Aims/hypothesis Epidemiological research indicates that long-chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) improve insulin resistance. The aim of this study was to investigate the effects of seafood consumption on insulin resistance in overweight participants during energy restriction. Methods In this 8 week dietary intervention, 324 participants (20-40 years, BMI 27.5-32.5 kg/m 2 , from Iceland, Spain and Ireland) were randomised by computer to one of four energyrestricted diets (−30E%) of identical macronutrient composition but different LC n-3 PUFA content: control (n=80; no seafood; single-blinded); lean fish (n=80; 150 g cod, three times/week); fatty fish (n=84; 150 g salmon, three times/ week); (4) fish oil (n=80; daily docosahexaenoic/eicosapentaenoic acid capsules, no other seafood; single-blinded). Fasting glucose, insulin, adiponectin, plasma triacylglycerol and fatty acids in erythrocyte membrane were measured at baseline and endpoint. Insulin resistance was calculated using the homeostasis model assessment of insulin resistance (HOMA-IR). Linear models with fixed effects and covariates were used to investigate the effects of seafood consumption on fasting insulin and HOMA-IR at endpoint in comparison with the control group. Results Of the participants, 278 (86%) completed the intervention. Fish oil intake was a significant predictor of fasting insulin and insulin resistance after 8 weeks, and this finding remained significant even after including weight loss, triacylglycerol reduction, increased LC n-3 PUFA in membranes or adiponectin changes as covariates in the statistical analysis. Weight loss was also a significant predictor of improvements. Conclusions/interpretation LC n-3 PUFA consumption during energy reduction exerts positive effects on insulin resistance in young overweight individuals, independently from changes in body weight, triacylglycerol, erythrocyte membrane or adiponectin.Trial registration: ClinicalTrials.gov NCT00315770.

Experts have called attention to the possible negative impact of the coronavirus disease 2019 (COVID-19)–related cytokine storm syndrome on the progression of leprosy-related disabilities. We assessed the frequency of reactional states in patients co-infected with Mycobacterium leprae and severe acute respiratory syndrome (SARS) coronavirus (CoV) 2 (SARS-CoV-2). We consecutively included patients during the first peak of the COVID-19 epidemic in Brazil and analyzed the expressions of genes encoding interleukin (IL)-1β, IL-6, IL-8, IL-10, IL-12A, IL-12B, and tumor necrosis factor-α in peripheral blood mononuclear cells. We included 64 leprosy patients and 50 controls. Twelve of the leprosy patients and 14 of the controls had been diagnosed with COVID-19. Co-infection was associated with increased IL-6 (P = 0.043) and IL-12B (P = 0.017) expression. The median disability grades were higher for leprosy/COVID-19 patients; however, the difference was not significant (P = 0.194). Patients co-infected with M. leprae and SARS-CoV-2 may experience a higher-grade proinflammatory state.

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Type 2 diabetes mellitus (T2DM) consists of a set of metabolic and endocrine disorders which evolve into deficiency in insulin action and hyperglycemia. Physical exercise is considered the main intervention to prevent and control T2DM. Literature has suggested that circulating microRNAs (miRs) help to understand responses to physical activity among diabetic patients. Thus, the aim of this study was to analyze the acute effect of two interventions (strength and cardiovascular) on the total, whole blood circulating concentrations of miR-126, miR-146a and miR-155 in older adults with and without T2DM. A total of 23 male and female older adults (68.2±5.3 years) participated in the trial, 13 of whom presented with controlled T2DM and 10 were nondiabetics. They underwent both interventions separately, performed with intensity from 60% to 70% of reserve heart rate. Glucose and miRs levels were quantified and compared across groups with baseline titers as covariables. Diabetic patients showed more reduction in serum blood glucose than nondiabetics, with a great magnitude of reduction after the strength training intervention, which was paralleled by a positive change of the whole blood circulating levels of miR-146a, but not of the other miRs. Our report supports evidence that miR-146a levels in peripheral blood leukocytes are negatively associated with a state of insulin resistance, which is suggested as a novel marker to trace response to antidiabetic interventions.

Recent evidence suggests changes in circulating microRNA levels may be promising biomarkers for the clinical diagnosis of Alzheimer disease (AD). We hypothesized that whole-blood microRNAs may be useful to identify individuals with established AD. For this purpose, a sample of community-dwelling women (≥55 years old) carrying the ApoE ∊4 allele were clinically evaluated using the American Psychiatric Association/ Diagnostic and Statistical Manual of Mental Disorders, Fourth edition and the Alzheimer Disease Assessment Scale–Cognitive Subscale criteria to diagnose probable AD, and the Clinical Dementia Rating scale to stage the dementia. A set of 25 mature microRNAs was rationally selected for evaluation based on experimental evidence of interaction with genes linked to the late-onset AD neuropathology. Whole-blood concentrations were determined by quantitative real-time polymerase chain reaction. Compared to patients without dementia, a median 3-fold decrease in miR-9 levels was found among patients with AD ( P = .001). Our findings support blood-borne miR-9 as a candidate biomarker for probable AD, embodied by evidence from the literature of its implication in amyloidogenesis.

Background and Aim. Frailty is a geriatric condition resulting from physiological changes covering the musculoskeletal, immune, and neuroendocrine systems, leading to a greater inflammatory state. The present research aimed to investigate the association of components of Fried’s frailty (as well as of the phenotype as a whole) with total serum levels of a panel of inflammatory mediators. Methods. One hundred and sixty-one very old patients (aged ≥80 years) devoid of cognitive decline were eligible for analyses. Clinical and biochemical data along with physical and cognitive assessments encompassing dual-energy X-ray scans and hand dynamometry were adopted to investigate frailty criteria, while circulating immune mediators (IFNγ, IL-2, IL-4, IL-6, IL-10, and TNFα) were assessed using high-throughput flow cytometry. Results. Preliminarily, IL-6 correlated positively with waist-to-hip ratio and C-reactive protein and negatively with glycemia. In analyses controlled for these factors, serum levels of IL-6 were comparatively augmented among the very old participants with reduced grip strength (OR = 3.299; 95% CI 1.08–6.09; p = 0.032 ) and among those with slow walk speed (OR = 2.460; 95% CI 1.16–7.05; p = 0.022 ). Conclusions. Our study shows a strong negative correlation of IL-6 levels with Fried’s frailty components of grip strength and walk speed in very old adults, regardless of confounding factors.

Background and Aim Due to the high incidence of vascular diseases, it is necessary to identify new circulating or structural markers for predicting risk for chronic diseases. Some studies suggest that MMP1 gene polymorphisms are associated with the enzyme expression levels in situ (e.g., in atherosclerotic plaques). Objectives Thus, the study of this polymorphism may help understanding the pathophysiology of coronary disease. Methods We performed cross-sectional clinical and laboratory evaluations (including measurement of intima-media thickness of carotid arteries) and genotyping of the MMP1 SNP rs495366 (A/G) in 366 elderly people. Results No significant differences between genotypes were noted for biochemical, metabolic, inflammatory, or clinical variables except for a significant difference in intima-media thickness for the left carotid artery and a trend toward significance for the right counterpart. Conclusion Carriers of the allele associated with lower MMP1 expression (allele A) presented greater carotid thickness. We suggest that the phenomenon can be explained by impaired remodeling of the arterial wall (poor degradation of collagen fibers in this scenario), yielding carotid wall thickening and a greater intrinsic risk for cerebrovascular events.

Metalloproteinases (MMPs) are involved in metastatic tumor processes, with changes in circulating levels detected in several cancer types. Here, we compare serum concentrations of metalloproteinase-1 (MMP-1) across individuals clinically diagnosed with prostate cancer (PCa) or benign prostatic hyperplasia (BPH), correcting results for the rs495366 single nucleotide polymorphism (SNP) that predisposes to differential MMP-1 levels. 196 men aged ≥50 years were followed at a university hospital urology outpatient clinic, with clinical, anthropometric, and rectal examinations performed by one urologist. Blood samples obtained prior to any clinical intervention provided baseline MMP-1 and total/free PSA levels as well as metabolic, hormonal, and inflammatory markers. The SNP was genotyped by real-time PCR. Participants with medical and/or laboratory profile compatible with malignancy composed the PCa group when confirmed by the Gleason scale. As expected, A-allele homozygotes showed reduced levels of MMP-1. Genotype-adjusted analyses revealed the mean MMP-1 level as 2-fold higher in PCa carriers compared to BPH patients. No other differences were found according to the prostatic condition or genotypic distribution, except for the expected raise in total and free PSA levels in PCa. In conclusion, increased serum levels of MMP-1 were observed in this context of prostatic malignancy compared to a benign phenotype, regardless of a genetic influence.