The purpose of this study was to determine if the mixed evidence of almond consumption on HbA1c stems from testing people with different body fat distributions (BFD) associated with different risks of glucose intolerance. A 6-month randomised controlled trial in 134 adults was conducted. Participants were randomly assigned to the almond (A) or control (C) group based on their BFD. Those in the almond group consumed 1·5 oz of almonds with their breakfast and as their afternoon snack daily. Those in the control group continued their habitual breakfast and afternoon snack routines. Body weight and composition were measured and blood samples were collected for determination of HbA1c, glycaemia and lipaemia at 0 and 6 months. Appetite ratings, energy intake and diet quality were collected at 0, 2, 4 and 6 months. Participants consuming almonds ingested 816 (sem 364) kJ/d more than participants in the control group (P = 0·03), but this did not result in any differences in body weight (A: –0·3 (sem 0·4), C: –0·4 (sem 0·4); P > 0·3). Participants in the almond, high android subcutaneous adipose tissue (SAT) group had a greater reduction in android fat mass percentage (A: –1·0 (sem 0·6), C: 1·1 (sem 0·6); P = 0·04), preserved android lean mass percentage (A: 0·9 (sem 0·6), C: –1 (sem 0·6); P = 0·04) and tended to decrease android visceral adipose tissue mass (A: –13 (sem 53) g, C: 127 (sem 53) g; P = 0·08) compared with those in the control, high SAT group. There were no differences in HbA1c between groups (A: 5·4 (sem 0·04), C: 5·5 (sem 0·04); P > 0·05). Thus, BFD may not explain the mixed evidence on almond consumption and HbA1c. Long-term almond consumption has limited ability to improve cardiometabolic health in those who are overweight and obese but otherwise healthy.

During menopause, women undergo a series of physiological changes that include a redistribution of fat tissue. This study was designed to investigate the effect of adding 10 g of cocoa-rich chocolate to the habitual diet of postmenopausal women daily on body composition. We conducted a 6-month, two-arm randomised, controlled trial. Postmenopausal women (57·2 (sd 3·6) years, n 132) were recruited in primary care clinics. Participants in the control group (CG) did not receive any intervention. Those of the intervention group (IG) received 10 g daily of 99 % cocoa chocolate in addition to their habitual diet for 6 months. This quantity comprises 247 kJ (59 kcal) and 65·4 mg of polyphenols. The primary outcomes were the between-group differences in body composition variables, measured by impendancemetry at the end of the study. The main effect of the intervention showed a favourable reduction in the IG with respect to the CG in body fat mass (–0·63 kg (95 % CI –1·15, –0·11), P = 0·019; Cohen’s d = –0·450) and body fat percentage (–0·79 % (95 % CI –1·31, –0·26), P = 0·004; Cohen’s d = –0·539). A non-significant decrease was also observed in BMI (–0·20 kg/m2 (95 % CI –0·44, 0·03), P = 0·092; Cohen’s d = –0·345). Both the body fat mass and the body fat percentage showed a decrease in the IG for the three body segments analysed (trunk, arms and legs). Daily addition of 10 g of cocoa-rich chocolate to the habitual diet of postmenopausal women reduces their body fat mass and body fat percentage without modifying their weight.

We aimed to identify the association of hydration status with insulin resistance (IR) and body fat distribution. A total of 14 344 adults participated in the Korea National Health and Nutrition Examination Survey 2008–2010. We used urine specific gravity (USG) to indicate hydration status, and HOMA-IR (homoeostasis model assessment of IR) and trunk:leg fat ratio (TLR) as primary outcomes. In multivariate logistic regression, the OR per 0·01 increase in USG for high IR was 1·303 (95 % CI 1·185, 1·433; P < 0·001). In multivariate generalised additive model plots, increased USG showed a J-shaped association with logarithmic HOMA-IR, with the lowest Akaike’s information criterion score of USG 1·030. Moreover, increased USG was independently associated with increased trunk fat, decreased leg fat and increased TLR. In mediation analysis, the proportion of mediation effects of USG on TLR via IR was 0·193 (95 % CI 0·132, 0·285; P < 0·001), while the proportion of mediation effects of USG on IR via TLR was 0·130 (95 % CI 0·086, 0·188; P < 0·001). Increased USG, a sign of low hydration status and presumably high vasopressin, was associated with IR and poor fat distribution. Direct effect of low hydration status may be more dominant than indirect effect via IR or fat distribution. Further studies are necessary to confirm our findings.

Body fat distribution, especially visceral fat accumulation, may contribute more than total fat mass per se to the development of metabolic and cardiovascular disorders. Early prevention highly improves health outcomes later in life, especially when considering such cumulative conditions as atherosclerosis. However, as these processes emerge to be partly reversible, dietary and lifestyle interventions at any age and health condition are greatly beneficial. Given the worldwide abundance of metabolic and cardiovascular disorders, the identification and implementation of strategies for preventing or reducing the accumulation of morbid fat tissues is of great importance for preventing and regressing atherosclerosis. This review focuses on dietary strategies and specific food components that were demonstrated to alter body fat distribution and regression of atherosclerosis. Different properties of various adipose depots (superficial subcutaneous, deep subcutaneous and visceral fat depots) and their contribution to metabolic and cardiovascular disorders are briefly discussed. Visceral obesity and atherosclerosis should be approached as modifiable rather than ineluctable conditions.

Excess body adiposity, especially abdominal obesity and ectopic fat accumulation, are key risk factors in the development of a number of chronic diseases. The advent of in vivo imaging methodologies that allow direct assessment of total body fat and its distribution have been pivotal in this process. They have helped to identify a number of sub-phenotypes in the general population whose metabolic risk factors are not commensurate with their BMI. At least two such sub-phenotypes have been identified: subjects with normal BMI, but excess intra-abdominal (visceral) fat (with or without increased ectopic fat) and subjects with elevated BMI (> 25 kg/m2) but low visceral and ectopic fat. The former sub-phenotype is associated with adverse metabolic profiles, while the latter is associated with a metabolically normal phenotype, despite a high BMI. Here, examples of these phenotypes are presented and the value of carrying out enhanced phenotypical characterisation of subjects in interventional studies discussed.

Age-related changes in leptin and adiponectin levels remain controversial, being affected by inconsistent normalisation for adiposity and body fat distribution in the literature. In a cross-sectional study on 210 Caucasians (127 women, eighty-three men, 18–78 years, BMI 16·8–46·8 kg/m2), we investigated the effect of age on adipokine levels independent of fat mass (FM measured by densitometry), visceral and subcutaneous adipose tissue volumes (VAT and SAT assessed by whole-body MRI). Adiponectin levels increased with age in both sexes, whereas leptin levels decreased with age in women only. There was an age-related increase in VAT (as a percentage of total adipose tissue, VAT%TAT), associated with a decrease in SATlegs%TAT. Adiposity was the main predictor of leptin levels, with 75·1 % of the variance explained by %FM in women and 76·6 % in men. Independent of adiposity, age had a minor contribution to the variance in leptin levels (5·2 % in women only). The variance in adiponectin levels explained by age was 14·1 % in women and 5·1 % in men. In addition, independent and inverse contributions to the variance in adiponectin levels were found for truncal SAT (explaining additional 3·0 % in women and 9·1 % in men) and VAT%TAT (explaining additional 13·0 % in men). In conclusion, age-related changes in leptin and adiponectin levels are opposite to each other and partly independent of adiposity and body fat distribution. Normalisation for adiposity but not for body fat distribution is required for leptin. Adiponectin levels are adversely affected by subcutaneous and visceral trunk fat.

Body fat distribution plays an important role in determining metabolic health. Whereas central obesity is closely associated with the development of CVD and type 2 diabetes, lower body fat appears to be protective and is paradoxically associated with improved metabolic and cardiovascular profiles. Physiological studies have demonstrated that fatty acid handling differs between white adipose tissue depots, with lower body white adipose tissue acting as a more efficient site for long-term lipid storage. The regulatory mechanisms governing these regional differences in function remain to be elucidated. Although the local microenvironment is likely to be a contributing factor, recent findings point towards the tissues being intrinsically distinct at the level of the adipocyte precursor cells (pre-adipocytes). The multi-potent pre-adipocytes are capable of generating cells of the mesenchymal lineage, including adipocytes. Regional differences in the adipogenic and replicative potential of these cells, as well as metabolic and biochemical activity, have been reported. Intriguingly, the genetic and metabolic characteristics of these cells can be retained through multiple generations when the cells are cultured in vitro. The rapidly emerging field of epigenetics may hold the key for explaining regional differences in white adipose tissue gene expression and function. Epigenetics describes the regulation of gene expression that occurs independently of changes in DNA sequence, for instance, DNA methylation or histone protein modification. In this review, we will discuss the contribution of DNA methylation to the determination of cells of adipogenic fate as well as the role DNA methylation may play during adipocyte terminal differentiation.

The aim of the present study was to describe and validate a computed tomography (CT) method to analyse adiposity distribution in Göttingen minipigs. Adiposity was evaluated in two groups of minipigs. In group 1 (n 8), measurements were performed before and after the induction of obesity. In group 2 (n 7), animals were fed rations designed to obtain heterogeneous adiposity before analyses. CT acquisitions were associated with anatomical, ultrasonography and body chemical measurements. Our CT method was based on acquisition of a single slice at a fixed anatomical landmark, calculation of individual X-ray density ranges for CT values and delineation of the three main adipose compartments (subcutaneous adipose tissue, SAT; retroperitoneal adipose tissue, RAT; and visceral adipose tissue, VAT). Our validation measures showed that the CT-scan method was accurate, sensitive and reliable. The CT data were found to be correlated with body weight, abdominal perimeter, ultrasonography, anatomical measurements and body chemical composition (from r 0·84 to 0·93, P < 0·001 for all), with a pitfall concerning the precise estimation of VAT. With increased body weight, the amount of adipose tissue increased and the relative proportion of SAT increased, whereas the relative proportion of RAT and VAT decreased (P < 0·001 for all). Adiposity measured by CT, and especially SAT, was found to be negatively correlated with insulin sensitivity (r 0·54, P < 0·05). In conclusion, a precise evaluation of the adipose compartments in minipigs was done by CT. Therefore, the use of Göttingen minipigs is relevant to further investigate the relationship between the different adipose tissues and obesity.

Dietary energy density (ED) may be a good predictor of weight gain because of its association with the regulation of appetite control signals. Among the participants of the ‘SUpplementation en VItamines et Mineraux AntioXydants’ prospective study, 2707 subjects were included in the present study. Changes in weight, waist circumference (WC), hip circumference (HC) and waist:hip ratio were calculated using measured data collected in 1995/1996 and 2001/2002. The mean changes in various anthropometric indicators according to baseline body-weight status (BMI <  or ≥ 25 kg/m2) and sex-specific tertiles of baseline ED level or 6-year changes in ED were compared by covariance analysis. In overweight subjects, weight gain was positively associated with high dietary ED at baseline (P for trend  =  0·03) and with increasing ED during the follow-up (P for trend  =  0·0008). Both the WC and HC changes were also positively related to baseline ED and change in ED in overweight subjects. However, the relationships observed for the WC and HC changes were no longer significant after adjustment for weight change. These results support the hypothesis of a deleterious effect of high-energy-dense diets on weight change for overweight subjects. This relationship could be mediated by physical activity level. Further research needs to be performed in other populations to determine whether ED could be effective strategies to prevent weight gain.

The prevalence of obesity, defined as a BMI of ≥30·0 kg/m2, has increased substantially over previous decades to about 20% in industrialized countries, and a further increase is expected in the future. Epidemiological studies have shown that obesity is a risk factor for: post-menopausal breast cancer; cancers of the endometrium, colon and kidney; malignant adenomas of the oesophagus. Obese subjects have an approximately 1·5–3·5-fold increased risk of developing these cancers compared with normal-weight subjects, and it has been estimated that between 15 and 45% of these cancers can be attributed to overweight (BMI 25·0–29·9 kg/m2) and obesity in Europe. More recent studies suggest that obesity may also increase the risk of other types of cancer, including pancreatic, hepatic and gallbladder cancer. The underlying mechanisms for the increased cancer risk as a result of obesity are unclear and may vary by cancer site and also depend on the distribution of body fat. Thus, abdominal obesity as defined by waist circumference or waist:hip ratio has been shown to be more strongly related to certain cancer types than obesity as defined by BMI. Possible mechanisms that relate obesity to cancer risk include insulin resistance and resultant chronic hyperinsulinaemia, increased production of insulin-like growth factors or increased bioavailability of steroid hormones. Recent research also suggests that adipose tissue-derived hormones and cytokines (adipokines), such as leptin, adiponectin and inflammatory markers, may reflect mechanisms linked to tumourigenesis.

The aim of this study was to measure the effects of 12 weeks of conjugated linoleic acid (CLA) supplementation on body composition, RER, RMR, blood lipid profiles, insulin sensitivity and appetite in exercising, normal-weight persons. In this double-blind, randomised, controlled trial, sixty-two non-obese subjects (twenty-five men, thirty-seven women) received either 3·9 g/d CLA or 3·9 g high-oleic acid sunflower oil for 12 weeks. Prior to and after 12 weeks of supplementation, oral glucose tolerance, blood lipid concentrations, body composition (dual-energy X-ray absorptiometry and computerised tomography scans), RMR, resting and exercising RER and appetite were measured. There were no significant effects of CLA on body composition or distribution, RMR, RER or appetite. During the oral glucose tolerance tests, mean plasma insulin concentrations (0, 30, 120 min) were significantly lower (P = 0·04) in women who supplemented with CLA (24·3 (sd 9·7) to 20·4 (sd 8·5) μU/ml) compared to high-oleic acid sunflower oil control (23·7 (sd 9·8) to 26·0 (sd 8·8) μU/ml). Serum NEFA levels in response to oral glucose were attenuated in both men and women in the CLA (P = 0·001) compared to control group. However, serum total cholesterol and LDL-cholesterol concentrations decreased in both groups and HDL-cholesterol concentrations decreased in women over 12 weeks (P = 0·001, P = 0·02, P = 0·02, respectively). In conclusion, mixed-isomer CLA supplementation had a favourable effect on serum insulin and NEFA response to oral glucose in non-obese, regularly exercising women, but there were no CLA-specific effects on body composition, energy expenditure or appetite.