immunology, Insulin Secretion, Interleukin-33 biosynthesis, Islets of Langerhans immunology, Islets of Langerhans pathology, Lymphocytes physiology, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Vitamin A physiology, Insulin metabolism, Interleukin-33 pharmacology, Islets of Langerhans drug effects, Lymphocytes drug effects, Myeloid Cells metabolism, Tretinoin metabolism
- Abstract
Pancreatic-islet inflammation contributes to the failure of β cell insulin secretion during obesity and type 2 diabetes. However, little is known about the nature and function of resident immune cells in this context or in homeostasis. Here we show that interleukin (IL)-33 was produced by islet mesenchymal cells and enhanced by a diabetes milieu (glucose, IL-1β, and palmitate). IL-33 promoted β cell function through islet-resident group 2 innate lymphoid cells (ILC2s) that elicited retinoic acid (RA)-producing capacities in macrophages and dendritic cells via the secretion of IL-13 and colony-stimulating factor 2. In turn, local RA signaled to the β cells to increase insulin secretion. This IL-33-ILC2 axis was activated after acute β cell stress but was defective during chronic obesity. Accordingly, IL-33 injections rescued islet function in obese mice. Our findings provide evidence that an immunometabolic crosstalk between islet-derived IL-33, ILC2s, and myeloid cells fosters insulin secretion., (Copyright © 2017 Elsevier Inc. All rights reserved.)
- Published
- 2017
- Full Text
- View/download PDF
21. Pancreatic α Cell-Derived Glucagon-Related Peptides Are Required for β Cell Adaptation and Glucose Homeostasis.
- Author
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Traub S, Meier DT, Schulze F, Dror E, Nordmann TM, Goetz N, Koch N, Dalmas E, Stawiski M, Makshana V, Thorel F, Herrera PL, Böni-Schnetzler M, and Donath MY
- Subjects
- Aging pathology, Animals, Diet, High-Fat, Diphtheria Toxin administration & dosage, Diphtheria Toxin pharmacology, Glucagon-Secreting Cells drug effects, Glucose Intolerance complications, Glucose Intolerance pathology, Glucose Tolerance Test, Humans, Insulin metabolism, Insulin Secretion, Insulin-Secreting Cells drug effects, Mice, Inbred C57BL, Mice, Knockout, Obesity complications, Obesity pathology, Proprotein Convertases metabolism, Rats, Stress, Physiological drug effects, Adaptation, Physiological, Glucagon metabolism, Glucagon-Like Peptide 1 metabolism, Glucagon-Secreting Cells metabolism, Glucose metabolism, Homeostasis drug effects, Insulin-Secreting Cells metabolism
- Abstract
Pancreatic α cells may process proglucagon not only to glucagon but also to glucagon-like peptide-1 (GLP-1). However, the biological relevance of paracrine GLP-1 for β cell function remains unclear. We studied effects of locally derived insulin secretagogues on β cell function and glucose homeostasis using mice with α cell ablation and with α cell-specific GLP-1 deficiency. Normally, intestinal GLP-1 compensates for the lack of α cell-derived GLP-1. However, upon aging and metabolic stress, glucose tolerance is impaired. This was partly rescued with the DPP-4 inhibitor sitagliptin, but not with glucagon administration. In isolated islets from these mice, glucose-stimulated insulin secretion was heavily impaired and exogenous GLP-1 or glucagon rescued insulin secretion. These data highlight the importance of α cell-derived GLP-1 for glucose homeostasis during metabolic stress and may impact on the clinical use of systemic GLP-1 agonists versus stabilizing local α cell-derived GLP-1 by DPP-4 inhibitors in type 2 diabetes., (Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.)
- Published
- 2017
- Full Text
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22. Postprandial macrophage-derived IL-1β stimulates insulin, and both synergistically promote glucose disposal and inflammation.
- Author
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Dror E, Dalmas E, Meier DT, Wueest S, Thévenet J, Thienel C, Timper K, Nordmann TM, Traub S, Schulze F, Item F, Vallois D, Pattou F, Kerr-Conte J, Lavallard V, Berney T, Thorens B, Konrad D, Böni-Schnetzler M, and Donath MY
- Subjects
- Animals, Cells, Cultured, Glucose metabolism, Humans, Inflammasomes metabolism, Insulin metabolism, Interleukin-1beta genetics, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, NLR Family, Pyrin Domain-Containing 3 Protein metabolism, Postprandial Period, Reactive Oxygen Species metabolism, Signal Transduction, Sodium-Glucose Transporter 2 metabolism, Diabetes Mellitus, Type 2 immunology, Inflammation immunology, Insulin-Secreting Cells physiology, Interleukin-1beta metabolism, Macrophages physiology
- Abstract
The deleterious effect of chronic activation of the IL-1β system on type 2 diabetes and other metabolic diseases is well documented. However, a possible physiological role for IL-1β in glucose metabolism has remained unexplored. Here we found that feeding induced a physiological increase in the number of peritoneal macrophages that secreted IL-1β, in a glucose-dependent manner. Subsequently, IL-1β contributed to the postprandial stimulation of insulin secretion. Accordingly, lack of endogenous IL-1β signaling in mice during refeeding and obesity diminished the concentration of insulin in plasma. IL-1β and insulin increased the uptake of glucose into macrophages, and insulin reinforced a pro-inflammatory pattern via the insulin receptor, glucose metabolism, production of reactive oxygen species, and secretion of IL-1β mediated by the NLRP3 inflammasome. Postprandial inflammation might be limited by normalization of glycemia, since it was prevented by inhibition of the sodium-glucose cotransporter SGLT2. Our findings identify a physiological role for IL-1β and insulin in the regulation of both metabolism and immunity.
- Published
- 2017
- Full Text
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23. Glucose-Dependent Insulinotropic Peptide Stimulates Glucagon-Like Peptide 1 Production by Pancreatic Islets via Interleukin 6, Produced by α Cells.
- Author
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Timper K, Dalmas E, Dror E, Rütti S, Thienel C, Sauter NS, Bouzakri K, Bédat B, Pattou F, Kerr-Conte J, Böni-Schnetzler M, and Donath MY
- Subjects
- Animals, Blood Glucose metabolism, Diabetes Mellitus, Experimental etiology, Diabetes Mellitus, Experimental metabolism, Humans, Insulin metabolism, Insulin Secretion, Mice, Mice, Inbred C57BL, Gastric Inhibitory Polypeptide metabolism, Glucagon-Like Peptide 1 biosynthesis, Glucagon-Secreting Cells metabolism, Insulin-Secreting Cells metabolism, Interleukin-6 metabolism
- Abstract
Background & Aims: Glucose-dependent insulinotropic peptide (GIP) induces production of interleukin 6 (IL6) by adipocytes. IL6 increases production of glucagon-like peptide (GLP)-1 by L cells and α cells, leading to secretion of insulin from β cells. We investigated whether GIP regulates GLP1 and glycemia via IL6., Methods: We obtained samples of human pancreatic islets and isolated islets from mice; human α cells and β cells were sorted by flow cytometry and incubated with GIP. Islets were analyzed by quantitative polymerase chain reaction and immunohistochemistry. BKS.Cg-Dock7m+/+ Leprdb/J db/db mice (diabetic mice) and db/+ mice, as well as C57BL/6J IL6-knockout mice (IL6-KO) and C57BL/6J mice with the full-length Il6 gene (controls), were fed a chow or a high-fat diet; some mice were given injections of recombinant GIP, IL6, GLP, a neutralizing antibody against IL6 (anti-IL6), lipopolysaccharide, and/or IL1B. Mice were given a glucose challenge and blood samples were collected and analyzed., Results: Incubation of mouse and human pancreatic α cells with GIP induced their production of IL6, leading to production of GLP1 and insulin secretion from pancreatic islets. This did not occur in islets from IL6-KO mice or in islets incubated with anti-IL6. Incubation of islets with IL1B resulted in IL6 production but directly reduced GLP1 production. Incubation of mouse islets with the sodium glucose transporter 2 inhibitor dapagliflozin induced production of GLP1 and IL6. Injection of control mice with GIP increased plasma levels of GLP1, insulin, and glucose tolerance; these effects were amplified in mice given lipopolysaccharide but reduced in IL6-KO mice or in mice given anti-IL6. Islets from diabetic mice had increased levels of IL1B and IL6, compared with db/+ mice, but injection of GIP did not lead to production of GLP1 or reduce glycemia., Conclusions: In studies of pancreatic islets from human beings and mice, we found that GIP induces production of IL6 by α cells, leading to islet production of GLP1 and insulin. This process is regulated by inflammation, via IL1B, and by sodium glucose transporter 2. In diabetic mice, increased islet levels of IL6 and IL1B might increase or reduce the production of GLP1 and affect glycemia., (Copyright © 2016 AGA Institute. Published by Elsevier Inc. All rights reserved.)
- Published
- 2016
- Full Text
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24. Adipose tissue adaptive response to trans-10,cis-12-conjugated linoleic acid engages alternatively activated M2 macrophages.
- Author
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Pini M, Touch S, Poirier H, Dalmas E, Niot I, Rouault C, Druart C, Delzenne N, Clément K, André S, and Guerre-Millo M
- Subjects
- Adaptation, Physiological, Adipose Tissue, White cytology, Animals, Cells, Cultured, Female, Macrophages immunology, Mice, Mice, Inbred C57BL, T-Lymphocytes drug effects, Adipose Tissue, White drug effects, Linoleic Acids, Conjugated pharmacology, Macrophage Activation, Macrophages drug effects
- Abstract
In mice, nutritional supplementation with the trans-10,cis-12 isomer of linoleic acid (t10,c12-CLA) promotes lipoatrophy, hyperinsulinemia, and macrophage infiltration in white adipose tissue (WAT). We explored the dynamics of these interrelated responses over 2 consecutive 7 d periods of t10,c12-CLA administration and withdrawal. t10,c12-CLA down-regulated lipogenic and lipolytic gene expression and increased collagen deposition, but with no evidence of cross-linking. An abundant CD45(+) cell infiltrate, comprising prominently CD206(+)CD11c(-) macrophages, was found in WAT in association with an anti-inflammatory gene signature. Infiltration of natural killer (NK) and dendritic cells contributed to WAT's innate immune response to t10,c12-CLA. Less abundant adaptive immune cells colonized WAT, including B, NK T, γδ T, and αβ T cells. By contrast, T-regulatory cell abundance was not affected. Interruption of treatment allowed recovery of WAT mass and normalization of insulinemia, coincident with regain of WAT homeostasis owing to a coordinated reversion of genic, structural, and immune deregulations. These data revealed a striking resilience of WAT after a short-term metabolic injury induced by t10,c12-CLA, which relies on alternatively activated M2 macrophage engagement. In addition, the temporal links between variations in WAT alterations and insulinemia upon t10,c12-CLA manipulation strengthen the view that WAT dysfunctional status is critically involved in altered glucose homeostasis., (© FASEB.)
- Published
- 2016
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25. The IL-1 Pathway in Type 2 Diabetes and Cardiovascular Complications.
- Author
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Herder C, Dalmas E, Böni-Schnetzler M, and Donath MY
- Subjects
- Animals, Humans, Insulin Resistance physiology, Obesity metabolism, Cardiovascular Diseases metabolism, Diabetes Mellitus, Type 2 metabolism, Interleukin-1 metabolism
- Abstract
Patients with type 2 diabetes (T2D) exhibit chronic activation of the innate immune system in pancreatic islets, in insulin-sensitive tissues, and at sites of diabetic complications. This results from a pathological response to overnutrition and physical inactivity seen in genetically predisposed individuals. Processes mediated by the proinflammatory cytokine interleukin-1 (IL-1) link obesity and dyslipidemia and have implicated IL-1β in T2D and related cardiovascular complications. Epidemiological, molecular, and animal studies have now assigned a central role for IL-1β in driving tissue inflammation during metabolic stress. Proof-of-concept clinical studies have validated IL-1β as a target to improve insulin production and action in patients with T2D. Large ongoing clinical trials will address the potential of IL-1 antagonism to prevent cardiovascular and other related complications., (Copyright © 2015 Elsevier Ltd. All rights reserved.)
- Published
- 2015
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26. Irf5 deficiency in macrophages promotes beneficial adipose tissue expansion and insulin sensitivity during obesity.
- Author
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Dalmas E, Toubal A, Alzaid F, Blazek K, Eames HL, Lebozec K, Pini M, Hainault I, Montastier E, Denis RG, Ancel P, Lacombe A, Ling Y, Allatif O, Cruciani-Guglielmacci C, André S, Viguerie N, Poitou C, Stich V, Torcivia A, Foufelle F, Luquet S, Aron-Wisnewsky J, Langin D, Clément K, Udalova IA, and Venteclef N
- Subjects
- Animals, Diet, High-Fat, Gene Expression Regulation, Humans, Inflammation drug therapy, Inflammation pathology, Insulin Resistance genetics, Macrophages, Mice, Obesity drug therapy, Obesity pathology, Transforming Growth Factor beta1 biosynthesis, Adipose Tissue, White metabolism, Inflammation genetics, Interferon Regulatory Factors genetics, Obesity genetics
- Abstract
Accumulation of visceral adipose tissue correlates with elevated inflammation and increased risk of metabolic diseases. However, little is known about the molecular mechanisms that control its pathological expansion. Transcription factor interferon regulatory factor 5 (IRF5) has been implicated in polarizing macrophages towards an inflammatory phenotype. Here we demonstrate that mice lacking Irf5, when placed on a high-fat diet, show no difference in the growth of their epididymal white adipose tissue (epiWAT) but they show expansion of their subcutaneous white adipose tissue, as compared to wild-type (WT) mice on the same diet. EpiWAT from Irf5-deficient mice is marked by accumulation of alternatively activated macrophages, higher collagen deposition that restricts adipocyte size, and enhanced insulin sensitivity compared to epiWAT from WT mice. In obese individuals, IRF5 expression is negatively associated with insulin sensitivity and collagen deposition in visceral adipose tissue. Genome-wide analysis of gene expression in adipose tissue macrophages highlights the transforming growth factor β1 (TGFB1) gene itself as a direct target of IRF5-mediated inhibition. This study uncovers a new function for IRF5 in controlling the relative mass of different adipose tissue depots and thus insulin sensitivity in obesity, and it suggests that inhibition of IRF5 may promote a healthy metabolic state during this condition.
- Published
- 2015
- Full Text
- View/download PDF
27. A role for interleukin-22 in the alleviation of metabolic syndrome.
- Author
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Dalmas E and Donath MY
- Subjects
- Animals, Humans, Insulin Secretion, Blood Glucose metabolism, Cytokines immunology, Diabetes Mellitus, Type 2 immunology, Endoplasmic Reticulum Stress immunology, Gene Expression Regulation immunology, Insulin metabolism, Insulin-Secreting Cells immunology
- Abstract
Increasing evidence points to a role for the immune system in the regulation of metabolism. Two new studies in mice indicate treatment with interleukin-22 restores mucosal immunity in diabetes and alleviates metabolic disease, resulting in improved glycemic control.
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- 2014
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28. T cell-derived IL-22 amplifies IL-1β-driven inflammation in human adipose tissue: relevance to obesity and type 2 diabetes.
- Author
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Dalmas E, Venteclef N, Caer C, Poitou C, Cremer I, Aron-Wisnewsky J, Lacroix-Desmazes S, Bayry J, Kaveri SV, Clément K, André S, and Guerre-Millo M
- Subjects
- Adipose Tissue pathology, Adult, Blotting, Western, Cell Line, Coculture Techniques, Diabetes Mellitus, Type 2 genetics, Female, Gene Amplification, Glycated Hemoglobin, Humans, Inflammation genetics, Male, Obesity genetics, Real-Time Polymerase Chain Reaction, T-Lymphocytes metabolism, Interleukin-22, Diabetes Mellitus, Type 2 metabolism, Inflammation pathology, Insulin Resistance genetics, Interleukin-1beta metabolism, Interleukins metabolism, Obesity metabolism
- Abstract
Proinflammatory cytokines are critically involved in the alteration of adipose tissue biology leading to deterioration of glucose homeostasis in obesity. Here we show a pronounced proinflammatory signature of adipose tissue macrophages in type 2 diabetic obese patients, mainly driven by increased NLRP3-dependent interleukin (IL)-1β production. IL-1β release increased with glycemic deterioration and decreased after gastric bypass surgery. A specific enrichment of IL-17- and IL-22-producing CD4(+) T cells was found in adipose tissue of type 2 diabetic obese patients. Coculture experiments identified the effect of macrophage-derived IL-1β to promote IL-22 and IL-17 production by human adipose tissue CD4(+) T cells. Reciprocally, adipose tissue macrophages express IL-17 and IL-22 receptors, making them sensitive to IL-17 and IL-22. IL-22 increased IL-1β release by inducing pro-IL-1β transcription through activation of C-Jun pathways in macrophages. In sum, these human data identified IL-1β and the T-cell cytokine IL-22 as key players of a paracrine inflammatory pathway previously unidentified in adipose tissue, with a pathological relevance to obesity-induced type 2 diabetes. These results provide an additional rationale for targeting IL-1β in obesity-linked type 2 diabetes and may have important implications for the conception of novel combined anti-IL-1β and anti-IL-22 immunotherapy in human obesity., (© 2014 by the American Diabetes Association.)
- Published
- 2014
- Full Text
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29. Intima-media thickness in severe obesity: links with BMI and metabolic status but not with systemic or adipose tissue inflammation.
- Author
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Dalmas E, Kahn JF, Giral P, Abdennour M, Bouillot JL, Fellahi S, Oppert JM, Clément K, Guerre-Millo M, and Poitou C
- Subjects
- Adult, Atherosclerosis etiology, Carotid Arteries diagnostic imaging, Carotid Intima-Media Thickness, Diabetes Mellitus, Type 2 complications, E-Selectin blood, Female, Humans, Inflammation complications, Male, Middle Aged, Obesity, Morbid complications, Risk, Adipose Tissue diagnostic imaging, Atherosclerosis diagnostic imaging, Body Mass Index, Obesity, Morbid diagnostic imaging
- Abstract
Objective: Obesity is associated with cardiovascular risk and a low-grade inflammatory state in both blood and adipose tissue (AT). Whether inflammation contributes to vascular alteration remains an open question. To test this hypothesis, we measured arterial intima-media thickness (IMT), which reflects subclinical atherosclerosis, in severely obese subjects and explored associations with systemic inflammation and AT inflammation., Research Design and Methods: IMT of the carotid artery (C-IMT) and IMT of the femoral artery (F-IMT) were measured in 132 nonobese (control) subjects (BMI 22.3 kg/m2; mean age 44.8 years) and 232 subjects who were severely obese without diabetes (OB/ND; n = 146; BMI 48.3 kg/m2; age 38.2 years) or severely obese with type 2 diabetes (OB/D; n = 86; BMI 47.0; age 49.4 years). In 57 OB/ND subjects, circulating soluble E-selectin, matrix metalloproteinase 9, myeloperoxidase, soluble intracellular adhesion molecule 1, soluble vascular cell adhesion molecule 1, tissue plasminogen activator inhibitor 1, cystatin C, cathepsin S, and soluble CD14 were measured in serum. AT macrophages were quantified by CD68 immunochemistry., Results: Both C-IMT and F-IMT increased in OB/ND and OB/D patients. In OB/ND patients, age was the sole independent determinant of IMT. No significant association was found with circulating inflammation-related molecules, number of CD68+ cells, or the presence of crown-like structures in visceral or subcutaneous AT of OB/ND patients., Conclusions: IMT increased with severe obesity but was not influenced by the degree of systemic inflammation or AT macrophage accumulation.
- Published
- 2013
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30. Variations in circulating inflammatory factors are related to changes in calorie and carbohydrate intakes early in the course of surgery-induced weight reduction.
- Author
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Dalmas E, Rouault C, Abdennour M, Rovere C, Rizkalla S, Bar-Hen A, Nahon JL, Bouillot JL, Guerre-Millo M, Clément K, and Poitou C
- Subjects
- Adult, Diabetes Mellitus, Type 2 immunology, Female, Gastric Bypass, Humans, Middle Aged, Obesity surgery, Cytokines blood, Dietary Carbohydrates administration & dosage, Energy Intake, Obesity immunology, Surgical Procedures, Operative, Weight Loss
- Abstract
Background: Obesity is considered a low-grade inflammatory state that improves with weight loss. In addition to acute-phase proteins, other cytokines might contribute to systemic inflammation., Objective: Our objective was to compare serum concentrations of a large panel of inflammation-related factors in obese and normal-weight subjects and to determine kinetic changes induced by caloric restriction., Design: The cohort comprised 14 normal-weight women and 51 obese women who were followed over 2 y after Roux-en-Y gastric bypass. Multiplexed proteomics were used to simultaneously assay 27 cytokines and growth factors in serum., Results: Concentrations of interleukin (IL)-9, IL-1-receptor antagonist, IL-10, interferon-γ-inducible protein 10, macrophage inflammatory protein 1β, monocyte chemoattractant protein 1, IL-8, RANTES (regulated upon activation, normal T cell expressed and secreted), monokine induced by interferon-γ, and vascular endothelial growth factor were found to be elevated in obesity. IL-10 was further elevated in diabetic obese patients, whereas eotaxin was found to be higher only in diabetic subjects. After surgery, many factors showed a biphasic pattern of variation, decreasing sharply at month 3 before rising back to presurgical values at month 6; these changes closely tracked similar kinetic changes in calorie and carbohydrate intake. After 1 y, an overall reduction in cytokines accompanied the reduction in body mass index and an amelioration in metabolic status., Conclusions: Obesity is associated with elevated circulating concentrations of a large panel of cytokines. Coordinated kinetic changes during weight loss suggest an early influence of calorie and carbohydrate intakes, whereas a longer-term reduction in corpulence might prevail in regulating circulating cytokine concentrations. This trial is registered at clincaltrials.gov as NCT00476658.
- Published
- 2011
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31. Krüppel-like factor 4 regulates macrophage polarization.
- Author
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Liao X, Sharma N, Kapadia F, Zhou G, Lu Y, Hong H, Paruchuri K, Mahabeleshwar GH, Dalmas E, Venteclef N, Flask CA, Kim J, Doreian BW, Lu KQ, Kaestner KH, Hamik A, Clément K, and Jain MK
- Subjects
- Adipose Tissue cytology, Adipose Tissue physiology, Animals, Cell Line, Escherichia coli immunology, Gene Expression, Humans, Insulin Resistance physiology, Kruppel-Like Factor 4, Kruppel-Like Transcription Factors genetics, Lipopolysaccharides pharmacology, Macrophage Activation drug effects, Macrophage Activation immunology, Macrophages drug effects, Mice, Mice, Knockout, NF-kappa B metabolism, Obesity physiopathology, STAT6 Transcription Factor genetics, STAT6 Transcription Factor metabolism, Wound Healing physiology, Cell Polarity, Kruppel-Like Transcription Factors metabolism, Macrophages cytology, Macrophages immunology
- Abstract
Current paradigms suggest that two macrophage subsets, termed M1 and M2, are involved in inflammation and host defense. While the distinct functions of M1 and M2 macrophages have been intensively studied - the former are considered proinflammatory and the latter antiinflammatory - the determinants of their speciation are incompletely understood. Here we report our studies that identify Krüppel-like factor 4 (KLF4) as a critical regulator of macrophage polarization. Macrophage KLF4 expression was robustly induced in M2 macrophages and strongly reduced in M1 macrophages, observations that were recapitulated in human inflammatory paradigms in vivo. Mechanistically, KLF4 was found to cooperate with Stat6 to induce an M2 genetic program and inhibit M1 targets via sequestration of coactivators required for NF-κB activation. KLF4-deficient macrophages demonstrated increased proinflammatory gene expression, enhanced bactericidal activity, and altered metabolism. Furthermore, mice bearing myeloid-specific deletion of KLF4 exhibited delayed wound healing and were predisposed to developing diet-induced obesity, glucose intolerance, and insulin resistance. Collectively, these data identify KLF4 as what we believe to be a novel regulator of macrophage polarization.
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- 2011
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32. Defining macrophage phenotype and function in adipose tissue.
- Author
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Dalmas E, Clément K, and Guerre-Millo M
- Subjects
- Adipose Tissue cytology, Animals, Cell Movement, Homeostasis, Humans, Macrophages cytology, Obesity immunology, Phenotype, Adipose Tissue immunology, Macrophages immunology
- Abstract
In obesity, chronic low-grade inflammation is thought to mediate the effects of increased adipose tissue mass on metabolic comorbidity. Of the different cell types that contribute to obesity-induced inflammation in adipose tissue, this review focuses on macrophages and their monocytes precursors. Mechanisms for monocyte recruitment to adipose tissue, and how both monocytes and macrophages are phenotypically modified in this environment in response to increasing fat mass, are considered. The versatile phenotype of adipose tissue macrophages might contribute not only to inflammatory and metabolic alterations, but could also help to maintain adipose tissue homeostasis in the setting of obesity., (Copyright © 2011 Elsevier Ltd. All rights reserved.)
- Published
- 2011
- Full Text
- View/download PDF
33. Comparative bench study of triggering, pressurization, and cycling between the home ventilator VPAP II and three ICU ventilators.
- Author
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Tassaux D, Strasser S, Fonseca S, Dalmas E, and Jolliet P
- Subjects
- Equipment Design, Humans, Technology Assessment, Biomedical, Home Care Services, Intensive Care Units, Positive-Pressure Respiration instrumentation, Ventilators, Mechanical standards
- Abstract
Objective: To compare triggering, pressurization, and cycling of the home ventilator VPAP II with those of three ICU ventilators (Evita 4, Galileo, and Servo 300)., Design and Setting: Two-compartment lung model study in a research laboratory, university hospital., Methods: One compartment was driven by an ICU ventilator to mimic "patient" inspiratory effort, while the other was connected to the tested ventilator. Pressure support of 10, 15, 20, and 25 cmH2O, and inspiratory efforts of 5, 10, 15, 20, and 25 cmH2O (inspiratory time 1 s) were used in normal, obstructive, and restrictive conditions. Triggering delay (Td), triggering workload, pressurization at 300 and 500 ms, and difference between the "patient's" inspiratory time and that of the ventilator were analyzed., Results: No difference was noted in triggering workload between VPAP II, Evita 4, and Galileo while Servo 300 had a lower value. Pressurization at 300 ms on Evita 4 and Servo 300 reached 75% of the ideal value, on Galileo 35%, and on VPAP II 45%. Pressurization at 500 ms on Evita 4 and Servo 300 reached 85% of the ideal value, on Galileo 50%, and on VPAP II 55%. Cycling was delayed in obstructive conditions and premature in restrictive conditions with each of the devices., Conclusions: The VPAP II performed as well as one ICU ventilator and less well than two. Home devices for noninvasive ventilation in acute respiratory failure outside the ICU could prove attractive as they are smaller, less costly, and easier to use than ICU machines.
- Published
- 2002
- Full Text
- View/download PDF
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