Dietary intervention-induced weight loss decreases macrophage content in adipose tissue of obese women

Kováčiková, Michaela; Sengenès, Coralie; Kováčová, Zuzana; Šiklová, Michaela; Klimčáková, Eva; Polàk, Jan; Rossmeislová, Lenka; Bajzova, Magda; Hejnova, J.; Hnevkovska, Zuzana; Bouloumié, Anne; Langin, Dominique; Štich, Vladimír

doi:10.1038/ijo.2010.112

Cited by 63 publications

(53 citation statements)

References 54 publications

(73 reference statements)

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“…Although this molecule can cause inflammation, inducing macrophages to secrete TNF-α and IL-6, thereby promoting insulin resistance, it also induces the production and activity of chemoattractant proteins such as monocyte chemotactic protein 1 (MCP-1), which promotes innate cellular immune responses and translocation in response to stimuli, such as HFD-induced adipose tissue hypertrophy and liver steatosis [39,40]. It is important to halt the production of inflammatory molecules, which are promoters of insulin resistance, so that macrophage infiltration is prevented, and any macrophages already infiltrating do not receive stimuli to remain infiltrated, as occurs with some drugs or with weight loss [41][42][43][44].…”

Section: Discussionmentioning

confidence: 99%

Modulation of gut microbiota by antibiotics improves insulin signalling in high-fat fed mice

et al. 2012

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Aims/hypothesis A high-fat dietary intake induces obesity and subclinical inflammation, which play important roles in insulin resistance. Recent studies have suggested that increased concentrations of circulating lipopolysaccharide (LPS), promoted by changes in intestinal permeability, may have a pivotal role in insulin resistance. Thus, we investigated the effect of gut microbiota modulation on insulin resistance and macrophage infiltration. Methods Swiss mice were submitted to a high-fat diet with antibiotics or pair-feeding for 8 weeks. Metagenome analyses were performed on DNA samples from mouse faeces. Blood was collected to determine levels of glucose, insulin, LPS, cytokines and acetate. Liver, muscle and adipose tissue proteins were analysed by western blotting. In addition, liver and adipose tissue were analysed, blinded, using histology and immunohistochemistry. Results Antibiotic treatment greatly modified the gut microbiota, reducing levels of Bacteroidetes and Firmicutes, overall bacterial count and circulating LPS levels. This modulation reduced levels of fasting glucose, insulin, TNF-α and IL-6; reduced activation of toll-like receptor 4 (TLR4), c-Jun N-terminal kinase (JNK), inhibitor of κ light polypeptide gene enhancer in B cells, kinase β (IKKβ) and phosphorylated IRS-1 Ser307; and consequently improved glucose tolerance and insulin tolerance and action in metabolically active tissues. In addition, there was an increase in portal levels of circulating acetate, which probably contributed to an increase in 5′-AMP-activated protein kinase (AMPK) phosphorylation in mice. We observed a striking reduction in crown-like structures (CLS) and F4/80 + macrophage cells in the adipose tissue of antibiotic-treated mice. Conclusions/interpretation These results suggest that modulation of gut microbiota in obesity can improve insulin signalling and glucose tolerance by reducing circulating LPS levels and inflammatory signalling. Modulation also appears to increase levels of circulating acetate, which activates AMPK and finally leads to reduced macrophage infiltration.

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Section: Discussionmentioning

confidence: 99%

Modulation of gut microbiota by antibiotics improves insulin signalling in high-fat fed mice

et al. 2012

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“…In addition, because various subpopulations of macrophages may exist and express distinct surface markers depending on the local microenvironment, different ATM markers could be identified in different macrophage subpopulations of adipose tissue. Several macrophage subpopulations have indeed been identified in human adipose tissue [23,27,35,36]. Studies investigating mRNA variations of specific macrophage subpopulations in different adipose tissue locations and/or in different groups of individuals are currently not available due to technical limitations.…”

Section: Discussionmentioning

confidence: 99%

Macrophage gene expression is related to obesity and the metabolic syndrome in human subcutaneous fat as well as in visceral fat

et al. 2011

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Aims/hypothesis Our goal was to identify a set of human adipose tissue macrophage (ATM)-specific markers and investigate whether their gene expression in subcutaneous adipose tissue (SAT) as well as in visceral adipose tissue (VAT) is related to obesity and to the occurrence of the metabolic syndrome. Methods ATM-specific markers were identified by DNA microarray analysis of adipose tissue cell types isolated from SAT of lean and obese individuals. We then analysed gene expression of these markers by reverse transcription quantitative PCR in paired samples of SAT and VAT from 53 women stratified into four groups (lean, overweight, obese and obese with the metabolic syndrome). Anthropometric measurements, euglycaemic-hyperinsulinaemic clamp, blood analysis and computed tomography scans were performed. Results A panel of 24 genes was selected as ATM-specific markers based on overexpression in ATM compared with other adipose tissue cell types. In SAT and VAT, gene expression of ATM markers was lowest in lean and highest in the metabolic syndrome group. mRNA levels in the two fat depots were negatively correlated with glucose disposal rate and positively associated with indices of adiposity and the metabolic syndrome. Conclusions/interpretation In humans, expression of ATMspecific genes increases with the degree of adiposity and correlates with markers of insulin resistance and the metabolic syndrome to a similar degree in SAT and in VAT.

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“…Conversely, caloric restriction attenuates WAT inflammation and improves glycemic status in obese humans and mice after prolonged periods of weight reduction or stabilization (10)(11)(12)(13)(14). These observations enlighten WAT plasticity in response to long-term modifications of energy balance and its close link with coordinated changes in metabolic status.…”

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confidence: 81%

Adipose tissue adaptive response totrans‐10,cis‐12‐conjugated linoleic acid engages alternatively activated M2 macrophages

et al. 2015

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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 2 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, gd T, and ab 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.-Pini, M., Touch, S., Poirier, H., Dalmas, E., Niot, I., Rouault, C., Druart, C., Delzenne, N., Clément, K., André, S., Guerre-Millo, M. Adipose tissue adaptive response to trans-10,cis-12-conjugated linoleic acid engages alternatively activated M2 macrophages. It is broadly agreed that accumulation of proinflammatory macrophages is a key component of white adipose tissue (WAT) response to nutrient overload in obesity. Through the release of an array of proinflammatory chemokines and cytokines, macrophages are thought to perpetuate and propagate inflammation in WAT, leading eventually to a chronic pathologic state. Although opposite in terms of excess vs. deficiency of fat mass, obesity and lipodystrophy share common WAT alterations, including inflammation and macrophage infiltration, as shown in several lipodystrophic mouse models (1-3) and in patients with HIV-associated lipodystrophy (4-6). Enhanced extracellular matrix (ECM) deposition and fibrosis are additional signatures of WAT pathology in both conditions (4,7,8). These local alterations are accompanied by systemic inflammation and insulin resistance, the most prevalent outcomes of WAT dysfunction common to obesity and lipodystrophy (9).The time frame necessary for WAT macrophage accumulation and insulin resistance to occur is usually long, ranging from months in mice fed a high-fat diet to years in obese humans. Conversely, caloric restriction attenuates WAT inflammation and improves glycemic status in obese humans and mice after prolonged periods of weight reducti...

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Dietary intervention-induced weight loss decreases macrophage content in adipose tissue of obese women

Cited by 63 publications

References 54 publications

Modulation of gut microbiota by antibiotics improves insulin signalling in high-fat fed mice

Modulation of gut microbiota by antibiotics improves insulin signalling in high-fat fed mice

Macrophage gene expression is related to obesity and the metabolic syndrome in human subcutaneous fat as well as in visceral fat

Adipose tissue adaptive response totrans‐10,cis‐12‐conjugated linoleic acid engages alternatively activated M2 macrophages

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