Previously, we have shown that satiety and metabolites increased after high-fat modified sham feeding (MSF). We assessed possible metabolic effects due to oral stimulation with a high-fat sham-fed ‘meal’, in comparison with a high-fat fed meal and with water, in the postprandial state. Fourteen healthy women (aged 18–40 years; BMI 22·5 (sd 3) kg/m2) were fed in energy balance during 4 d with a 50 % enegy as carbohydrate, 15 % energy as protein and 35 % energy as fat menu. On day 4, subjects were given one out of three test lunches, 5 h after a high-fat breakfast, in random order: a high-fat MSF lunch, water (W) or the same lunch to be eaten (E), during their 36 h stay in the respiration chamber, where substrate oxidation, 24 h energy expenditure (EE) and appetite profile were measured. Oral fat stimulation by MSF increased EE (W 6·3 (sd 0·8) v. MSF 6·9 (sd 1·0) kJ/min and E 6·8 (sd 0·7) kJ/min; P < 0·04) for 1 h, increased plasma insulin concentrations (t = 15; W 10·0 (sd 3·4) v. MSF 13·2 (sd 4·0) v. E 22·3 (sd 3·3) units/l; P < 0·0001), attenuated changes in plasma NEFA concentrations (t = 15, W 432 (sd 108) v. MSF 418 (sd 146) v. E 282 (sd 72) μmol/l; P < 0·0001), plasma TAG concentrations (t = 60; W 1092 (sd 548) v. MSF 1116 (sd 493) μmol/l and E 1350 (sd 352) μmol/l; P < 0·02) and plasma glycerol concentrations (t = 15, W 87 (sd 29) v. MSF 74 (sd 34) μmol/l and E 67 (sd 18) μmol/l; P < 0·03). Over a longer period of time, MSF had no effects on substrate oxidation, diet-induced thermogenesis or total EE. In addition to the previously observed metabolic effects of oral stimulation with fat, EE is stimulated up to 1 h after the MSF meal.

Balanced glucose metabolism ensures optimal fetal growth with long-term health implications conferred on both mother and child. We examined whether supplementation of probiotics with dietary counselling affects glucose metabolism in normoglycaemic pregnant women. At the first trimester of pregnancy 256 women were randomised to receive nutrition counselling to modify dietary intake according to current recommendations or as controls; the dietary intervention group was further randomised to receive probiotics (Lactobacillus rhamnosus GG and Bifidobacterium lactis Bb12; diet/probiotics) or placebo (diet/placebo) in a double-blind manner, whilst the control group received placebo (control/placebo). Blood glucose concentrations were lowest in the diet/probiotics group during pregnancy (baseline-adjusted means 4·45, 4·60 and 4·56 mmol/l in diet/probiotics, diet/placebo and control/placebo, respectively; P = 0·025) and over the 12 months' postpartum period (baseline-adjusted means 4·87, 5·01 and 5·02 mmol/l; P = 0·025). Better glucose tolerance in the diet/probiotics group was confirmed by a reduced risk of elevated glucose concentration compared with the control/placebo group (OR 0·31 (95 % CI 0·12, 0·78); P = 0·013) as well as by the lowest insulin concentration (adjusted means 7·55, 9·32 and 9·27 mU/l; P = 0·032) and homeostasis model assessment (adjusted means 1·49, 1·90 and 1·88; P = 0·028) and the highest quantitative insulin sensitivity check index (adjusted means 0·37, 0·35 and 0·35; P = 0·028) during the last trimester of pregnancy. The effects observed extended over the 12-month postpartum period. The present study demonstrated that improved blood glucose control can be achieved by dietary counselling with probiotics even in a normoglycaemic population and thus may provide potential novel means for the prophylactic and therapeutic management of glucose disorders.

A single bout of prolonged, moderate-intensity endurance exercise lowers fasting and postprandial TAG concentrations the next day. However, the TAG-lowering effect of exercise is dose-dependent and does not manifest after light exercise of low energy cost ( < 2 MJ). We aimed to investigate whether superimposing mild energy intake restriction to such exercise, in order to augment total energy deficit, potentiates the hypotriacylglycerolaemic effect. Eight healthy, sedentary, premenopausal women (age 27·1 (sem 1·3) years; BMI 21·8 (sem 0·9) kg/m2) performed two oral fat tolerance tests in the morning on two different occasions: once after a single bout of light exercise (100 min at 30 % of peak oxygen consumption; net energy expenditure 1·04 (sem 0·01) MJ) coupled with mild energy intake restriction (1·39 (sem 0·22) MJ) on the preceding day, and once after resting coupled with isoenergetic feeding on the preceding day (control). Fasting plasma TAG, TAG in the TAG-rich lipoproteins (TRL-TAG) and serum insulin concentrations were 18, 34 and 30 % lower, respectively, after exercise plus diet compared with the control trial (P < 0·05). Postprandial concentrations of plasma TAG and TRL-TAG were 19 and 27 % lower after exercise plus diet compared with the control condition (P < 0·01), whereas postprandial insulin concentrations were not different. It is concluded that a combination of light exercise along with mild hypoenergetic diet may be a practical and feasible intervention to attenuate fasting and postprandial triacylglycerolaemia, especially for people who cannot exercise for prolonged periods of time at moderate-to-high intensities, such as many sedentary individuals.

n-3 long-chain PUFA (n-3 LC-PUFA) may improve cardiovascular and inflammatory diseases. The effects of n-3 LC-PUFA-supplemented dairy products on inflammation and immunological parameters, biomarkers of oxidative stress, serum lipids, and on disease activity were determined in patients with rheumatoid arthritis (RA). Forty-five subjects (forty-three females and two males) were randomly divided into two groups in a double-blind, placebo-controlled cross-over study. Both groups received placebo or verum products consecutively for 3 months with a 2-month washout phase between the two periods. Blood samples were taken at the beginning and at the end of each period. The dairy products generally improved serum lipids by increasing HDL and lowering lipoprotein a. The n-3 LC-PUFA supplements act to lower TAG. Additionally, a decreased lipopolysaccharide-stimulated cylo-oxygenase-2 expression was found in patients who had consumed the enriched dairy products. The majority of the CD analysed were not influenced, although n-3 LC-PUFA did suppress the immune response as lymphocytes and monocytes were found to be significantly decreased. The n-3 LC-PUFA did not increase the biomarkers of oxidative stress such as 8-iso-PGF2α and 15-keto-dihydro PGF2α, and DNA damage like 7,8-dihydro-8-oxo-2′-deoxyguanosine. The long-term consumption of dairy products (2 × 12 weeks) diminished the excretion of hydroxypyridinium crosslinks, and favoured the diastolic blood pressure. The consumption of moderate doses of n-3 LC-PUFA in combination with dairy products did not improve the disease activity. However, there is evidence of cardioprotective effects. Furthermore, the long-term consumption of dairy products acts against the cartilage and bone destruction in RA.

An increased risk of renal cell carcinoma (RCC) has been linked with obesity. However, there is limited information about the contribution of dietary fat and fat-related food groups to RCC risk. A population-based case–control study of 406 cases and 2434 controls aged 40–85 years was conducted in Iowa (1986–89). For 323 cases and 1820 controls from the present study, information on dietary intake from foods high in fat nutrients and other lifestyle factors was obtained using a mailed questionnaire. Cancer risks were estimated by OR and 95 % CI, adjusting for age, sex, smoking, obesity, hypertension, physical activity, alcohol and vegetable intake and tea and coffee consumption. In all nutrient analyses, energy density estimates were used. Dietary nutrient intake of animal fat, saturated fat, oleic acid and cholesterol was associated with an elevated risk of RCC (OR = 1·9, 95 % CI 1·3, 2·9, Ptrend < 0·001; OR = 2·6, 95 % CI 1·6, 4·0, Ptrend < 0·001; OR = 1·9, 95 % CI 1·2, 2·9, Ptrend = 0·01; OR = 1·9, 95 % CI 1·3, 2·8, Ptrend = 0·006, respectively, for the top quartile compared with the bottom quartile of intake). Increased risks were also associated with high-fat spreads, red and cured meats and dairy products (OR = 2·0, 95 % CI 1·4, 3·0, Ptrend = 0·001; OR = 1·7, 95 % CI 1·0, 2·2, Ptrend = 0·01; OR = 1·8, 95 % CI 1·2, 2·7, Ptrend = 0·02; OR = 1·6, 95 % CI 1·1, 2·3, Ptrend = 0·02, respectively). In both the food groups and nutrients, there was a significant dose–response with increased intake. Our data also indicated that the association of RCC with high-fat spreads may be stronger among individuals with hypertension. These findings deserve further investigation in prospective studies.

The objective of this study was to provide data on malnutrition prevalence in hospitals, nursing homes and home-care organisations in The Netherlands in a nationally representative sample, and to assess the factors such as age, sex, time since admission, ward type and disease for identifying patients at high risk of malnutrition. A cross-sectional, multi-centre design with a standardised questionnaire was used to measure the prevalence of malnutrition. Nutritional status was assessed by BMI, undesired weight loss and nutritional intake. In this study, 12 883 patients were included. The prevalence of malnutrition was the highest in hospitals (23·8 %), followed by home-care organisations (21·7 %) and nursing homes (19·2 %). Logistic regression analysis revealed no association with age, time since admission and ward type. Being female was associated with malnutrition only in nursing homes. Blood diseases, gastrointestinal tract diseases, infection, chronic obstructive pulmonary disease, dementia and cancer were the factors associated with malnutrition in hospitals. Dementia was associated with malnutrition in nursing homes, while gastrointestinal tract diseases, diabetes mellitus and cancer were the associated factors in home care. This study shows that malnutrition is still a substantial problem in hospitals, nursing homes and home care in The Netherlands. Malnutrition is a problem for more than one in five patients. Despite growing attention to the problem, more continued alertness is required.

Generalised skinfold equations developed in the 1970s are commonly used to estimate laboratory-measured percentage fat (BF%). The equations were developed on predominately white individuals using Siri's two-component percentage fat equation (BF%-GEN). We cross-validated the Jackson–Pollock (JP) generalised equations with samples of young white, Hispanic and African–American men and women using dual-energy X-ray absorptiometry (DXA) as the BF% referent criterion (BF%-DXA). The cross-sectional sample included 1129 women and men (aged 17–35 years). The correlations between BF%-GEN and BF%-DXA were 0·85 for women and 0·93 for men. Analysis of measurement error showed that BF%-GEN underestimated BF%-DXA of men and women by 1·3 and 3·0 %. General linear models (GLM) confirmed that BF%-GEN systematically underestimated BF%-DXA of Hispanic men and women, and overestimated BF%-DXA of African–American men. GLM were used to estimate BF%-DXA from the JP sum of skinfolds and to account for race/ethnic group bias. The fit statistics (R and standard error of the estimate; see) of the men's calibration model were: white, R 0·92, see 3·0 %; Hispanic, R 0·91, see 3·0 %; African–American, R 0·95, see 2·6 %. The women's statistics were: white and African–American, R 0·86, see 3·8 %; Hispanic, R 0·83, see 3·4 %. These results showed that BF%-GEN and BF%-DXA were highly correlated, but the error analyses documented that the generalised equations lacked accuracy when applied to these racially and ethnically diverse men and women. The inaccuracy was linked to the body composition and race/ethnic differences between these Training Intervention and Genetics of Exercise Response (TIGER) study subjects and the men and women used to develop the generalised equations in the 1970s and using BF%-DXA as the referent criterion.

Inflammation and endothelial activation are associated with an increased risk of CVD and epidemiological evidence suggests an association between levels of markers of inflammation or endothelial activation and the intake of fruit. Also, vitamin E, a fat-soluble antioxidant, has anti-inflammatory properties. We performed a randomised 2 × 2 factorial, crossover trial to determine the effect of orange and blackcurrant juice (500 ml/d) and vitamin E (15 mg RRR-α-tocopherol/d) supplementation on markers of inflammation and endothelial activation in forty-eight patients with peripheral arterial disease. Patients were randomly allocated to two dietary supplements from the four possible combinations of juice and vitamin E: juice+vitamin E; juice+placebo; reference beverage (sugar drink)+vitamin E; and reference beverage+placebo. The supplementations were given for 28 d, separated by a 4-week wash-out period. Analysis of main effects showed that juice decreased C-reactive protein (CRP) by 11 % and fibrinogen by 3 % while the reference drink increased CRP by 13 % and fibrinogen by 2 % (P < 0·008 and P < 0·002, respectively). No significant differences were measured for IL-6 and the endothelial activation markers von Willebrand factor, tissue-plasminogen activator and plasmin activator inhibitor-1. Vitamin E supplementation had no significant effects on the various markers. We observed no significant interaction between juice and vitamin E. In this study, orange and blackcurrant juice reduced markers of inflammation, but not markers of endothelial activation, in patients with peripheral arterial disease, relative to sugar drinks.

Measurements of body composition are crucial in identifying HIV-infected patients at risk of malnutrition. No information is available on the validity of indirect body composition methods in African HIV-infected outpatients. Our first aim was to test the validity of fifteen published equations, developed in whites, African-Americans and/or Africans who were or not HIV-infected, for predicting total body water (TBW) from bioelectrical impedance analysis (BIA) in HIV-infected patients. The second aim was to develop specific predictive equations. Thirty-four HIV-infected patients without antiretroviral treatment and oedema at the beginning of the study (age 39 (sd 7) years, BMI 18·7 (sd 3·7) kg/m2, TBW 30·4 (sd 7·2) kg) were measured at inclusion then 3 and 6 months later. In the resulting eighty-eight measurements, we compared TBW values predicted from BIA to those measured by 2H dilution. Range of bias values was 0·1–4·3 kg, and errors showed acceptable values (2·2–3·4 kg) for fourteen equations and a high value (10·4) for one equation. Two equations developed in non-HIV-infected subjects showed non-significant bias and could be used in African HIV-infected patients. In the other cases, poor agreement indicated a lack of validity. Specific equations developed from our sample showed a higher precision of TBW prediction when using resistance at 1000 kHz (1·7 kg) than at 50 kHz (2·3 kg), this latter precision being similar to that of the valid published equations (2·3 and 2·8 kg). The valid published or developed predictive equations should be cross-validated in large independent samples of African HIV-infected patients.

Lactation is known to be associated with a transient loss of bone mineral density (BMD) during 3–6 months post-partum. Bone changes during lactation in women consuming low dietary calcium are not sufficiently studied. The present longitudinal study examined the BMD changes during lactation in undernourished women and the relationship of bone changes to the nutritional status. Whole-body bone mineral content and BMD at hip, lumbar spine and forearm were assessed using dual-energy X-ray absorptiometry in thirty-six lactating women from the low socio-economic group at four time points – within 1 month after delivery (baseline), and at 6, 12 and 18 months after delivery. Maternal body composition and biochemical parameters of bone metabolism were estimated at the same time. It was observed that femoral neck BMD reduced by 4·6 % at 6 months, but recovery to the baseline was incomplete at 18 months with a deficit of 2 %. Hip BMD reduction at 6 months was transient. Lumbar spine BMD did not show significant loss at 6 months and BMD increased by 3·6 and 6·3 % at 12 and 18 months, respectively. Regression analyses indicated that baseline lean mass was the most important determinant of bone preservation at femoral neck, hip as well as whole body, whereas baseline body weight was the most important determinant of per cent gain in lumbar spine. Maternal nutritional status as indicated by body weight and lean mass appears to influence the lactation-related BMD changes in undernourished women from the low socio-economic group in India.

We previously demonstrated that safflower seed extract (SSE) and its major antioxidant constituents, serotonin hydroxycinnamic acid amides, suppressed LDL oxidation in vitro, decreased plasma autoantibody titres to oxidized LDL and attenuated atherosclerotic lesion formation in apoE-deficient mice. In this report, we examined whether SSE, rich in serotonin derivatives, could affect markers of oxidative stress, inflammation and aortic stiffness in healthy human subjects. Twenty Japanese male volunteers were studied at baseline, after 2·1 g SSE supplementation daily (providing 290 mg serotonin derivatives/d) for 4 weeks, and after a 4-week washout period. Significant reductions in circulating oxidized LDL, autoantibody titres to malondialdehyde-modified LDL, the soluble form of vascular cell adhesion molecule-1 (sVCAM-1), and urinary 8-isoprostane were observed after a 4-week intervention. Although there were no statistically significant differences in blood pressure or brachial–ankle pulse wave velocity (baPWV), an index of arterial stiffness, baPWV was lower than baseline in eleven of twenty subjects and was accompanied by a reduction in blood pressure. Statistically significant negative correlations were observed between the extent of initial cardiovascular risk markers (autoantibody titres, 8-isoprostane, sVCAM-1 and baPWV) and the effect of intervention. This suggested that individuals with elevated oxidative stress, inflammation, and/or arterial stiffness may receive more benefit from SSE supplementation.

The aim of the present study was to analyse the association between adherence to the Mediterranean diet and self-perceived mental and physical health function, controlled for confounding effects of age, smoking, BMI, alcohol consumption, educational level, leisure-time physical activity and the presence of chronic conditions. A random sample of the 35–74-year-old population (3910 men and 4285 women) of Gerona, Spain, was examined in 2000 and 2005 in two independent population-based cross-sectional surveys. Dietary intake was assessed using a validated FFQ. The Mediterranean diet score (MDS) was calculated according to tertile distribution of energy-adjusted food consumption considered characteristic for the Mediterranean region. Health-related quality of life was measured using the SF-12 questionnaire. Alcohol consumption, leisure-time physical activity and smoking habits were recorded. Weight and height were measured. Age-adjusted linear regression analysis revealed a significant (P < 0·01) direct association of the MDS with self-reported mental and physical health in both sexes. An increase of 5 units of the MDS was directly associated with changes of 0·74 and 1·15 units in men and women, respectively, in the mental component score after controlling for potential confounders. The age-adjusted direct association of the MDS with self-reported scoring of physical health remained stable after adjusting for several confounders in men but was attenuated in women. Adherence to the Mediterranean diet was associated with higher scoring for self-perceived health.

Polymorphisms of the ABCG5 and ABCG8 genes interfere with cholesterol absorption and synthesis. We determined whether common polymorphisms of these genes regulate the responses of serum cholesterol and vascular function during long-term inhibition of cholesterol absorption. Mildly to moderately hypercholesterolaemic subjects (n 282) completed a 1-year study consuming plant stanol or sterol ester (2 g stanol or sterol) or control spread. Serum cholesterol and non-cholesterol sterols, markers of cholesterol absorption and synthesis, and variables of vascular function and structure were analysed in relation to common polymorphisms of ABCG5 and ABCG8. At baseline, subjects with the 54K allele of ABCG8 had higher brachial endothelial-dependent flow-mediated dilatation than those without it (5·79 (se 0·31) v. 4·46 (se 0·44) %; P = 0·049), and subjects with the 632V allele of ABCG8 had larger brachial artery diameter than those without it. Polymorphisms of ABCG5 and ABCG8 were neither associated with serum cholesterol reduction nor changes in cholesterol metabolism or in vascular function. However, in subjects with the 400K allele of ABCG8, intima media thickness (IMT) was increased in all groups more than in those without it (P < 0·05). In conclusion, serum cholesterol lowering with absorption inhibition was not associated with polymorphic sites of ABCG5 and ABCG8. However, regulation of baseline cholesterol metabolism and vascular function and structure, and IMT progression during 1 year seemed to share some of the common polymorphic sites of these genes, suggesting a gene-regulated interaction between cholesterol metabolism and vascular function and structure.

Added sugars are often viewed as ‘empty calories’, negatively impacting micronutrient intakes, yet reviews consider the evidence inconclusive. This study aimed to quantify associations between dietary added sugars (as a percentage of energy) and micronutrient intake and biochemical status in the National Diet and Nutrition Survey. Using data from 1688 British children aged 4–18 years who completed 7 d weighed dietary records in 1997, micronutrient intakes were examined across quintiles of added sugars. After excluding low energy reporters, mean dietary intakes of most nutrients exceeded the reference nutrient intake, except for zinc. Compared with quintile 1 (9 % added sugars), high consumers in quintile 5 (23 % added sugars) had micronutrient intakes ranging from 24 % lower to 6 % higher (mean 14 % lower). Zinc intakes in quintile 1 v. quintile 5 averaged 93 % v. 78 % of reference nutrient intake; magnesium 114 % v. 94 %; iron 115 % v. 100 %; and vitamin A 111 % v. 92 %, respectively. Plasma levels of magnesium, zinc and carotenoids did not vary across quintiles, but weak negative correlations were observed with serum ferritin and transferrin saturation. Plasma selenium was inversely correlated with added sugars (r − 0·17; P < 0·0001) but there was no association with glutathione peroxidase. The impact of added sugars on micronutrient intakes appears modest overall but may have relevance for children consuming inadequate amounts of nutrient-rich foods coupled with a diet high in added sugars (approximately 23 %). Further work is needed to explore the impact of different sources of added sugars and to refine assessments of inadequate intakes and status.

High prevalences of vitamin D deficiency have been reported in non-Western immigrants moving to Western countries, including Norway, but there is limited information on vitamin D status in infants born to immigrant mothers. We aimed to describe the vitamin D status and potentially correlated factors among infants aged 6 weeks and their mothers with Pakistani, Turkish or Somali background attending child health clinics in Norway. Eighty-six healthy infants and their mothers with immigrant background were recruited at the routine 6-week check-up at nine centres between 2004 and 2006. Venous or capillary blood was collected at the clinics from the mother and infant, and serum separated for analysis of 25-hydroxyvitamin D (s-25(OH)D) and intact parathyroid hormone (s-iPTH). The mean maternal s-25(OH)D was 25·8 nmol/l, with 57 % below 25 nmol/l and 15 % below 12·5 nmol/l. Of the mothers, 26 % had s-iPTH>5·7 pmol/l. For infants, mean s-25(OH)D was 41·7 nmol/l, with 47 % below 25 nmol/l and 34 % below 12·5 nmol/l. s-25(OH)D was considerably lower in the thirty-one exclusively breast-fed infants (mean 11·1 nmol/l; P < 0·0001). Use of vitamin D supplements and education showed a positive association with maternal s-25(OH)D. There was no significant association between mother's and child's s-25(OH)D, and no significant ethnic or seasonal variation in s-25(OH)D for mothers or infants. In conclusion, there is widespread vitamin D deficiency in immigrant mothers and their infants living in Norway. Exclusively breast-fed infants who did not receive vitamin D supplements had particularly severe vitamin D deficiency.

The impact of nutrition on the epigenetic machinery has increasingly attracted interest. The aim of the present study was to demonstrate the effects of various diets on methylation and gene expression. The antioxidative enzyme mitochondrial superoxide dismutase (MnSOD) was chosen as the model system because epigenetic regulation has been previously shown in cell lines for this gene. Promoter methylation and gene expression of MnSOD in buccal swabs from three sample groups were analysed. The three groups included: (1) forty vegetarians (aged 20–30 years); (2) age-matched omnivores; (3) elderly omnivores (aged>85 years). A 3-fold increase in the expression of the MnSOD gene was associated with decreased CpG methylation of the analysed promoter region in the vegetarian group compared with the age-matched omnivores group. Expression and promoter methylation of the MnSOD gene in elderly omnivores showed no significant differences compared with younger omnivores. In accordance with previous findings in various tissues, DNA global methylation was found to be significantly higher (30 %) in buccal swabs of younger subjects (independent of the diet), than in those of elderly omnivores. In the control experiment which was designed to verify the findings of the human buccal swab studies, the Caco-2 cell line was treated with zebularine. Results of the control study showed a 6-fold increase of MnSOD expression, an approximately 40 % decreased methylation of specified CpG in the MnSOD promoter and a 50 % reduction of global DNA methylation. These results indicate that diet affects the epigenetic regulation of human MnSOD.

Previous studies have demonstrated that the n-3 fatty acid EPA improves insulin resistance induced by high-fat diets. The aim of the present study was to investigate the potential role of visfatin and apelin in the insulin-sensitising effects of EPA ethyl ester. The effects of EPA on muscle and adipose GLUT mRNA, as well as on liver glucokinase (GK) and glucose-6-phosphatase (G6Pase) activity, were investigated. Male Wistar rats fed on a standard diet or a high-fat cafeteria diet were daily treated by oral administration with EPA ethyl ester (1 g/kg) for 5 weeks. A significant decrease (P < 0·01) in white adipose tissue (WAT) visfatin mRNA levels was found in the cafeteria-fed rats, which was reversed by EPA administration (P < 0·05). Moreover, a negative relationship was observed between homeostatic model assessment (HOMA) and the visfatin:total WAT ratio. In contrast, cafeteria-diet feeding caused a significant increase (P < 0·01) in apelin mRNA in visceral WAT. EPA increased (P < 0·01) apelin gene expression, and a negative relationship between HOMA index with visceral apelin mRNA and serum apelin:total WAT ratio was also observed. EPA treatment did not induce changes in skeletal muscle GLUT1, GLUT4 or insulin receptor mRNA levels. Neither liver GK and G6Pase activity nor the GK:G6Pase ratio was modified by EPA. These data suggest that somehow the insulin-sensitising effects of EPA could be related to its stimulatory action on both visfatin and apelin gene expression in visceral fat, while changes in skeletal muscle GLUT, as well as in hepatic glucose production, are not likely to be the main contributing factors in the improvement in insulin resistance induced by EPA.

Anthropometric indices of adiposity include BMI, waist circumference and waist:height ratio. In the recruitment phase of a prospective cohort study carried out between 1998 and 2002 we studied a population sample of 11 786 white Caucasian non-pregnant women in Southampton, UK aged 20–34 years, and explored the extent to which proposed cut-off points for the three indices identified the same or different women and how these indices related to adiposity. Height, weight and waist circumference were measured and fat mass was estimated from skinfold thicknesses; fat mass index was calculated as fat mass/height1·65. Of the subjects, 4869 (42 %) women were overweight (BMI ≥ 25 kg/m2) and 1849 (16 %) were obese (BMI ≥ 30 kg/m2). A total of 890 (8 %) subjects were not overweight but had a waist circumference ≥ 80 cm and 748 (6 %) subjects were overweight but had a waist circumference < 80 cm (6 %). Of the women, 50 % had a BMI ≥ 25 kg/m2 or a waist circumference ≥ 80 cm or a waist:height ratio ≥ 0·5. Of the variation in fat mass index, 85 % was explained by BMI, 76 % by waist circumference and 75 % by waist:height ratio. Our findings demonstrate that many women are differentially classified depending on which index of adiposity is used. As each index captures different aspects of size in terms of adiposity, there is the need to determine how the three indices relate to function and how they can be of use in defining risk of ill health in women.