White adipose tissue is a key endocrine and secretory organ, releasing multiple adipokines, many of which are linked to inflammation and immunity. During the expansion of adipose tissue mass in obesity there is a major inflammatory response in the tissue with increased expression and release of inflammation-related adipokines, including IL-6, leptin, monocyte chemoattractant protein-1 and TNF-α, together with decreased adiponectin production. We proposed in 2004 (Trayhurn & Wood, Br J Nutr92, 347–355) that inflammation in adipose tissue in obesity is a response to hypoxia in enlarged adipocytes distant from the vasculature. Hypoxia has now been directly demonstrated in adipose tissue of several obese mouse models (ob/ob, KKAy, diet-induced) and molecular studies indicate that the level of the hypoxia-inducible transcription factor, hypoxia-inducible factor-1α, is increased, as is expression of the hypoxia-sensitive marker gene, GLUT1. Cell- culture studies on murine and human adipocytes show that hypoxia (induced by low O2 or chemically) leads to stimulation of the expression and secretion of a number of inflammation-related adipokines, including angiopoietin-like protein 4, IL-6, leptin, macrophage migration inhibitory factor and vascular endothelial growth factor. Hypoxia also stimulates the inflammatory response of macrophages and inhibits adipocyte differentiation from preadipocytes. GLUT1 gene expression, protein level and glucose transport by human adipocytes are markedly increased by hypoxia, indicating that low O2 tension stimulates glucose utilisation. It is suggested that hypoxia has a pervasive effect on adipocyte metabolism and on overall adipose tissue function, underpinning the inflammatory response in the tissue in obesity and the subsequent development of obesity-associated diseases, particularly type 2 diabetes and the metabolic syndrome.

The study of hypoxia in adipose tissue in relation to obesity is timely, since some very recent studies have put these topics in a physiological context.

There is a growing appreciation that it is not just the total intake of dietary Se that is important to health but that the species of Se ingested may also be important. The present review attempts to catalogue what is known about Se species in foods and supplements and the health effects in which they are implicated. The biosynthetic pathways involved in Se assimilation by plants and the way in which Se species are metabolised in animals are presented in order to give an insight into the species likely to be present in plant and animal foods. Known data on the species of Se in the food chain and in food supplements are tabulated along with their concentrations and the analytical methodology used. The latter is important, since identification that is only based on retention-time matching with authentic standards must be considered as tentative: for evidence of structural confirmation, fragmentation of the molecular ion in addition to MS data is required. Bioavailability, as normally defined, is higher for organic Se species. Health effects, both beneficial and toxic, thought to be associated with specific Se species are described. Potent anti-tumour effects have been attributed to the low-molecular-weight species, Se-methyl-selenocysteine and its γ-glutamyl-derivative, found in a number of edible plants of the Allium and Brassica families. There remain considerable gaps in our knowledge of the forms of Se that naturally occur in foods. Without adequate knowledge of Se speciation, false conclusions may be drawn when assessing Se requirements for optimal health.

Following the publication of the landmark trial of Clark et al. in 1996 that appeared to show that Se could reduce the risk of cancer, awareness of the importance of Se to human health has markedly increased. As a result, there is now much more aggressive marketing of Se supplements and functional foods, even in situations where additional consumption of Se is inappropriate. The present review addresses how Se gets into the food chain, the wide variability in Se content of foods and the very different levels of intake between countries and regions. Though it is clear that there are adverse consequences for health of both deficient and excessive intake, health effects at intermediate levels of intake are less certain. Thus it is difficult to define optimal intake which depends on a large number of factors, such as which functions of Se are most relevant to a particular disease state, which species of Se is most prominent in the Se source, which health condition is being considered, the adequacy or otherwise of intake of other nutrients, the presence of additional stressors, and lastly whether the ability to make selenoproteins may be compromised. These complexities need to be understood, particularly by policy makers, in order to make informed judgments. Potential solutions for increasing Se intake, where required, include agronomic biofortification and genetic biofortification or, for individuals, increased intake of naturally Se-rich foods, functional foods or supplements. The difficulties of balancing the risks and benefits in relation to Se intake are highlighted.

The loss of weight was analysed in a group of sixty overweight/obese women of childbearing age (20–35 years) according to their initial vitamin D status. Subjects were randomly assigned to one of two slightly hypocaloric diets: Diet V, in which the consumption of vegetables was increased, or Diet C, in which the relative consumption of cereals (especially breakfast cereals) was increased. Dietetic, anthropometric and biochemical data were collected at the start of the study and again at 2 weeks after dividing the women into groups depending on their having an initial serum 25-hydroxyvitamin D (25(OH)D) concentration of < 50 nmol/l (LD) or ≥ 50 nmol/l (HD). Dietary intervention led to a reduction in energy intake, body weight and BMI in all groups. The HD women showed greater body fat losses during the study than the LD women (1·7 (sd 1·8) kg compared to 0·5 (sd 0·8) kg). A better vitamin D status therefore aided the loss of body fat over the experimental period (OR 0·462; CI 0·271, 0·785; P < 0·001). However, when the dietary groups were analysed separately, this effect was only seen in the C subjects (OR 0·300; CI 0·121, 0·748; P < 0·001). The present results suggest that women with a better vitamin D status respond more positively to hypocaloric diets and lose more body fat; this was especially clear among the C subjects who had a greater vitamin D supply during the experimental period.

Epoxyxanthophylls (epoxide-containing xanthophylls), a group of carotenoids, are ubiquitously distributed in edible plants. Among them, neoxanthin in green leafy vegetables and fucoxanthin in brown algae have been reported to exhibit an antiproliferative effect on several human cancer cells in vitro. However, there is little information about the intestinal absorption and metabolic fate of dietary epoxyxanthophylls in humans. To estimate the intestinal absorption of neoxanthin and fucoxanthin in humans, we evaluated the plasma epoxyxanthophyll concentrations before and after 1-week dietary interventions with spinach (Spinacia oleracea) and wakame (Undaria pinnatifida). The epoxyxanthophylls and their metabolites in the plasma extracts were determined by HPLC after partial purification and concentration with solid-phase extraction cartridges. Even after 1 week of spinach intake (3·0 mg neoxanthin/d), the plasma concentrations of neoxanthin and its metabolites (neochrome stereoisomers) remained very low (about 1 nmol/l), whereas those of β-carotene and lutein were markedly increased. Similarly, the plasma concentration of fucoxanthinol, a gastrointestinal metabolite of fucoxanthin, was < 1 nmol/l after 1 week of wakame intake (6·1 mg fucoxanthin/d). These results indicated that the plasma response to dietary epoxyxanthophylls was very low in humans even after 1-week intake of epoxyxanthophyll-rich diets.

Induction of an altered phenotype by prenatal under-nutrition involves changes in the epigenetic regulation of specific genes. We investigated the effect of feeding pregnant rats a protein-restricted (PR) diet with different amounts of folic acid on the methylation of individual CpG dinucleotides in the hepatic PPARα promoter in juvenile offspring, and the effect of the maternal PR diet on CpG methylation in adult offspring. Pregnant rats (five per group) were fed 180 g/kg casein (control) or 90 g/kg casein with 1 mg/kg folic acid (PR), or 90 g/kg casein and 5 mg/kg folic acid (PRF). Offspring were killed on postnatal day 34 (five males and females per group) and day 80 (five males per group). Methylation of sixteen CpG dinucleotides in the PPARα promoter was measured by pyrosequencing. Mean PPARα promoter methylation in the PR offspring (4·5 %) was 26 % lower than controls (6·1 %) due to specific reduction at CpG dinucleotides 2 (40 %), 3 (43 %), 4 (33 %) and 16 (48 %) (P < 0·05). There was no significant difference in methylation at these CpG between control and PRF offspring. Methylation of CpG 5 and 8 was higher (47 and 63 %, respectively, P < 0·05) in the PRF offspring than control or PR offspring. The methylation pattern in day 80 PR offspring was comparable to day 34 PR offspring. These data show for the first time that prenatal nutrition induces differential changes to the methylation of individual CpG dinucleotides in juvenile rats which persist in adults.

Resistance exercise is recommended to individuals following high-protein diets in order to augment changes in body composition. However, alterations in macronutrient composition may compromise physical performance. The present study investigated the effects of an isoenergetic high-protein diet on upper and lower limb strength and fatigue during high-intensity resistance exercise. Ten recreationally active women, aged 25–40 years, followed a control diet (55, 15 and 30 % of energy from carbohydrate, protein and fat, respectively) and a high-protein diet (respective values, 30, 40 and 30) for 7 d each in a random counterbalanced design. Each participant underwent strength testing of upper limb (isometric handgrip strength and endurance) and lower limb (four sets of sixteen maximal knee flexions and extensions on an isokinetic dynamometer) before and after applying each diet. Body weight, body fat and RER were significantly reduced following the high-protein diet (P < 0·05). No differences were found between diets in any of the strength performance parameters (handgrip strength, handgrip endurance, peak torque, total work and fatigue) or the responses of heart rate, systolic and diastolic arterial pressure, blood lactate and blood glucose to exercise. Women on a short-term isoenergetic high-protein, moderate-fat diet maintained muscular strength and endurance of upper and lower limbs during high-intensity resistance exercise without experiencing fatigue earlier compared with a control diet.

Oxysterols arise from the enzymic or non-enzymic oxidation of cholesterol and have been shown to be cytotoxic to certain cell lines. In particular, apoptosis induced by the oxysterol 7β-hydroxycholesterol (7β-OH) has been associated with the generation of oxidative stress, cytochrome c release and caspase activation. Due to the fundamental importance of apoptosis in pathological processes, the identification of substances capable of modulating this form of cell death is now actively researched. The objective of the present study was to investigate if apigenin, lycopene and astaxanthin could inhibit 7β-OH-induced apoptosis in U937 cells. Pretreatment with 0·1 μm-astaxanthin protected against apoptosis, while lycopene did not oppose the adverse effects of 7β-OH. At low concentrations, apigenin did not protect against oxysterol-induced apoptosis; however, at higher concentrations it intensified cell death. Additionally, we investigated the effect of 7β-OH, apigenin and astaxanthin on the activation of the serine threonine kinase Akt (phosphorylated Akt:Akt ratio) to determine whether the effect on cell viability and growth was linked to the Akt signalling pathway. Akt activation was decreased in the oxysterol-treated cells compared with control cells; however, this did not attain significance. Interestingly, activation of Akt was significantly reduced compared with control cells following incubation with apigenin and astaxanthin both in the absence and in the presence of 7β-OH. Our data suggest that apigenin, lycopene and astaxanthin failed to protect against 7β-OH-induced apoptosis, and the decrease in cell viability and the increase in apoptotic nuclei induced by the antioxidants appear to be associated with down regulation of Akt activity.

Colonic fermentation products, SCFA, have various effects on colonic functions. Here, we found that physiological concentrations of SCFA immediately promote epithelial barrier function in the large intestine. Solutions of mixed and individual SCFA were applied to the caecal walls mounted on Ussing-type chambers. Transepithelial electrical resistance (TER) increased rapidly and reached a peak 35 % higher than that in the control specimen within 10 min post application of the SCFA mixture (80 acetate, 40 propionate, 20 butyrate (mmol/l)). The Lucifer yellow permeability, a paracellular transport marker, was dose-dependently reduced by the mixed SCFA, acetate and propionate solutions. Inhibition of monocarboxylate transporter-1 did not influence the increase in TER with acetate; however, lowering the pH (from 7·5 to 5·5) clearly enhanced the effect of acetate. Non-metabolizable, bromo and chloro derivatives of SCFA also increased TER. These results suggest that passive diffusion of SCFA is dominant and the metabolism of SCFA is not required for the promotive effect of SCFA on barrier function. We also observed that individual SCFA dose-dependently increased TER in T84 and Caco-2 cells, which indicates that SCFA directly stimulate epithelial cells. Depletion of membrane cholesterol and inhibitors of phosphatidylinositol-3 kinase and Gq protein attenuated the acetate-mediated promotive effect. Finally, we found that the mucosal application of the SCFA mixture dose-dependently suppressed [3H] mannitol transport from the caecal lumen to the mesenteric blood in the anaesthetized rats. We conclude that physiological concentrations of SCFA immediately enhance barrier function of the colonic epithelium through cholesterol-rich microdomain in the plasma membrane.

The aim of the present study was to determine whether the addition of soluble fibre in the diet affected protein metabolism in the intestinal tissues, some visceral organs and in skeletal muscle. A diet supplemented with pectin (80 g/kg) was fed to young growing rats and the effect on organ mass and protein metabolism in liver, spleen, small and large intestines and gastrocnemius muscle was monitored and compared with the control group. Protein synthesis rates were determined by measuring [13C]valine incorporation in tissue protein. In the pectin-fed rats compared with the controls, DM intake and body weight gain were reduced (9 and 20 %, respectively) as well as gastrocnemius muscle, liver and spleen weights (6, 14 and 11 %, respectively), but the intestinal tissues were increased (64 %). In the intestinal tissues all protein metabolism parameters (protein and RNA content, protein synthesis rate and translational efficiency) were increased in the pectin group. In liver the translational efficiency was also increased, whereas its protein and RNA contents were reduced in the pectin group. In gastrocnemius muscle, protein content, fractional and absolute protein synthesis rates and translational efficiency were lower in the pectin group. The stimulation of protein turnover in intestines and liver by soluble fibre such as pectins could be one of the factors that explain the decrease in muscle turnover and whole-body growth rate.

The aim of this study was to examine the responses of uric acid, antioxidant defences and pro-oxidant variables after a high-fat meal. Twenty-five healthy persons without criteria for the metabolic syndrome, underwent a high-fat meal with Supracal® (60 g fat). Measurements were made at baseline and 3 h after the meal of TAG, uric acid, HDL-cholesterol, total proteins and oxidative stress. Following the high-fat meal, we detected a significant increase in pro-oxidative variables and a decrease in antioxidative variables. The uric acid concentrations were significantly lower after the high-fat meal and the reduction correlated significantly with the oxidative stress variables. The inverse relation between reduced uric acid and increased carbonylated proteins remained in multiple regression analysis. We conclude that uric acid is a powerful antioxidant and its reduction following a high-fat meal may be related with its acute antioxidative action.

A wide range of factors can be attributed to the syndrome of fatty liver observed in some cultured fish species. The objective of the study was therefore to quantify different hepatocyte ultrastructural features as potentially influenced by twelve nutritional and husbandry factors, in order to discriminate the most influent factors in Eurasian perch (Perca fluviatilis), a typical carnivorous temperate fish species. Twenty-four groups of juveniles (initial weight 57·6 (sd 14·4) g) were intensively reared for 116 d and fed sixteen different isoproteic diets. The distribution of the experimental treatments was based on a multivariate fractional factorial design (L24 212) with either high (+1) or low ( − 1) level of each of the following factors: diet (lipid and protein sources, lipid content, astaxanthin enrichment), feeding level, daily and weekly distribution frequency, fish density, initial weight heterogeneity, temperature, photoperiod, and light spectrum. Liver lipid droplets, glycogen, mitochondria and rough endoplasmic reticulum (RER) were semi-quantified and analysed by a soft imaging system using transmission electronic microscopy photographs. Important variability of hepatocyte ultrastructural features was observed. The present study confirms that the rearing temperature, through its influences in the general metabolic activity, seems to be the main factor modifying mainly lipid droplet accumulation and RER development. However, factors that could be pooled under the designation of factors leading to food accessibility and lipid and protein quality intensify or compensate the effect of temperature.

After birth, the gastrointestinal (GI) tract undergoes vast structural and functional adaptations to be able to digest mother's milk and later, during the weaning period, solid food. Studies on germ-free animals have shown the role of the gut microbiota for stimulating GI maturation, but which groups are involved is unclear. In the present study, we administered the probiotic bacterium, Lactobacillus plantarum 299v (Lp299v), in the drinking water to pregnant and lactating rat dams until their pups had reached an age of 14 d. It was found that Lp299v colonizing the mothers were also able to colonize the pups, which had an impact on their gut growth and function. The small intestine, pancreas and liver weighed more in the 14 d-old pups born from dams exposed to Lp299v than in the control pups from dams given only water. Furthermore, the Lp299v pups showed decreased gut permeability. Despite a heavier spleen in the Lp299v pups, as compared to the control pups, no significant increase in the acute-phase protein, haptoglobin, was found. In conclusion, the results reported here clearly show that manipulating the maternal microflora by exposing expecting mothers to a Gram-positive, probiotic bacterium prior to parturition and during lactation impacts the gut growth and function in the offspring.

Strategies to manipulate the intestinal microbiota have been considered to promote immune health. The aim of the present study was to examine whether fructo-oligosaccharide, a typical prebiotic, could suppress antigen-specific skin inflammation by favourably changing the population of intestinal microbiota. Female BALB/c mice were fed a synthetic diet with or without fructo-oligosaccharide supplementation for 3 weeks and were then epicutaneously immunised with 2,4-dinitrofluorobenzene. Afterwards, mice continued to receive their respective diets. At 5 d after immunisation, the mice were ear challenged with the hapten. Ear swelling after the challenge was significantly reduced in the mice fed the diet supplemented with fructo-oligosaccharide than in mice fed the control diet. To characterise the change in the intestinal microbiota, DNA samples isolated from fresh faeces were subjected to PCR–denaturing gradient gel electrophoresis and real-time PCR based on 16S rDNA gene sequences. Dietary fructo-oligosaccharide altered the composition of intestinal microbiota. The numbers of bifidobacteria, but not lactobacilli, were significantly higher in mice fed the fructo-oligosaccharide-supplemented diet than in mice fed the control diet. Ear swelling was negatively correlated with the numbers of bifidobacteria in the faeces. Sequence analysis revealed that Bifidobacterium pseudolongum was the most predominant bifidobacteria in the intestine of mice fed the fructo-oligosaccharide-supplemented diet. These results suggest that consumption of fructo-oligosaccharide reduces contact hypersensitivity, which is associated with proliferation of B. pseudolongum in the intestinal tract of mice.

Fish oils (FO) – rich in EPA and DHA – may protect against colitis development. Moreover, inflammatory bowel disease patients have elevated colonic arachidonic acid (AA) proportions. So far, effects of dietary AA v. FO on colitis have never been examined. We therefore designed three isoenergetic diets, which were fed to mice for 6 weeks preceding and during 7 d dextran sodium sulfate colitis induction. The control diet was rich in oleic acid (OA). For the other two diets, 1·0 % (w/w) OA was exchanged for EPA+DHA (FO group) or AA. At 7 d after colitis induction, the AA group had gained weight (0·46 (sem 0·54) g), whereas the FO and OA groups had lost weight ( − 0·98 (sem 0·81) g and − 0·79 (sem 1·05) g, respectively; P < 0·01 v. AA). The AA group had less diarrhoea than the FO and OA groups (P < 0·05). Weight and length of the colon, histological scores and cytokine concentrations in colon homogenates showed no differences. Myeloperoxidase concentrations in plasma and polymorphonuclear cell infiltration in colon were decreased in the FO group as compared with the OA group. We conclude that in this mice model an AA-enriched diet increased colonic AA content, but did not result in more colonic inflammation as compared with FO- and OA-enriched diets. As we only examined effects after 7 d and because the time point for evaluating effects seems to be important, the present results should be regarded as preliminary. Future studies should further elucidate differential effects of fatty acids on colitis development in time.

In mammals, (n-3) PUFA and conjugated linoleic acids (CLA) act as activators of PPARα and alter nuclear concentrations of sterol regulatory element-binding proteins (SREBP) in the liver, and thereby influence hepatic lipid catabolism and synthesis. In this study, we investigated the hypothesis that (n-3) PUFA and CLA exert similar effects in the liver of laying hens. Thirty hens (64 weeks old) were fed diets containing 30 g/kg of sunflower oil (control), fish oil (salmon oil) or CLA in TAG form (containing predominantly cis-9, trans-11 CLA and trans-10, cis-12 CLA) for 5 weeks. Hens fed fish oil had a higher expression of some PPARα target genes and a lower nuclear concentration of SREBP-2 in the liver and lower concentrations of cholesterol and TAG in plasma than control hens. Nuclear concentration of SREBP-1 and its target genes involved in lipogenesis were not altered in hens fed fish oil. Hens fed CLA had increased concentrations of TAG and cholesterol in the liver. However, their mRNA levels of PPARα target genes and nuclear concentrations of SREBP-1 and SREBP-2 as well as mRNA levels of their target genes in the liver were largely unchanged compared to control hens. The results of this study suggest that (n-3) PUFA cause a moderate activation of PPARα and lower cholesterol synthesis but do not impair fatty acid synthesis in the liver of laying hens. CLA lead to an accumulation of TAG and cholesterol in the liver of hens by mechanisms to be elucidated in further studies.

The usefulness of the glycaemic index (GI) of a food for practical advice for individuals with diabetes or the general population depends on its reliability, as estimated by intra-class coefficient (ICC), a measure having values between 0 and 1, with values closer to 1 indicating better reliability. We aimed to estimate the ICC of the postprandial blood glucose response to glucose and white bread, instant mashed potato and chickpeas using the incremental area under the curve (iAUC) and the GI of these foods. The iAUC values were determined in twenty healthy individuals on three and four occasions for white bread and glucose, respectively, and for potato and chickpeas on a single occasion. The ICC of the iAUC for white bread and glucose were 0·50 (95 % CI 0·27, 0·73) and 0·49 (95 % CI 0·22, 0·75), respectively. The mean GI of white bread was 81 (95 % CI 74, 90) with a reliability of 0·27 indicating substantial within-person variability. The GI of mashed potato and chickpeas were 87 (95 % CI 76, 101) and 28 (95 % CI 22, 37) respectively with ICC of 0·02 and 0·40.The ICC of the iAUC were moderate and those of the GI fair or poor, indicating the heterogeneous nature of individuals' responses. The unpredictability of individual responses even if they are the result of day-to-day variation places limitations on the clinical usefulness of GI. If the very different GI of potato and chickpeas are estimates of an individual's every-day response to different foods, then the GI of foods may provide an indication of the GI of a long-term diet.

The impact of apo E phenotypes on applicability of relative cholesterol synthesis (lathosterol:cholesterol) and absorption (ratios of cholestanol, campesterol and sitosterol to cholesterol) during diets of various cholesterol and fat content is unclear. We examined and compared with each other both relative and absolute synthesis and absorption among twenty-nine men, of whom eight, nine and twelve had apo E phenotypes 2 (2/2, 2/3, 2/4), 3 (3/3) and 4 (3/4, 4/4), respectively. Serum lipids, lipoproteins, sterols and cholesterol metabolism were examined on four subsequent diets: high-cholesterol high-fat (home diet; HD), low-cholesterol low-fat (LCLF), high-cholesterol low-fat (HCLF) and low-cholesterol high-fat (LCHF). LDL-cholesterol (LDL-C) level was about 40 % lower (P < 0·05) in apo E2 than apo E3 and E4 groups irrespective of dietary fat and cholesterol. Serum proportions of phytosterols were determined apo E-dependently on LCLF and HCLF, and those of lathosterol, cholestanol and campesterol were increased in apo E2 and E3 groups (P < 0·05 for each v. HD). Serum proportion of sitosterol reflected almost consistently apo E phenotype (r range+0·308 to+0·383; P range 0·214–0·011). Relative cholesterol synthesis and absorption reflected respective absolute values during each diet in the apo E4 group (r range+0·713 to+0·893; P < 0·05 for each), but only during HD (r+0·594; P = 0·015) in the apo E2+E3 group. The consumption of a high amount of fat did not interfere with cholesterol metabolism or serum levels of LDL-C differently in apo E phenotypes. Surrogate sterol markers of cholesterol metabolism reflected absolute ones (especially in the apo E4 group) and apo E phenotypes despite variable amounts of dietary cholesterol and fat.

This study aimed to investigate the clinical usefulness of an anthropometrically based method for estimating leg lean volume (LLV) in patients with chronic obstructive pulmonary disease (COPD) who presented or not with nutritional depletion. We prospectively evaluated a group of forty-eight patients (thirty-eight males) with moderate to severe COPD (Global Initiative for Chronic Obstructive Lung disease stages II–IV) who underwent a 6 min walking test and knee isokinetic dynamometry. Leg lean mass (muscle mass plus bone) was determined by dual-energy X-ray absorptiometry (DEXA) with derivation of its respective volume: these values were compared with those obtained by the truncated cones method first described by Jones and Pearson in 1969. As expected, depleted patients (n 19) had reduced exercise capacity and impaired muscle performance as compared to non-depleted subjects (P < 0·01). The mean bias of the LLV differences between anthropometry and DEXA were 0·40 litre (95 % CI − 0·59, 1·39) and 0·50 litre (95 % CI − 1·08, 2·08) for depleted and non-depleted patients, respectively. Anthropometrically and DEXA-based estimates correlated similarly with muscle functional attributes. A ROC curve analysis revealed that leg height-corrected LLV values had acceptable sensitivity and specificity to identify depleted patients (area under the curve 0·93 (range 0·86–1·00); P < 0·001). Moreover, patients with LLV ≤ 9·2 litres/m (the best cut-off value according to the ROC curve) had significantly lower exercise capacity and muscle performance than their counterparts (P < 0·05). In conclusion, an anthropometrically based method of estimating LLV (Jones and Pearson method) was shown to present with clinically acceptable accuracy and external validity in depleted and non-depleted patients with stable COPD.