Odorous emissions of synthetic turf and its relationship with local communities.

Synthetic turf has been a mainstay of field sports and local communities for decades, and in that time, has faced both community and government pressure to ensure its safety and fitness for purpose. Considerable research and regulations have been applied to synthetic turf with regards to its safety, construction, potential toxicity, sports impact, as well as environmental considerations. However, very little attention has been paid to reports of odorous impacts from synthetic turf fields. This is problematic as odours are both a source of most complaints by communities towards other industries, as well as the fact that synthetic turf has a unique placement within communities themselves. It is wholly possible that the concerns surrounding synthetic turf are being modulated by the odours that the fields themselves produce through previously identified psychological mechanisms. As a result, ensuring good standards for synthetic turf with regards to odorous emissions should be benchmarked for community acceptability. This review investigates prior research into synthetic turf with regards to identified volatile organic compounds emitted, as well as proposing the means by which community stakeholders engage with synthetic turf, as well as how they should be consulted. From here, this review provides trajectories for future research within this space, and how regulatory bodies should address potential issues. This research space is currently in its infancy and therefore information relating to synthetic turf odour factors must be carefully considered.

Capsular inflammation after immediate breast reconstruction - Gene expression patterns and inflammatory cell infiltration in irradiated and non-irradiated breasts.

BACKGROUND: Capsular contracture following post-mastectomy radiotherapy (PMRT) is commonly seen in patients undergoing implant-based immediate breast reconstruction (IBR). Further understanding of the underlying biology is needed for the development of preventive or therapeutic strategies. Therefore, we conducted a comparative study of gene expression patterns in capsular tissue from breast cancer patients who had received versus those who had not received PMRT after implant-based IBR. METHODS: Biopsies from irradiated and healthy non-irradiated capsular tissue were harvested during implant exchange following IBR. Biopsies from irradiated (n = 13) and non-irradiated (n = 12) capsules were compared using Affymetrix microarrays to identify the most differentially regulated genes. Further analysis using immunohistochemistry was performed in a subset of materials to compare the presence of T cells, B cells, and macrophages. RESULTS: Enrichment testing using Gene Ontology (GO) analysis revealed that the 227 most differentially expressed genes were mainly involved in an inflammatory response. Twenty-one GO biological processes were identified [p < 0.05, false discovery rate (FDR) < 5%], several with B-cell-associated inflammation. Cell-type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT) analysis identified macrophages as the most common inflammatory cell type in both groups, further supported by immunostaining of CD68. Radiation remarkably increased B-cell infiltration in the capsular region of biopsies, as quantified by immunostaining of CD20 (p = 0.016). CONCLUSIONS: Transcript analysis and immunohistochemistry revealed inflammatory responses in capsular biopsies regardless of radiotherapy. However, the radiation response specifically involved B-cell-associated inflammatory responses.

The evolution of multicellular complexity: the role of relatedness and environmental constraints.

A major challenge in evolutionary biology has been to explain the variation in multicellularity across the many independently evolved multicellular lineages, from slime moulds to vertebrates. Social evolution theory has highlighted the key role of relatedness in determining multicellular complexity and obligateness; however, there is a need to extend this to a broader perspective incorporating the role of the environment. In this paper, we formally test Bonner's 1998 hypothesis that the environment is crucial in determining the course of multicellular evolution, with aggregative multicellularity evolving more frequently on land and clonal multicellularity more frequently in water. Using a combination of scaling theory and phylogenetic comparative analyses, we describe multicellular organizational complexity across 139 species spanning 14 independent transitions to multicellularity and investigate the role of the environment in determining multicellular group formation and in imposing constraints on multicellular evolution. Our results, showing that the physical environment has impacted the way in which multicellular groups form, highlight that environmental conditions might have affected the major evolutionary transition to obligate multicellularity.

Multicellular group formation in Saccharomyces cerevisiae.

Understanding how and why cells cooperate to form multicellular organisms is a central aim of evolutionary biology. Multicellular groups can form through clonal development (where daughter cells stick to mother cells after division) or by aggregation (where cells aggregate to form groups). These different ways of forming groups directly affect relatedness between individual cells, which in turn can influence the degree of cooperation and conflict within the multicellular group. It is hard to study the evolution of multicellularity by focusing only on obligately multicellular organisms, like complex animals and plants, because the factors that favour multicellular cooperation cannot be disentangled, as cells cannot survive and reproduce independently. We support the use of Saccharomyces cerevisiae as an ideal model for studying the very first stages of the evolution of multicellularity. This is because it can form multicellular groups both clonally and through aggregation and uses a family of proteins called 'flocculins' that determine the way in which groups form, making it particularly amenable to laboratory experiments. We briefly review current knowledge about multicellularity in S. cerevisiae and then propose a framework for making predictions about the evolution of multicellular phenotypes in yeast based on social evolution theory. We finish by explaining how S. cerevisiae is a particularly useful experimental model for the analysis of open questions concerning multicellularity.

Importance of 2,4,6-Trichloroanisole (TCA) as an odorant in the emissions from anaerobically stabilized dewatered biosolids.

Odours from stabilized biosolids after anaerobic digestion of wastewater sludge can cause local community impact. Apart from the well-known odorants such as sulfur compounds, contributions from other volatile organic compounds (VOCs) to nuisance odours is limited. The presence of compounds with low odour detection thresholds (ODTs) at low concentrations, can present challenges for analytical identification. Thirty-six biosolids samples were taken after anaerobic stabilisation and dewatering at a wastewater treatment plant, Sydney, Australia. Biosolid cake samples were stored outside in loosely covered trays under aerobic conditions, however without interactions with soil microorganisms as it would be in reality. All biosolids cake samples were analysed over a period of 35 days. Emissions were collected onto Tenax TA sorbent tubes using a U.S. EPA flux hood method at storage days 1, 3, 7, 10, 14, 21 and 35. Gas chromatography (GC) coupled with mass spectrometer detector (MSD) and an olfactory detection port (ODP) was used to identify a musty/moldy/earthy type odorant in the biosolids emissions as 2,4,6-trichloroanisole (TCA). Measured odour intensities, classified on a scale from 1 to 4, and odour characters were specified by three ODP assessors. TCA was identified in all biosolid cake emissions. The measured odour intensities of the TCA did not significantly alter as the biosolids were aged, however varied between biosolids cakes. Due to its odour intensity, 85% frequency of detection and its low ODT, which is orders of magnitudes lower than sulfur compounds, TCA should be considered as a potential odorant of concern in biosolids emissions.

Emissions of volatile sulfur compounds (VSCs) throughout wastewater biosolids processing.

Volatile sulfur compounds (VSCs) are important contributors to nuisance odours from the processing of wastewater sludge and biosolids. However, emission characteristics are difficult to predict as they vary between sites and are likely to be affected by biosolids processing configuration and operation. VSC emissions from biosolids throughout 6 wastewater treatment plants (WWTPs) in Sydney, Australia were examined in this study. H2S was the VSC found at the highest concentrations throughout the WWTPs, with concentrations ranging from 7 to 39,000µg/m3. Based on odour activity values (OAVs), H2S was typically also the most dominant odorant. However, methyl mercaptan (MeSH) was also found to be sensorially important in the biosolids storage areas given its low odour detection threshold (ODT). High concentrations of VOSCs such as MeSH in the storage areas were shown to potentially interfere with H2S measurements using the Jerome 631-X H2S sensor and these interferences should be investigated in more detail. The VSC composition of emissions varied throughout biosolids processing as well as between the different WWTPs. The primary sludge and biosolids after dewatering and during storage, were key stages producing nuisance odours as judged by the determination of OAVs. Cluster analysis was used to group sampling locations according to VSC emissions. These groups were typically the dewatered and stored biosolids, primary and thickened primary sludge, and waste activated sludge (WAS), thickened WAS, digested sludge and centrate. Effects of biosolids composition and process operation on VSC emissions were evaluated using best subset regression. Emissions from the primary sludge were dominated by H2S and appeared to be affected by the presence of organic matter, pH and Fe content. While volatile organic sulfur compounds (VOSCs) emitted from the produced biosolids were shown to be correlated with upstream factors such as Fe and Al salt dosing, anaerobic digestion and dewatering parameters.

Unrepresented community odour impact: Improving engagement strategies.

Complaints for odour causing industry continue to increase in numeracy and severity. One assessment approach using Gas Chromatography-Mass Spectrometry/Olfactometry (GC-MS/O), has been used primarily to identify priority odourants within a standardised panel. We investigated the variation of response between participants of average and high olfactory sensitivity, and discovered that current GC-MS/O methodologies do not represent the entirety of community odour impact. Based on these results we constructed a Biosolids Processing Odour Wheel followed by a Community Odour Wheel for use by untrained community members and site operators. By using the information gathered from this research, as well as odour testing workshops for a wastewater treatment plant's staff and community surrounding the facility, we established a communicative system, which was subsequently incorporated into an online dynamic odour observation platform. This platform provides the WWTP with meaningful information from the community, as well as a common language for which to discuss environmental malodour with all stakeholders.

Distribution and sensorial relevance of volatile organic compounds emitted throughout wastewater biosolids processing.

A diverse range of volatile organic compounds (VOCs) are emitted from wastewater biosolids processing. Odorous emissions are predominately made up of volatile sulfur compounds (VSCs) which are typically the only odorants measured. However, a range of VOCs are known to contribute to malodours yet previous studies often overlook the contribution of VOCs in comparison with VSCs. This study aims to evaluate how emissions are affected by different biosolids processing configurations, and if any non-sulfur VOCs should be included in odour measurement and management. Non-sulfur VOCs emitted from biosolids throughout six wastewater treatment plants in the Sydney, Australia region were measured at six locations on average twice each week over 2-3weeks at each site. Variations in types of VOCs emitted throughout and between the sites were assigned to differences in WWTP processing configurations, plant operation and variations in industrial and municipal flows to the sewer network, referred to as sewer catchments. The presence of VOCs is likely due to biotic generation as well as industrial or residential additions to the sewer network. The dewatered and stored biosolids samples had the highest levels of VOC emissions. Sensorially important odorants were p-cresol and butanoic acid, based on the frequency of detection and odour activity values. Other compounds with a high risk of nuisance impacts were trimethylamine, indole and phenol emitted from the dewatered and stored biosolids, and volatile fatty acids from the anaerobic digester inlet and outlet at one particular site. The findings show that non-sulfur VOCs should be added to odorant monitoring campaigns at WWTPs. Identification of VOCs as sensorially important odorants opens opportunities for the more efficient management of nuisance odours, through targeted odour control or process improvement.

Sulfur flows and biosolids processing: Using Material Flux Analysis (MFA) principles at wastewater treatment plants.

High flows of sulfur through wastewater treatment plants (WWTPs) may cause noxious gaseous emissions, corrosion of infrastructure, inhibit wastewater microbial communities, or contribute to acid rain if the biosolids or biogas is combusted. Yet, sulfur is an important agricultural nutrient and the direct application of biosolids to soils enables its beneficial re-use. Flows of sulfur throughout the biosolids processing of six WWTPs were investigated to identify how they were affected by biosolids processing configurations. The process of tracking sulfur flows through the sites also identified limitations in data availability and quality, highlighting future requirements for tracking substance flows. One site was investigated in more detail showing sulfur speciation throughout the plant and tracking sulfur flows in odour control systems in order to quantify outflows to air, land and ocean sinks. While the majority of sulfur from WWTPs is removed as sulfate in the secondary effluent, the sulfur content of biosolids is valuable as it can be directly returned to soils to combat the potential sulfur deficiencies. Biosolids processing configurations, which focus on maximising solids recovery, through high efficiency separation techniques in primary sedimentation tanks, thickeners and dewatering centrifuges retain more sulfur in the biosolids. However, variations in sulfur loads and concentrations entering the WWTPs affect sulfur recovery in the biosolids, suggesting industrial emitters, and chemical dosing of iron salts are responsible for differences in recovery between sites.

Odorous volatile organic compound (VOC) emissions from ageing anaerobically stabilised biosolids.

Opportunities for the beneficial re-use of biosolids are limited by nuisance odour emissions. Volatile organic compounds (VOCs) from anaerobically stabilised biosolids were measured to identify compounds that could contribute to the overall odour character of nuisance emissions. Flux hood sampling and chemical analysis were used to identify VOCs emitted from biosolids as they were stored in ambient conditions. Compounds emitted varied as the biosolid cakes were stored for a period of 50 days. VOCs detected in the biosolids are likely to occur from catchment sources as well as abiotic and biotic generation in the wastewater processing and the biosolids as they are stored. Odour activity values (OAVs) were used to compare odorants. Trimethylamine was the only VOC detected that exceeded the sulfur compounds in terms of OAVs. Other compounds such as limonene, ethyl methyl benzene and acetic acid were detected at concentrations exceeding their olfactory detection limits, however at lower OAVs than sulfur compounds.

Jejunal perforation: an unusual presentation of metastatic cutaneous squamous cell carcinoma (SCC) in an immunosuppressed patient.

We report the rare occurrence of a small bowel perforation secondary to a metastatic cutaneous squamous cell carcinoma (cSCC). A 70-year-old woman, who had previously undergone renal transplantation, presented with severe, sudden-onset abdominal pain. She was peritonitic on initial examination, with evidence of free intra-abdominal air on radiographic imaging. During an exploratory laparotomy, she was found to have a perforated jejunum secondary to disseminated metastases seen throughout her peritoneum. Following histopathological analysis, as well as further imaging studies, the primary malignancy was eventually identified as a cSCC on her upper back. Palliative care was started and the patient died 8 weeks following her initial presentation.

Multicellular group formation in response to predators in the alga Chlorella vulgaris.

A key step in the evolution of multicellular organisms is the formation of cooperative multicellular groups. It has been suggested that predation pressure may promote multicellular group formation in some algae and bacteria, with cells forming groups to lower their chance of being eaten. We use the green alga Chlorella vulgaris and the protist Tetrahymena thermophila to test whether predation pressure can initiate the formation of colonies. We found that: (1) either predators or just predator exoproducts promote colony formation; (2) higher predator densities cause more colonies to form; and (3) colony formation in this system is facultative, with populations returning to being unicellular when the predation pressure is removed. These results provide empirical support for the hypothesis that predation pressure promotes multicellular group formation. The speed of the reversion of populations to unicellularity suggests that this response is due to phenotypic plasticity and not evolutionary change.

Ceramides are associated with inflammatory processes in human mediastinal adipose tissue.

BACKGROUND AND AIM: Ceramides are poorly characterized in human adipose tissue. The aim of this study was to investigate concentrations of different ceramide species in human subcutaneous and visceral adipose tissue depots and to determine associations between ceramides and global gene expression profiles. METHODS AND RESULTS: Concentrations of six ceramide species were determined in plasma and in subcutaneous and mediastinal adipose tissue from 10 overweight subjects (BMI 29.4 ± 4.9 kg/m(2)). In the adipose tissue biopsies gene expression arrays were performed and relationships between ceramides and gene expression analyzed. Immunostaining of the two adipose tissue depots was performed in an independent group of 10 patients. Mediastinal adipose tissue contained significantly higher concentrations (p < 0.05) of all six ceramide species than the subcutaneous depot. Of the six ceramides in plasma, concentrations of only two (Cer d18:1/18:0 and Cer d18:1/22:0) correlated significantly (p < 0.05) with the corresponding species in mediastinal adipose tissue, but there were no significant correlations between ceramides in plasma and subcutaneous adipose tissue. Multivariate analysis identified significant correlations between the total ceramide concentration and global gene expression within mediastinal, but not subcutaneous adipose tissue, according to cross-validation. Gene ontology analysis of genes related to ceramides in the mediastinal depot revealed that genes positively correlated with ceramides were associated mainly with immune and inflammatory categories, while genes negatively correlated with ceramides were associated mainly with lipid and carbohydrate metabolism. CONCLUSIONS: Ceramides in human mediastinal adipose tissue may be involved in inflammation and lipid and carbohydrate metabolism.

Human mediastinal adipose tissue displays certain characteristics of brown fat.

BACKGROUND: The amount of intra-thoracic fat, of which mediastinal adipose tissue comprises the major depot, is related to various cardiometabolic risk factors. Autopsy and imaging studies indicate that the mediastinal depot in adult humans could contain brown adipose tissue (BAT). To gain a better understanding of this intra-thoracic fat depot, we examined possible BAT characteristics of human mediastinal in comparison with subcutaneous adipose tissue. MATERIALS AND METHODS: Adipose tissue biopsies from thoracic subcutaneous and mediastinal depots were obtained during open-heart surgery from 33 subjects (26 male, 63.7±13.8 years, body mass index 29.3±5.1 kg m(-2)). Microarray analysis was performed on 10 patients and genes of interest confirmed by quantitative PCR (qPCR) in samples from another group of 23 patients. Adipocyte size was determined and uncoupling protein 1 (UCP1) protein expression investigated with immunohistochemistry. RESULTS: The microarray data showed that a number of BAT-specific genes had significantly higher expression in the mediastinal depot than in the subcutaneous depot. Higher expression of UCP1 (24-fold, P<0.001) and PPARGC1A (1.7-fold, P=0.0047), and lower expression of SHOX2 (0.12-fold, P<0.001) and HOXC8 (0.14-fold, P<0.001) in the mediastinal depot was confirmed by qPCR. Gene set enrichment analysis identified two gene sets related to mitochondria, which were significantly more highly expressed in the mediastinal than in the subcutaneous depot (P<0.01). No significant changes in UCP1 gene expression were observed in the subcutaneous or mediastinal depots following lowering of body temperature during surgery. UCP1 messenger RNA levels in the mediastinal depot were lower than those in murine BAT and white adipose tissue. In some mediastinal adipose tissue biopsies, a small number of multilocular adipocytes that stained positively for UCP1 were observed. Adipocytes were significantly smaller in the mediastinal than the subcutaneous depot (cross-sectional area 2400±810 versus 3260±980 µm(2), P<0.001). CONCLUSIONS: Human mediastinal adipose tissue displays some characteristics of BAT when compared with the subcutaneous depot at microscopic and molecular levels.

A common variant in PNPLA3, which encodes adiponutrin, is associated with liver fat content in humans.

AIMS/HYPOTHESIS: It has recently been suggested that the rs738409 G allele in PNPLA3, which encodes adiponutrin, is strongly associated with increased liver fat content in three different ethnic groups. The aims of the present study were as follows: (1) to try to replicate these findings in European individuals with quantitative measures of hepatic fat content; (2) to study whether the polymorphism influences hepatic and adipose tissue insulin sensitivity; and (3) to investigate whether PNPLA3 expression is altered in the human fatty liver. METHODS: We genotyped 291 Finnish individuals in whom liver fat had been measured using proton magnetic resonance spectroscopy. Hepatic PNPLA3 expression was measured in 32 participants. Hepatic and adipose tissue insulin sensitivities were measured using a euglycaemic-hyperinsulinaemic (insulin infusion 0.3 mU kg(-1) min(-1)) clamp technique combined with infusion of [3-(3)H]glucose in 109 participants. RESULTS: The rs738409 G allele in PNPLA3 was associated with increased quantitative measures of liver fat content (p = 0.011) and serum aspartate aminotransferase concentrations (p = 0.002) independently of age, sex and BMI. Fasting serum insulin and hepatic and adipose tissue insulin sensitivity were related to liver fat content independently of genotype status. PNPLA3 mRNA expression in the liver was positively related to obesity (r = 0.62, p < 0.0001) and to liver fat content (r = 0.58, p = 0.025) in participants who were not morbidly obese (BMI < 40 kg/m(2)). CONCLUSIONS/INTERPRETATION: A common variant in PNPLA3 increases the risk of hepatic steatosis in humans.

Fatty acid desaturases in human adipose tissue: relationships between gene expression, desaturation indexes and insulin resistance.

AIMS/HYPOTHESIS: Fatty acid desaturases introduce double bonds into growing fatty acid chains. The key desaturases in humans are Delta5-desaturase (D5D), Delta6-desaturase (D6D) and stearoyl-CoA desaturase (SCD). Animal and human data implicate hepatic desaturase activities in insulin resistance, obesity and dyslipidaemia. However, the role of desaturase activity in adipose tissue is uncertain. We therefore evaluated relationships between adipose mRNA expression, estimated desaturase activities (fatty acid ratios) in adipose tissue and insulin resistance. METHODS: Subcutaneous adipose tissue mRNA expression of D5D (also known as FADS1), D6D (also known as FADS2) and SCD was determined in 75 individuals representative of the study population of 294 healthy 63-year-old men. Desaturation indexes (product/substrate fatty acid ratios) were generated from adipose tissue fatty acid composition in all individuals. Insulin resistance was defined as the upper quartile of the updated homeostasis model assessment (HOMA-2) index. RESULTS: The relevant desaturation indexes (16:1/16:0, 18:1/18:0, 20:4/20:3 and 18:3/18:2) reflected expression of SCD, but not of D5D or D6D in adipose tissue. Insulin-resistant individuals had a higher adipose tissue 18:1/18:0, but not 16:1/16:0 ratio than insulin-sensitive individuals. Individuals with a high adipose tissue 18:1/18:0 ratio were 4.4-fold (95% CI 1.8-11.8) more likely to be insulin resistant [threefold (95% CI 1.1-8.6) after adjustment for waist circumference and plasma triacylglycerol]. In a multiple regression model predicting HOMA-2, the independent effect of the 18:1/18:0 ratio was borderline (p=0.086). CONCLUSIONS/INTERPRETATION: Adipose tissue desaturation indexes of SCD reflect the expression of the gene encoding the enzyme in this tissue. Elevated SCD activity within adipose tissue is closely coupled to the development of insulin resistance.

Increased expression of the macrophage markers and of 11beta-HSD-1 in subcutaneous adipose tissue, but not in cultured monocyte-derived macrophages, is associated with liver fat in human obesity.

OBJECTIVE: To determine whether increased expression of macrophage markers and of inflammatory markers in subcutaneous adipose tissue is associated with liver fat in human obesity. We also determined whether expression of TNF (gene encoding TNF-alpha), HSD11B1 (gene encoding 11beta-HSD-1) and RETN (gene encoding resistin) in cultured monocyte-derived macrophages differs between obese/overweight and non-obese subjects. DESIGN: Cross-sectional comparison of obese/overweight and non-obese subjects with respect to adipose tissue gene expression, gene expression in monocyte-derived macrophages, liver fat content and in vivo insulin sensitivity. SUBJECTS: Adipose tissue gene expression, gene expression in monocyte-derived macrophages, liver fat content and in vivo insulin sensitivity: 10 healthy non-obese (24.2+/-1.0 kg/m(2)) and 10 healthy obese/overweight (33.1+/-1.7 kg/m(2)) women. Gene expression in monocyte-derived macrophages: seven healthy non-obese (22.1+/-0.7 kg/m(2)) and seven healthy obese/overweight (36.9+/-2.2 kg/m(2)) women. MEASUREMENTS: Adipose tissue biopsies and blood samples for isolation of peripheral mononuclear cells were taken after an overnight fast. Liver fat content was measured using magnetic resonance proton spectroscopy. Whole body insulin sensitivity was measured using the hyperinsulinemic euglycemic clamp technique. Expression levels of TNF, HSD11B1, RETN and the macrophage markers CD68 and ITGAM were determined by real-time PCR. RESULTS: In adipose tissue, expression of HSD11B1, ITGAM and CD68 was significantly increased in the obese/overweight as compared to the non-obese group. Expression of all these genes was closely positively correlated with liver fat content and inversely correlated with whole body insulin sensitivity. The associations between expression of CD68, ITGAM and HSD11B1 and liver fat were independent of obesity. There were no differences in TNF, HSD11B1, RETN or CD68 gene expression basally or after stimulation with lipopolysaccharide in monocyte-derived macrophages between obese/overweight and non-obese subjects. CONCLUSION: Accumulation of fat in the liver is associated with increased adipose tissue inflammation independent of obesity.

Fatty acid handling protein expression in adipose tissue, fatty acid composition of adipose tissue and serum, and markers of insulin resistance.

OBJECTIVE: Proteins involved in cellular fatty acid (FA) uptake and metabolism may be of relevance in the context of disturbed FA metabolism associated with insulin resistance. Therefore this study investigated relationships between FA handling protein mRNA expression in adipose tissue, FA composition of adipose tissue and serum, and markers of insulin resistance. SUBJECTS: 75 subjects with a range of insulin sensitivities recruited from a cohort of 294 healthy 63-year-old Swedish men. MEASUREMENTS: Anthropometric and biochemical variables (e.g. waist-hip-ratio (WHR) and homeostasis model assessment (HOMA) index of insulin sensitivity), FA composition of the subcutaneous (s.c.) gluteal adipose tissue, serum nonesterified FA (NEFA) and serum phospholipid compartments (by gas-liquid chromatography; n = 294), and mRNA levels of FA handling proteins (adipocyte and keratinocyte lipid binding proteins, fatty acid transport protein (FATP) -1 and -4, CD36/fatty acid translocase, plasma membrane fatty acid binding protein, and acyl-CoA synthase-1 (ACS1)) in s.c. gluteal adipose tissue (by quantitative real-time polymerase chain reaction; n = 75). RESULTS: ACS1 expression was negatively correlated with measures of insulin resistance and central obesity (ACS1 versus HOMA: r = -0.28, P<0.05; ACS1 versus WHR: r = -0.23, P<0.05), with an opposite trend for FATP4. Further analysis of ACS1 expression levels revealed correlations with adipose tissue 16:0 (r = -0.27, P<0.05) and NEFA 16:1 (r = 0.29, P<0.05), FA composition variables which in turn correlated with HOMA index (r = 0.39, P<0.001 and r = -0.23, P<0.05, respectively, n = 75). Moreover, NEFA 16:1 predicted ACS1 expression independently of HOMA, WHR and adipose tissue 16:0 in multiple regression analysis (standardized coefficient = 0.27, P<0.05). CONCLUSION: Significant associations were found between measures of insulin sensitivity, adipose tissue FA handling protein expression, and specific FA composition variables. Although causal relationships could not be identified these findings suggest a role of FA handling proteins in relation to insulin sensitivity, via their involvement in FA trafficking and metabolism. In particular they indicate links between ACS1 activity, the distribution of 16:0 and 16:1, and insulin sensitivity, which may be of physiological relevance.

Acute in vivo effects of insulin on gene expression in adipose tissue in insulin-resistant and insulin-sensitive subjects.

AIMS/HYPOTHESIS: We determined the response of selected genes to in vivo insulin in adipose tissue in 21 non-diabetic women. MATERIALS AND METHODS: The women were divided into insulin-sensitive and -resistant groups based on their median whole-body insulin sensitivity (8.7+/-0.4 vs 4.2+/-0.3 mg kg(-1) min(-1) for insulin-sensitive vs -resistant group). Subcutaneous adipose tissue biopsies were obtained before and after 3 and 6 h of i.v. maintained euglycaemic hyperinsulinaemia. Adipose tissue mRNA concentrations of facilitated glucose transporter, member 1 (SLC2A1, previously known as GLUT1), facilitated glucose transporter, member 4 (SLC2A4, previously known as GLUT4), peroxisome proliferator-activated receptor gamma ( PPARG), peroxisome proliferator-activated receptor gamma co-activator 1alpha (PPARGC1A), 11beta-hydroxysteroid dehydrogenase-1 (HSD11B1), TNF, adiponectin (ADIPOQ), IL6 and the macrophage marker CD68 were measured using real-time PCR. RESULTS: Basal expression of 'insulin-sensitivity genes' SLC2A4 and ADIPOQ was lower while that of 'insulin-resistance genes', HSD11B1 and IL6 was significantly higher in the insulin-resistant than in the insulin-sensitive group. Insulin significantly increased expression of 'insulin-sensitivity genes' SLC2A4, PPARG, PPARGC1A and ADIPOQ in the insulin-sensitive group, while only expression of PPARG and PPARGC1A was increased in the insulin-resistant group. The expression of 'insulin-resistance genes' HSD11B1 and IL6 was increased by insulin in the insulin-resistant group, but insulin failed to increase HSD11B1 expression in the insulin-sensitive group. At 6 h, expression of HSD11B1, TNF and IL6 was significantly higher in the insulin-resistant than in the insulin-sensitive group. IL6 expression increased significantly more in response to insulin in the insulin-resistant than in the insulin-sensitive group. CD68 was overexpressed in the insulin-resistant as compared with the insulin-sensitive group at both 0 and 6 h. CONCLUSIONS/INTERPRETATION: These data suggest that genes adversely affecting insulin sensitivity hyperrespond to insulin, while genes enhancing insulin sensitivity hyporespond to insulin in insulin-resistant human adipose tissue in vivo.