Anthocyanins are naturally occurring compounds abundant in the human diet. Evidence has accumulated regarding the positive association of their intake with healthy biological effects. The microbiota has just been started to be considered as a metabolic organ, hence contributing to the metabolism of phenolic compounds and, consequently, to their bioavailability and the biological effects displayed by them. This review aimed to compile information regarding interaction of anthocyanins with the microbiota, from two perspectives: (i) identification of their colonic metabolites as potential bioactive molecules and (ii) their role as prebiotic agents. These perspectives are key points in anthocyanin metabolomics. Several metabolites have been identified after anthocyanin consumption with potential health benefits, in particular phenolic acids and simple phenols. On the other hand, microbiota modulation is closely related to several physiological impairments, and its modulation has been considered as a possible mechanism by which phenolic compounds may exert their effect.

In the past decades, obesity and associated metabolic complications have reached epidemic proportions. For the study of these pathologies, a number of animal models have been developed. However, a direct comparison between Wistar and Sprague-Dawley (SD) Rat as models of high-fat (HF) diet-induced obesity has not been adequately evaluated so far. Wistar and SD rats were assigned for 2 experimental groups for 17 weeks: standard (St) and high-fat (HF) diet groups. To assess some of the features of the metabolic syndrome, oral glucose tolerance tests, systolic blood pressure measurements and blood biochemical analysis were performed throughout the study. The gut microbiota composition of the animals of each group was evaluated at the end of the study by real-time PCR. HF diet increased weight gain, body fat mass, mesenteric adipocyte's size, adiponectin and leptin plasma levels and decreased oral glucose tolerance in both Wistar and SD rats. However, the majority of these effects were more pronounced or earlier detected in Wistar rats. The gut microbiota of SD rats was less abundant in Bacteroides and Prevotella but richer in Bifidobacterium and Lactobacillus comparatively to the gut microbiota of Wistar rats. Nevertheless, the modulation of the gut microbiota by HF diet was similar in both strains, except for Clostridium leptum that was only reduced in Wistar rats fed with HF diet. In conclusion, both Wistar and SD Rat can be used as models of HF diet-induced obesity although the metabolic effects caused by HF diet seemed to be more pronounced in Wistar Rat. Differences in the gut microbial ecology may account for the worsened metabolic scenario observed in Wistar Rat.

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A B S T R A C TBackground: The role of persistent organic pollutants (POPs) with endocrine disrupting activity in the aetiology of obesity and other metabolic dysfunctions has been recently highlighted. Adipose tissue (AT) is a common site of POPs accumulation where they can induce adverse effects on human health. Objectives: To evaluate the presence of POPs in human visceral (vAT) and subcutaneous (scAT) adipose tissue in a sample of Portuguese obese patients that underwent bariatric surgery, and assess their putative association with metabolic disruption preoperatively, as well as with subsequent body mass index (BMI) reduction. Methods: AT samples (n¼ 189) from obese patients (BMI Z35) were collected and the levels of 13 POPs were determined by gas chromatography with electroncapture detection (GC-ECD). Anthropometric and biochem-ical data were collected at the time of surgery. BMI variation was evaluated after 12 months and adipocyte size was measured in AT samples. Results: Our data confirm that POPs are pervasive in this obese population (96.3% of detection on both tissues), their abundance increasing with age (RS ¼ 0.310, po0.01) and duration of obesity (RS ¼ 0.170, po0.05). We observed a difference in AT depot POPs storage capability, with higher levels of ΣPOPs in vAT (213.97204.2 compared to 155.17147.4 ng/g of fat, po0.001), extremely relevant when evaluating their metabolic impact. Furthermore, there was a positive correlation between POP levels and the presence of metabolic syndrome components, namely dysglycaemia and hypertension, and more importantly with cardiovascular risk (RS ¼ 0.277, po0.01), with relevance for vAT (RS ¼ 0.315, po0.01). Finally, we observed an interesting relation of higher POP levels with lower weight loss in older patients. Conclusion: Our sample of obese subjects allowed us to highlight the importance of POPs stored in AT on the development of metabolic dysfunction in a context of obesity, shifting the focus to their metabolic effects and not only for their recognition as environmental obesogens.

Ethanol seems to enhance Cy3glc metabolism that appears to be compromised in overweight and obese individuals.

The World Health Organization promotes salt iodisation to control iodine deficiency. In Portugal, the use of iodised salt in school canteens has been mandatory since 2013. The present study aimed to evaluate iodine status in school-aged children (6–12 years) and to monitor the use of iodised salt in school canteens. A total of 2018 participants were randomly selected to participate in a cross-sectional survey in northern Portugal. Children’s urine and salt samples from households and school canteens were collected. A lifestyle questionnaire was completed by parents to assess children’s eating frequency of iodine food sources. Urinary iodine concentration (UIC) was measured by inductively coupled plasma-mass spectrometry. The median UIC was 129 µg/L which indicates the adequacy of iodine status and 32% of the children had UIC < 100 µg/L. No school canteen implemented the iodised salt policy and only 2% of the households were using iodised salt. Lower consumption of milk, but not fish, was associated with a higher risk of iodine deficiency. Estimation of sodium intake from spot urine samples could be an opportunity for adequate monitoring of population means. Implementation of iodine deficiency control policies should include a monitoring program aligned with the commitment of reducing the population salt intake.

Endocrine-disrupting chemicals such as p,p’-dichlorodiphenyldichloroethylene (p,p’-DDE), are bioaccumulated in the adipose tissue (AT) and have been implicated in the obesity and diabetes epidemic. Thus, it is hypothesized that p,p’-DDE exposure could aggravate the harm of an obesogenic context. We explored the effects of 12 weeks exposure in male Wistar rats’ metabolism and AT biology, assessing a range of metabolic, biochemical and histological parameters. p,p’-DDE -treatment exacerbated several of the metabolic syndrome-accompanying features induced by high-fat diet (HF), such as dyslipidaemia, glucose intolerance and hypertension. A transcriptome analysis comparing mesenteric visceral AT (vAT) of HF and HF/DDE groups revealed a decrease in expression of nervous system and tissue development-related genes, with special relevance for the neuropeptide galanin that also revealed DNA methylation changes at its promoter region. Additionally, we observed an increase in transcription of dipeptidylpeptidase 4, as well as a plasmatic increase of the pro-inflammatory cytokine IL-1β. Our results suggest that p,p’-DDE impairs vAT normal function and effectively decreases the dynamic response to energy surplus. We conclude that p,p’-DDE does not merely accumulate in fat, but may contribute significantly to the development of metabolic dysfunction and inflammation. Our findings reinforce their recognition as metabolism disrupting chemicals, even in non-obesogenic contexts.

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