Abdominal adipocyte populations in women with visceral obesity

Visceral obesity is independently related to numerous cardiometabolic alterations, with adipose tissue dysfunction as a central feature. Objective: To examine whether omental (OM) and subcutaneous (SC) adipocyte size populations in women relate to visceral obesity, cardiometabolic risk factors and adipocyte lipolysis independent of total adiposity. Design and Methods: OM and SC fat samples were obtained during gynecological surgery in 60 women [mean age: 46.1±5.9 years; mean BMI: 27.1±4.5 kg/m2 (range: 20.3-41.1 kg/m2)]. Fresh samples were treated with osmium tetroxide and were analyzed with a Multisizer Coulter. Cell size distributions were computed for each sample with exponential and Gaussian function fits. Results: Computed tomography-measured visceral fat accumulation was the best predictor of larger cell populations as well as the percentage of small cells in both OM and SC fat (p<0.0000 for all). Accordingly, women with visceral obesity had larger cells in the main population and higher proportion of small adipocytes independent of total adiposity (p≤0.05). Using linear regression analysis, we found that women characterized by larger-than-predicted adipocytes in either OM or SC adipose tissue presented higher visceral adipose tissue area, increased percentage of small cells and HOMAir index as well as higher OM adipocyte isoproterenol-, forskolin- and dibutyryl cAMP- stimulated lipolysis compared to women with smaller-than predicted adipocytes, independent of total adiposity (p≤0.05). Conclusion: Excess visceral adipose tissue accumulation is a strong marker of both adipocyte hypertrophy and increased number of small cells in either fat compartment, which relates to higher insulin resistance index and lipolytic response, independent of total adiposity

Vapor phase mediated cellular uptake of sub 5 nm nanoparticles

Nanoparticles became an important and wide-used tool for cell imaging because of their unique optical properties. Although the potential of nanoparticles (NPs) in biology is promising, a number of questions concerning the safety of nanomaterials and the risk/benefit ratio of their usage are open. Here, we have shown that nanoparticles produced from silicon carbide (NPs) dispersed in colloidal suspensions are able to penetrate into surrounding air environment during the natural evaporation of the colloids and label biological cells via vapor phase. Natural gradual size-tuning of NPs in dependence to the distance from the NP liquid source allows progressive shift of the fluorescence color of labeled cells in the blue region according to the increase of the distance from the NP suspension. This effect may be used for the soft vapor labeling of biological cells with the possibility of controlling the color of fluorescence. However, scientists dealing with the colloidal NPs have to seriously consider such a NP's natural transfer in order to protect their own health as well as to avoid any contamination of the control samples

Impact of Carbon Fluoroxide Nanoparticles on Cell Proliferation

Cytotoxicity of fluorescent carbon fluoroxide (CFO) nanoparticles (NPs) was studied in a label-free manner on several cancer and non-cancer cell lines. A direct cytotoxic effect of the CFO NPs was clearly observed by a suppression of cell proliferation. The real-time measurement of cell activities allowed to quantify the impact of the uptaken NPs on cell proliferation and after washout of the NPs from the cell culture medium. The results show more toxic effects of the CFO NPs on cancer than on non-cancer cell lines. The notion of NPs biocompatibility must be related to a maximum concentration value of the NPs acceptable for a given cell type. Furthermore, the cytotoxicity effects of NPs should be studied not only during their direct exposure to cells but also after their washout from the culture medium

Insulin prevents fatty acid induced increase of adipocyte size

International audienceMetabolic disorders related to obesity are largely dependent on adipose tissue hypertrophy, which involves adipocyte hypertrophy and increased adipogenesis. Adiposize is regulated by lipid accumulation as a result of increased lipogenesis (mainly lipid uptake in mature adipocytes) and reduced lipolysis. Using realtime 2D cell culture analyses of lipid uptake, we show (1) that high glucose concentration (4.5 g/L) was required to accumulate oleic acid increasing lipid droplet size until unilocularization similar to mature adipocytes in few days, (2) oleic acid reduced Peroxisome-Proliferator Activated Receptor Gamma (PPARG) gene transcription and (3) insulin counteracted oleic acid-induced increase of lipid droplet size. Although the lipolytic activity observed in high versus low glucose (1 g/L) conditions was not altered, insulin was found to inhibit oleic acid induced gene transcription required for lipid storage such as Cell Death Inducing DFFA Like Effectors (CIDEC) and G0S2 (G0 switch gene S2), possibly through PPARA activity. Although this signalling pathway requires more detailed investigation, the results point out the differential mechanisms involved in the pro-adipogenic effect of insulin in absence versus its protective effect on adiposity in presence of oleic acid uptake

FABP4 Controls Fat Mass Expandability (Adipocyte Size and Number) through Inhibition of CD36/SR-B2 Signalling

Adipose tissue hypertrophy during obesity plays pleiotropic effects on health. Adipose tissue expandability depends on adipocyte size and number. In mature adipocytes, lipid accumulation as triglycerides into droplets is imbalanced by lipid uptake and lipolysis. In previous studies, we showed that adipogenesis induced by oleic acid is signed by size increase and reduction of FAT/CD36 (SR-B2) activity. The present study aims to decipher the mechanisms involved in fat mass regulation by fatty acid/FAT-CD36 signalling. Human adipose stem cells, 3T3-L1, and its 3T3-MBX subclone cell lines were used in 2D cell cultures or co-cultures to monitor in real-time experiments proliferation, differentiation, lipolysis, and/or lipid uptake and activation of FAT/CD36 signalling pathways regulated by oleic acid, during adipogenesis and/or regulation of adipocyte size. Both FABP4 uptake and its induction by fatty acid-mediated FAT/CD36-PPARG gene transcription induce accumulation of intracellular FABP4, which in turn reduces FAT/CD36, and consequently exerts a negative feedback loop on FAT/CD36 signalling in both adipocytes and their progenitors. Both adipocyte size and recruitment of new adipocytes are under the control of FABP4 stores. This study suggests that FABP4 controls fat mass homeostasis

Hysteresis of White Adipose Tissue

International audienceObjective: This study was performed to analyze the modifications within adipose tissue during calorie restriction and more specifically to state whether hysteresis occurs during fat mass reduction. Method: Rats male Wistar increased their body weight by 130 g under control conditions and were then submitted to a calorie restriction (CR) at 30% or 60% of control. Experiment has been stopped when the body weight of the group CR60% returned back to its initial value. Samples of retroperitoneal adipose tissue were collected by biopsies along the study. Adipose cell size was analyzed using multisizer IV (Beckman Coulter) to determine the size distribution curves during natural growth and after calorie restriction. Results: After CR60%, body weights and adipose tissue masses were similar to the ones at the beginning of the experiment. Adipose cell size distribution curve was shifted to the left compared to the one of initial control. Adipose cell sizes were significantly lower after CR60% than those of control at the beginning of the experiment. Conclusions: These results state for the first time that hysteresis occurs in white adipose tissue after calorie restriction. The composition of adipose tissue after calorie restriction was significantly different than the one of initial control. After significant weight loss, organisms must be considered as different from the initial controls, they are most likely governed by different regulations which will have to be identified

Pro-inflammatory cytokines and cell interactions between pbmc and synoviocytes induce retraction and formation of pseudopodia

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