Adipose tissue macrophages and their polarization in health and obesity

Catrysse, Leen; Loo, Geert

doi:10.1016/j.cellimm.2018.03.001

Cited by 78 publications

(81 citation statements)

References 57 publications

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“…Upon exceeding its expansion capacity by an enlargement in the size of adipocytes (hypertrophy), an increase in the number of adipocytes (hyperplasia) or both, WAT becomes dysfunctional and promotes the recruitment of immune cells, which ultimately leads to a low‐grade inflammatory state . Self‐sustained lipolysis orchestrates the accumulation of monocyte‐derived macrophages in the obese WAT, where they polarize or switch from an M2 anti‐inflammatory phenotype toward an M1 pro‐inflammatory phenotype . Such a pathological WAT remodeling particularly occurs with long‐lasting ingestion of Westernized, high‐fat diets (HFDs) rich in saturated fatty acids (SFAs) in both humans and murine models .…”

Section: Introductionmentioning

confidence: 99%

“…[8,9] Self-sustained lipolysis orchestrates the accumulation of monocytederived macrophages in the obese WAT, [10] where they polarize or switch from an M2 anti-inflammatory phenotype toward an M1 proinflammatory phenotype. [11][12][13] Such a pathological WAT remodeling particularly occurs with long-lasting ingestion of Westernized, high-fat diets (HFDs) rich in saturated fatty acids (SFAs) in both humans and murine models. [14][15][16][17] Conversely, a growing body of evidence points the benefits from replacing dietary SFAs with monounsaturated fatty acids (MUFAs) or omega-3 polyunsaturated fatty acids (PUFAs) on blood lipid and WAT homeostasis.…”

Section: Introductionmentioning

confidence: 99%

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Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Paz

Naranjo

López

et al. 2019

Molecular Nutrition Food Res

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Scope Obesity is a principal causative factor of metabolic syndrome. Niacin potently regulates lipid metabolism. Replacement of saturated fatty acids by MUFAs or inclusion of omega‐3 long‐chain PUFAs in the diet improves plasma lipid levels. However, the potential benefits of niacin in combination with MUFAs or omega‐3 long‐chain PUFAs against white adipose tissue (WAT) dysfunction in the high fat diet (HFD)‐induced metabolic syndrome are unknown. Methods and results Male Lepob/obLDLR−/− mice are fed a chow diet or HFDs based on milk cream (21% kcal), olive oil (21% kcal), or olive oil (20% kcal) plus 1% kcal from eicosapentaenoic and docosahexaenoic acids, including immediate‐release niacin (1% w/v) in drinking water, for 8 weeks. Mice are then phenotyped. Dietary MUFAs are identified as positive regulators of adipose NAD+ signaling pathways by triggering NAD+ biosynthesis via the salvage pathway. This coexists with overexpression of genes involved in recognition of NAD+ and fatty acids, a surrounding lipid environment dominated by exogenous oleic acid and an alternatively activated macrophage profile, which culminate in a healthy expansion of WAT and improvement of several hallmarks that typify the metabolic syndrome. Conclusion Niacin in combination with dietary MUFAs can favor WAT homeostasis in the development of HFD‐induced obesity and metabolic syndrome.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Paz

Naranjo

López

et al. 2019

Molecular Nutrition Food Res

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“…The aim of this study was to determine the proportion of CD204+ macrophages within the entire population of macrophages in the adipose tissue of obese patients in relation to T2D. Immunohistochemical staining for CD68 is an accepted pan-macrophages marker, while CD204 serves as a useful marker differentiation associated with the M2 subtype of macrophages 1,2 . Most recent studies describe more complex forms of macrophage activation than the previous M1/M2 model.…”

Section: Discussionmentioning

confidence: 99%

“…18 ), we can conclude that both CD68+ and CD204+ macrophages evaluated in our specimens are so called a resident macrophage type 17 . In obesity, these cells proliferate and additionally, meta bolic signals (such as high insulin, free acids, high glucose, oxidized low-density lipoprotein, oxidized phospholipids) can change the phenotype of these macrophages and they can become metabolically activate 1,18 .…”

Section: Discussionmentioning

confidence: 99%

Macrophages of the subcutaneous and omental fatty tissue in obese patients: Immunohistochemical phenotyping of M2 subtypes in relation to type 2 diabetes

Chylíková¹,

Dvořáčková²,

Čížková³

et al. 2020

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background and Aims. Macrophages are linked to the initiation of the chronic inflammation believed to underlie the changes taking place in the white fatty tissue of obese people. Both the number of macrophages, but their functional status, play an important role in the development of inflammation. Classically, macrophages are divided into two types: pro-inflammatory (M1) and anti-inflammatory (M2) types, and based on current immunological studies, further views on the functional distribution of macrophages are suggested. In this study, we evaluated the M1 and M2 macrophages ratio in obese subjects with, or without diabetes. To identify all macrophages, we used CD68 expression, while CD204 expression is typically used for the M2 macrophage. Materials and Methods. During bariatric surgery, carried out in obese people with and without type 2 diabetes (T2D), we obtained subcutaneous adipose tissue from the navel and omental adipose tissue. We also obtained the same tissue from people with a physiological range of BMI from a judicial autopsy. Applying immunohistochemical staining anti-CD68 and anti-CD204, we carried out a quantitative evaluation of the number of macrophages. Results. We found CD68+ and CD204+ positive macrophages in perivascular spaces and between fat cells, both isolated and in larger infiltrates. They were also present in so-called "crown-like structures" (CLS) around dying adipocytes. Quantitative analysis showed an increased number of macrophages in all obese patients compared to the control group of non-obese, individuals without T2D. The most striking observation was the macrophage increase in the visceral fatty tissue of diabetics. The number of CD68 and CD204 positive macrophages was statistically significantly smaller in patients without T2D. Conclusion. We demonstrated a significantly greater number of macrophages in visceral adipose tissue, especially in patients with T2D. Our results also show a positive correlation between the presence of T2D and the total number of macrophages; a significantly greater number of macrophages were found in visceral adipose tissue, especially in patients with T2D.

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“…Macrophages also mediate lipogenesis and adipogenesis in adipose tissue (Appari et al, ; Catrysse and van Loo, ). Excessive energy intake will be absorbed and stored in differentiated adipocytes to maintain the energy balance in the body and for occasional emergency use (Greenberg et al, ; Vegiopoulos et al, ).…”

Section: Discussionmentioning

confidence: 99%

β‐Cypermethrin Alleviated the Inhibitory Effect of Medium from RAW 264.7 Cells on 3T3‐L1 Cell Maturation into Adipocytes

Wang

Jin

et al. 2020

Lipids

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Studies have elucidated that pyrethroids induce adipogenesis. It is also known that macrophages can affect the homeostasis of adipose tissue. However, whether and how the β-cypermethrin (β-CYP)-mediated inhibition of the macrophages affects adipogenesis remain unknown. To explore the effects of β-CYP on adipogenesis through modulating the function of macrophages, 3T3-L1 cells, a preadipocyte cell line, were exposed to culture medium from either RAW 264.7 cells, a macrophage cell line (RM), or β-CYP-treated RAW 264.7 cells (CRM). CRM decreased the inhibitory effects of RM treatment on cell proliferation and adipogenesis, as lipid accumulation, the CEBPA content, and Fasn and Acaca expression in 3T3-L1 cells were higher following CRM treatment than following RM treatment through the higher levels of the demethylated CEBPA promoter in 3T3-L1 cells. However, the medium from β-CYPand Nacetyl-L-cysteine-cotreated RAW 264.7 cells (CNRM) partially restored the inhibitory effects of RAW 264.7 cells on 3T3-L1 cells that had been reduced by CRM, indicating that β-CYP might reduce the cytotoxicity and inhibitory effects of RAW 264.7 cells on the adipogenesis of 3T3-L1 cells through elevating ROS levels in RAW 264.7 cells. Moreover, exposure to β-CYP downregulated the TNF-α secretion in RAW 264.7 cells. In conclusion, these data demonstrated that β-CYP affected the function of RAW 264.7 cells, alleviating their inhibitory effects on adipogenesis and CEBPA demethylation in 3T3-L1 cells. β-CYP might achieve these effects through downregulating the secretion of TNF-α via elevating ROS levels in RAW 264.7 cells. Our experiments provide a new perspective on the obesogenic effect of pyrethroids.

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Adipose tissue macrophages and their polarization in health and obesity

Cited by 78 publications

References 57 publications

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Monounsaturated Fatty Acids in a High‐Fat Diet and Niacin Protect from White Fat Dysfunction in the Metabolic Syndrome

Macrophages of the subcutaneous and omental fatty tissue in obese patients: Immunohistochemical phenotyping of M2 subtypes in relation to type 2 diabetes

β‐Cypermethrin Alleviated the Inhibitory Effect of Medium from RAW 264.7 Cells on 3T3‐L1 Cell Maturation into Adipocytes

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