Arachidonic Acid In Adipose Tissue Research Articles

APOE4 mice rely more on the plasma DHA than APOE3 mice, especially in glia morphology and cognitive performance.

AbstractBackgroundThe metabolism of docosahexaenoic acid (DHA), an omega‐3 fatty acid, is different in APOE4 carriers. Brain relies on the plasma DHA pool for its need but the plasma‐liver‐brain axis in relation to cognition remains obscure. We hypothesized that this relation is compromised in APOE4 mice considering the differences in fatty acid metabolism between APOE3 and APOE4 mice.MethodMale and female APOE3 and APOE4 mice were fed either a diet enriched with DHA (0.7 g DHA/100 g diet) or a control diet for 8 months. Barnes maze and object recognition tests were performed in mice. Immunofluorescence was eprformed on parafin embeded brain slides with GFAP and IBA‐1 and multiplex cytokines were measured in hippocampus protein extracts.ResultIn the cortex, a genotype effect was found where APOE4 mice had higher concentration of DHA than APOE3 mice fed the control diet. APOE4 mice had 20‐30% lower plasma DHA and arachidonic acid (AA) concentrations, adipose tissue AA concentrations than APOE3 mice, independent of diet. In APOE4 mice, there was a significant correlation between plasma DHA and scores on the Barnes maze and with better recognition index. In addition, APOE4 mice fed the DHA diet had lower hippocampal concentrations of interleukin‐7, lipopolysaccharide‐induced CXC chemokine and monocyte chemoattractant protein 1, and higher concentration of interferon‐gamma compared to APOE4 mice fed the control diet. We also found that a diet rich in DHA enhances reactive astrogliosis and ramified microglia morphology in APOE4 mice.ConclusionAltogether, our data support that APOE4 mice rely more on the plasma DHA than APOE3 mice, especially in cognitive performance and astrocytes and microglia morphology. Any disturbance in plasma DHA metabolism might have a greater impact on cognition in APOE4 carriers.

The Insulin-Sensitizer Pioglitazone Remodels Adipose Tissue Phospholipids in Humans.

The insulin-sensitizer pioglitazone exerts its cardiometabolic benefits in type 2 diabetes (T2D) through a redistribution of body fat, from ectopic and visceral areas to subcutaneous adipose depots. Whereas excessive weight gain and lipid storage in obesity promotes insulin resistance and chronic inflammation, the expansion of subcutaneous adipose by pioglitazone is associated with a reversal of these immunometabolic deficits. The precise events driving this beneficial remodeling of adipose tissue with pioglitazone remain unclear, and whether insulin-sensitizers alter the lipidomic composition of human adipose has not previously been investigated. Using shotgun lipidomics, we explored the molecular lipid responses in subcutaneous adipose tissue following 6months of pioglitazone treatment (45mg/day) in obese humans with T2D. Despite an expected increase in body weight following pioglitazone treatment, no robust effects were observed on the composition of storage lipids (i.e., triglycerides) or the content of lipotoxic lipid species (e.g., ceramides and diacylglycerides) in adipose tissue. Instead, pioglitazone caused a selective remodeling of the glycerophospholipid pool, characterized by a decrease in lipids enriched for arachidonic acid, such as plasmanylethanolamines and phosphatidylinositols. This contributed to a greater overall saturation and shortened chain length of fatty acyl groups within cell membrane lipids, changes that are consistent with the purported induction of adipogenesis by pioglitazone. The mechanism through which pioglitazone lowered adipose tissue arachidonic acid, a major modulator of inflammatory pathways, did not involve alterations in phospholipase gene expression but was associated with a reduction in its precursor linoleic acid, an effect that was also observed in skeletal muscle samples from the same subjects. These findings offer important insights into the biological mechanisms through which pioglitazone protects the immunometabolic health of adipocytes in the face of increased lipid storage.

Interactions between 5-Lipoxygenase Polymorphisms and Adipose Tissue Contents of Arachidonic and Eicosapentaenoic Acids Do Not Affect Risk of Myocardial Infarction in Middle-Aged Men and Women in a Danish Case-Cohort Study

Background: The 5-lipoxygenase pathway has been linked to atherothrombotic disease, and a functional tandem repeat polymorphism in the arachidonate lipoxygenase-5 (ALOX-5) gene has been associated with the risk of myocardial infarction (MI). Interestingly, 2 studies have reported an interaction between dietary intakes of the ALOX-5 substrates, arachidonic acid (AA) and eicosapentaenoic acid (EPA), and genotype.Objective: We investigated whether the interactions between the ALOX-5 tandem repeat polymorphism (rs59439148) and adipose tissue AA and EPA were associated with incident MI.Methods: In the Danish Diet, Cancer and Health study, we conducted a case-cohort study including 3089 participants with incident MI identified from national registries and a randomly selected subcohort of 3000 participants. Participants were men and women with a median age of 56 y at baseline and no previous history of cancer. Adipose tissue and blood samples were collected at baseline along with comprehensive questionnaires on lifestyle and demographic data. The ALOX-5 tandem repeat polymorphism was genotyped by multititer plate sequencing. Associations were analyzed by using Cox proportional hazards models.Results: We observed a higher risk of MI for homozygous carriers of the variant alleles in the fifth quintile of AA content than for the reference group with the lowest quintile of AA and carrying the wild-type allele (HR: 3.02; 95% CI: 1.41, 6.44). In contrast, homozygotes for the variant alleles tended to have a higher risk of MI when comparing the lowest quintile of EPA content with the reference group with the highest quintile of EPA and carrying the wild-type allele (HR: 2.15; 95% CI: 0.91, 5.09; P = 0.08). Although our results suggested interactions between the polymorphism and adipose tissue AA and EPA, a quantitative evaluation of interaction by calculating the relative excess risk due to interactions was not significant.Conclusions: Adipose tissue EPA and AA and the ALOX-5 tandem repeat polymorphism did not significantly interact to affect the risk of MI. However, the results should be replicated in larger, heterogeneous populations.

Dietary Cocoa Reduces Adipose Tissue Inflammation in High‐ Fat Fed Obese Mice

In diet‐induced obesity, adipose tissue (AT) is in a chronic state of inflammation predisposing the development of insulin‐resistance, type 2 diabetes and cardiovascular complications. Cocoa (Theobroma cacao) is a polyphenol‐rich food with putative anti‐inflammatory activities; however, little research has been done to support the role of cocoa in modulating inflammation in obese subjects, and the mechanism of action remains to be fully elucidated. The objective of the present study is to determine the effects of dietary cocoa supplementation on AT inflammation in high‐fat (HF)‐fed mice. Male C57BL/6J mice were fed a HF diet (HF group), a HF diet with 8% (w/w) unsweetened cocoa powder (HFC group), or a low‐fat diet for 18 weeks. Cocoa supplementation significantly decreased pro‐inflammatory gene expression (Il6, Il12b, Nos2 and Emr1) in the stromal vascular fraction of AT by 40–62% compared to HF group (P < 0.05). Protein expression of adipose‐specific phospholipase A2 was reduced by 53% in HFC mice (P < 0.05). Moreover, AT arachidonic acid (AA) levels were positively correlated with adiposity (r = 0.56, P < 0.01) and cocoa‐supplemented mice had 33% lower levels of AA compared to HF control (P < 0.05). These results demonstrate the anti‐inflammatory effects of cocoa in obese mice and provide mechanistic biomarkers for further investigation.Grant Funding Source: Dept. of Food Science of The Pennsylvania State University

Adipose tissue arachidonic acid content is associated with the expression of 5-lipoxygenase in atherosclerotic plaques

BackgroundThe content of arachidonic acid in adipose tissue is positively associated with the risk of myocardial infarction, whereas the content of eicosapentaenoic acid in adipose tissue has been reported to be negatively associated with the risk of myocardial infarction. Both arachidonic acid and eicosapentaenoic acid are substrates for the synthesis of pro-inflammatory leukotrienes and leukotrienes derived from eicosapentaenoic acid are generally much less potent. In this study we hypothesized that a high content of arachidonic acid in adipose tissue would reflect a high formation of arachidonic acid derived leukotrienes and a high expression of 5-lipoxygenase in atherosclerotic plaques. Likewise, we hypothesized that a high content of eicosapentaenoic acid in adipose tissue would reflect a low formation of arachidonic acid derived leukotrienes and a low expression of 5-lipoxygenase in plaques.MethodsIn a cross sectional study we included 45 consecutive subjects undergoing femoral thrombendarterectomy. The expression of 5-lipoxygenase in plaques was assessed by a semi-automated image analysis computer programme after immunohistochemical staining with mono-clonal 5-lipoxygenase antibodies. Leukotriene B4 and cysteinyl leukotriene formation from stimulated femoral artery plaques was quantified using ELISA methods. The fatty acid content of adipose tissue biopsies from the thigh was analyzed using gas chromatography. Associations between variables were assessed by Pearson correlations and were further explored in a multivariable linear regression model adjusting for potential confounders.ResultsA high content of arachidonic acid in adipose tissue was associated with a higher expression of 5-lipoxygenase in plaques (r = 0.32, p = 0.03), but no significant associations with leukotriene B4 (r = 0.22, p = 0.14) and cysteinyl leukotriene (r = −0.11, p = 0.46) formation was seen. No significant associations were found between the content of eicosapentaenoic acid in adipose tissue and 5-lipoxygenase expression or leukotriene formation in plaque.ConclusionsAdipose tissue arachidonic acid contents correlated positively with the expression of 5-lipoxygenase in plaques. This association might represent a causal link between adipose tissue arachidonic acid and the risk of myocardial infarction but confirmatory studies are needed.

Adipose tissue arachidonic acid content is associated with the risk of myocardial infarction: A Danish case-cohort study

ObjectiveThe primary aim of the study was to evaluate the association between adipose tissue arachidonic acid (AA) content and the risk of myocardial infarction (MI). The secondary aim was to assess the correlation between adipose tissue AA and dietary intake of AA and linoleic acid (LA). MethodsWe conducted a case-cohort study nested within the Danish prospective Diet, Cancer and Health (DCH) study. After appropriate exclusions, the study included 2134 incident MI cases. Gluteal adipose tissue biopsies were collected at recruitment, and the fatty acid composition was determined by gas chromatography. A weighted Cox proportional hazards model was used to evaluate the association between adipose tissue AA content and the risk of MI. ResultsAfter adjusting for confounders we found a positive association between adipose tissue AA content and the risk of MI. Hazard ratios (HR) of MI relative to the lowest quintile of adipose tissue AA content, increased across quintiles; second quintile (HR 1.19 95%CI: 0.97–1.45), third (HR 1.24 95%CI: 1.02–1.52), fourth (HR 1.28 95%CI: 1.03–1.60), and fifth quintile (HR 1.39 95%CI: 1.10–1.77). Adipose tissue AA levels were not correlated with dietary intake of AA (r=0.03, 95%CI: −0.01, 0.06) and weakly negatively correlated with dietary intake of LA (r=−0.12, 95%CI: −0.15, −0.08). ConclusionsThe adipose tissue content of AA was positively associated with the risk of MI but did not correlate with dietary intake of neither AA nor LA.

Abstract 18506: A High Adipose Tissue Arachidonic Acid Content is Associated with a Higher Risk of Myocardial Infarction: A Danish Case Cohort Study

Background: Some, but not all studies have reported a positive association between the content of arachidonic acid (AA) in adipose tissue and the risk of coronary heart disease. However, unlike most other polyunsaturated fatty acids, the content of AA in adipose tissue does not seem to reflect the dietary intake of neither AA nor the endogenous source and precursor of AA, linoleic acid (LA). Aim: The primary aim of the study was to evaluate the association between adipose tissue AA content and the risk of myocardial infarction (MI). The secondary aim was to assess the correlation between adipose tissue AA and dietary intake of AA and LA, as assessed from a validated 192 item food frequency questionnaire. Methods: We conducted a case-cohort study nested within the Danish Prospective Diet, Cancer and Health (DCH) study. After appropriate exclusions, the study included 2,134 incident MI cases and 3,021 control subjects. Gluteal adipose tissue biopsies were collected at recruitment, and the fatty acid composition (in percentage of total fatty acids) was determined by gas chromatography. A weighted Cox proportional hazards model with sex-specific baseline hazards and age as time axis, was used to evaluate the association between adipose tissue AA content and the risk of MI. Results: In the crude analysis we observed a significant positive association between adipose AA content and the risk of MI. Although attenuated, the association remained significant when relevant potential confounders were included, where the hazard ratios (HR) of MI relative to the lowest quintile increased across quintiles; two (HR 1.16 95%CI: 0.95-1.41), three (HR 1.18 95%CI: 0.97-1.43) four (HR 1.20 95%CI: 0.97-1.49), and five (HR 1.29 95%CI: 1.03-1.61) (P for trend = 0.048). Adipose tissue AA levels were not correlated with dietary intake of AA (r = 0.03, 95%CI: -0.01, 0.06) and negatively correlated with dietary intake of LA (r = -0.12, 95%CI: -0.15, -0.08). Conclusions: The adipose tissue content of AA was positively associated with the risk of MI. Adipose tissue AA was not associated with dietary intake of neither AA nor LA and this apparently complex regulation of AA levels in adipose tissue is not well understood and needs to be explored further in future studies.

Pro-inflammatory Phospholipid Arachidonic Acid/Eicosapentaenoic Acid Ratio of Dysmetabolic Severely Obese Women

Fatty acids (FAs) and adipokines such as adiponectin or interleukin-6 (IL-6) are known to modulate inflammation and the development of metabolic syndrome. Whether FA composition assessed in plasma triacylglycerols (TAGs), phospholipids (PLs) and non-esterified fatty acids (NEFAs) and adipose tissue (AT) PLs differed between dysmetabolic and non-dysmetabolic severely obese women remains to be established. Whether the plasma and/or AT arachidonic acid (AA)/eicosapentaenoic acid (EPA) ratio in the PL sub-fraction may be associated with adipokine AT gene expression needs to be examined. FA composition was measured in plasma lipid classes and in the TAG and PL sub-fractions of subcutaneous abdominal and omental ATs of severely obese women paired for age and adiposity but showing a dysmetabolic profile (n = 13) or not (n = 14). FA profile was assessed by gas chromatography. Plasma and AT mRNA concentrations of adiponectin and IL-6 were measured by ELISA and real-time polymerase chain reaction, respectively. Plasma adiponectin and FA concentrations in the NEFA sub-fraction were, respectively, lower and higher in dysmetabolic than in non-dysmetabolic women (p < 0.05). Despite similar FA levels in the PL sub-fraction, the AA/EPA ratio was higher in plasma and ATs (p < 0.005), because of an EPA decrease in plasma and subcutaneous abdominal fat vs. an AA increase in the omental depot. The AA/EPA ratio was negatively associated with adiponectin concentrations in plasma and subcutaneous abdominal AT (0.01 < p < 0.05). Metabolic dysfunction is associated with a pro-inflammatory phospholipid AA/EPA ratio in plasma and ATs, and an altered adiponectin secretion that could contribute to developing metabolic syndrome.

An Association Between Dietary Arachidonic Acid, Measured in Adipose Tissue, and Ulcerative Colitis

Dietary arachidonic acid, an n-6 polyunsaturated fatty acid (n-6 PUFA), might be involved in the etiology of ulcerative colitis (UC). We performed a prospective cohort study to determine whether high levels of arachidonic acid in adipose tissue samples (which reflects dietary intake) are associated with UC. We analyzed data collected from 57,053 men and women in the EPIC-Denmark Prospective Cohort Study from 1993 to 1997. Adipose tissue biopsy samples were collected from gluteal regions at the beginning of the study, the cohort was monitored over subsequent years, and participants who developed UC were identified. A subcohort of 2510 randomly selected participants were used as controls. Concentrations of arachidonic acid were measured in adipose tissue samples. In the analysis, arachidonic acid levels were divided into quartiles; relative risks (RR) were calculated and adjusted for smoking, use of aspirin and nonsteroidal anti-inflammatory drugs, and levels of n-3 PUFAs. A total of 34 subjects (56% men) developed incident UC at a median age of 58.8 years (range, 50.0-69.0 years). Those in the highest quartile for arachidonic acid concentrations in adipose tissue had an RR for UC of 4.16 (95% confidence interval [CI]: 1.56-11.04); a trend per 0.1% increase in arachidonic acid of 1.77 in RR was observed (95% CI: 1.38-2.27). The fraction attributed the highest levels of arachidonic acid was 40.3%. Individuals with the highest relative concentrations of arachidonic acid in adipose tissue have a significantly greater risk of developing UC. Dietary modifications might therefore prevent UC or reduce disease symptoms.

Adipose tissue arachidonic acid and the metabolic syndrome in Costa Rican adults

Arachidonic acid, a precursor to a series of inflammatory mediators, may contribute to the development of insulin resistance. We examined the association between adipose tissue arachidonic acid and the metabolic syndrome in Costa Rica, a country in which the metabolic syndrome is highly prevalent. The 484 study participants each provided a fasting blood sample and an adipose tissue biopsy that was analyzed for fatty acid composition. Criteria for the metabolic syndrome were those established in the Third Report of the National Cholesterol Education Program Expert Panel. The data were analyzed by multivariate logistic regression. Subjects with greater adipose tissue arachidonic acid content had an increasing risk of the metabolic syndrome across quintiles: odds ratio (95% confidence interval), 1.00; 1.51 (0.78-2.91); 2.40 (1.26-4.55); 3.50 (1.84-6.66); and 6.01 (3.11-11.61); test for trend, P<0.0001, after adjustment for age, gender and area of residence. Further adjustment for metabolic risk factors, including adipose fatty acids and body mass index, did not significantly modify the result. Adipose tissue arachidonic acid was also independently associated with abdominal obesity, hypertriglyceridemia, elevated fasting glucose, and high blood pressure. This study identifies arachidonic acid as an important independent marker of metabolic dysregulation. A better understanding of the role of this fatty acid in the pathogenesis of the metabolic syndrome is warranted.

Arachidonic Acid in Adipose Tissue Is Associated with Nonfatal Acute Myocardial Infarction in the Central Valley of Costa Rica

Arachidonic acid (AA), a precursor of prothrombotic eicosanoids, is potentially atherogenic, but epidemiologic data are scarce. We evaluated the hypothesis that increased AA in adipose tissue is associated with increased risk of nonfatal acute myocardial infarction (MI), and if so, whether this association is related to dietary or adipose tissue linoleic acid. We studied the association between AA and MI in 466 cases of a first nonfatal acute MI, matched on age, gender, and residence to 466 population controls. Fatty acids (FA) were assessed by GC in adipose tissue samples collected from all subjects. Odds ratios (OR) and 95% CI were calculated from multivariate conditional logistic regression models. Subjects in the highest quintile of adipose tissue AA (0.64% of total FA) had a higher risk of nonfatal acute MI than those in the lowest quintile (0.29% of total FA), after adjusting for potential confounders including (n-3) and trans FAs (OR = 1.94, 95% CI: 1.07, 3.53, P for trend = 0.026). Adipose tissue AA was not correlated with dietary AA (r = 0.07), linoleic acid (r = 0.04), or other dietary (n-6) FAs, or with adipose tissue linoleic acid (r = -0.07). These data suggest that the association between MI and adipose tissue AA is not related to dietary intake of (n-6) FAs including linoleic acid. Better understanding of the metabolic factors that increase AA in adipose tissue is urgently needed.

Association of adipose tissue arachidonic acid content with BMI and overweight status in children from Cyprus and Crete.

The relationships between n-3 and n-6 fatty acids in subcutaneous fat, BMI and overweight status were investigated in eighty-eight children from Crete and Cyprus. Overweight status, BMI and serum lipid levels were similar in children at both locations, but Cretan children had higher levels of total MUFA than Cypriot children (62.2 (sd 2.8) v. 52.2 (sd 2.8) % area, respectively, P<0.001) and consequently Cypriot children had higher levels of total saturated, polyunsaturated, trans, n-3 and n-6 fatty acids. Cypriot children had also higher levels of individual n-3 and n-6 fatty acids, specifically linoleic, alpha-linolenic and dihomo-gamma-linolenic acids. The variance of BMI was better explained (38.2 %) by adipose tissue arachidonic acid content than any other n-3 and n-6 fatty acids. Mean levels of arachidonic acid, dihomo-gamma-linolenic acid and docosahexaenoic acid were higher in overweight and obese subjects. All obese subjects fell in the 4th quartile of arachidonic acid levels, whereas 88.9 % of overweight subjects fell in the 3rd and 4th quartile of arachidonic acid. These results indicate positive associations between adipose tissue arachidonic acid and BMI and overweight status. Further research could clarify whether this association is causal.

Tissue levels of fish fatty acids and risk of colorectal adenomas: a case-control study (Netherlands).

Epidemiological and animal studies have suggested that a high ratio of n-3 fish fatty acids to arachidonic acid (AA), might protect against colorectal carcinogenesis. Competition of n-3 and n-6 fatty acids, especially AA, for the enzyme cyclooxygenase-2 may be responsible for this effect. To examine the relation between fish intake and colorectal adenomas, data from a Dutch case-control study were analysed. All 52 cases and 57 controls filled out a food questionnaire, underwent a full colonic examination and have had a fat biopsy from the buttock. Intake of fish and fish fatty acids was inversely associated with colorectal adenomas although not statistically significant. For the ratio of fish fatty acids to AA, the ORs in the second and third tertile were 1.2 and 0.8 (p-trend = 0.78). Tissue levels of fish fatty acids were inversely associated and tissue levels of AA were positively associated with adenomas, although not statistically significant. However, the OR for the ratio of fish fatty acids to AA was 0.2 in the second and third tertile (p-trend = 0.002). In line with the hypothesis, a high ratio of fish fatty acids to AA in adipose tissue was associated with a lower risk of colorectal adenomas.

Prostacyclin as a critical prostanoid in adipogenesis

Adipose cell differentiation from adipoblasts to preadipose and to adipose cells is a multistep process. Terminal differentiation of preadipose cells expressing early markers to adipose cells expressing late and very late markers and accumulating triacylglycerol requires a combination of circulating and locally-produced hormones. Prostacyclin (PGI 2), one of the major metabolites of arachidonic acid in adipose tissue, has been shown to exert autocrine and paracrine adipogenic effects in vitro. As discussed herein, multiple arguments support the proposition that PGI 2 is a key prostanoid involved in adipogenesis.

Modulation of vascular tone and glycerol levels measured by in situ microdialysis in rat adipose tissue.

Changes in blood flow induced by the beta-adrenoceptor agonist isoproterenol (Iso) and a stable analogue of the major metabolite of arachidonic acid in adipose tissue, carbaprostacyclin (cPGI2), have been studied in rat periepididymal fat pad with in situ microdialysis measuring the distribution ratio of 0.2% ethanol in the dialysate (outflow) to that in the perfusate (inflow) (O/I ratio). Local perfusions of 1 microM cPGI2 or 1 microM Iso led to reversible decreases of the O/I ratio that were similar to the decrease induced by the vasodilating reference drug hydralazine (Hydra, 630 microM). Interestingly, a continuous perfusion of Hydra at a submaximal vasodilating concentration (63 microM) was sufficient to prevent further vasodilatation induced by Iso or cPGI2. To take advantage of this observation, experiments were designed to evaluate the influence of the vasodilating effect of Iso or cPGI2 on the ability of either to induce lipolysis in vivo. The results showed that the vasodilating effect of Iso could contribute to glycerol removal from the extracellular fluid and demonstrate that cPGI2 was devoid of lipolytic activity.

Differentiation of preadipose cells: paracrine role of prostacyclin upon stimulation of adipose cells by angiotensin-II.

Prostacyclin (PGI2), the major metabolite of arachidonic acid in adipose tissue, has been shown to play a key role in the process of preadipose cell differentiation in vitro. Moreover, angiotensin-II (Ang II) is able to induce the production of PGI2 in suspensions of isolated adipocytes as well as in the interstitial fluid of rat adipose tissue. A possible role of Ang II in the control of the autocrine-paracrine adipogenic effect of PGI2 has been investigated, using cells of the Ob1771 preadipocyte clonal line cultured in serum-free chemically defined medium. Whereas both preadipose and adipose cells were able to produce PGI2 upon exposure to arachidonic acid, only adipose cells were able to do so when challenged with Ang II. In agreement with this observation, the ability of Ang II to induce preadipose cells to differentiate required the simultaneous presence of differentiated cells. Such coculture experiments show that the promoting effect of Ang II on preadipose cell differentiation was strongly reduced by aspirin, antibodies able to neutralize PGI2, and the AT2 receptor antagonist PD123177, but not by the AT1 receptor antagonist losartan. Together, these results support Ang II as being able, by means of binding to a receptor of the AT2 subtype present in adipose cells, to control the adipogenic effect of PGI2 through a paracrine mode of action.

Fatty acid composition of adipose tissue and serum micronutrients in relation to common rheumatic complaints in Swedish adults 50-70 years old.

Biochemical markers of nutritional status, such as adipose tissue fatty acid composition and circulating levels of micronutrients, may reflect dietary habits, but may also be related to inflammatory activity. We examined the relationship between common rheumatic complaints such as osteo-arthrosis, arthralgia, tendinitis, low-back pain, and neck pain, and the composition of adipose tissue fatty acids, serum concentrations of retinol, ascorbic acid, alpha-tocopherol and selenium in 502, out of 900 randomly selected individuals 50-70 years old. Compared with control subjects the rheumatic group as a whole (p less than 0.01) as well as subgroups like those with arthralgia (p less than 0.01), subacromial shoulder pain (p less than 0.03), and low-back pain (p less than 0.05), had decreased proportions of adipose tissue arachidonic acid. The abnormalities correlated with the duration of the symptom-free period preceding adipose tissue sampling and could not be explained by the evaluation of possible confounding factors. Regarding other fatty acids and micronutrients there were no differences between symptomatic subjects and controls. One explanation for the low proportion of adipose tissue arachidonic acid may be increased eicosanoid production.