Key points• Contradictory findings have been reported concerning the function of irisin and its precursor gene, skeletal muscle FNDC5, in energy homeostasis and metabolic health, and the associated regulatory role of exercise and PGC-1α.• We analysed the effects of different short-and long-term exercise regimens on muscle FNDC5and PGC-1α, and serum irisin, and studied the associations of irisin and FNDC5 with health parameters.• FNDC5 and serum irisin did not change after acute aerobic, long-term endurance training or endurance training combined with resistance exercise (RE) training, or associate with metabolic disturbances. A single RE bout increased FNDC5 mRNA in young, but not older men (27 vs. 62 years). Changes in PGC-1α or serum irisin were not consistently accompanied by changes in FNDC5.• Our data suggest that the effects of exercise on FNDC5 and irisin are not consistent, and that their role in health is questionable. Moreover, the regulatory mechanisms should be studied further.Abstract Recently, contradictory findings have been reported concerning the function of irisin and its precursor gene, skeletal muscle FNDC5, in energy homeostasis, and the associated regulatory role of exercise and PGC-1α. We therefore evaluated whether muscle FNDC5 mRNA and serum irisin are exercise responsive and whether PGC-1α expression is associated with FNDC5 expression. The male subjects in the study performed single exercises: (1) 1 h low-intensity aerobic exercise (AE) (middle-aged, n = 17), (2) a heavy-intensity resistance exercise (RE) bout (young n = 10, older n = 11) (27 vs. 62 years), (3) long-term 21 weeks endurance exercise (EE) training alone (twice a week, middle-aged, n = 9), or (4) combined EE and RE training (both twice a week, middle-aged, n = 9). Skeletal muscle mRNA expression was analysed by quantitative PCR and serum irisin by ELISA. No significant changes were observed in skeletal muscle PGC-1α, FNDC5 and serum irisin after AE, EE training or combined EE + RE training. However, a single RE bout increased PGC-1α by 4-fold in young and by 2-fold in older men, while FNDC5 mRNA only increased in young men post-RE, by 1.

The study aimed to assess whether aerobic exercise (AEx) training and a fibre-enriched diet can reduce hepatic fat content (HFC) and increase glycaemic control in pre-diabetic patients with non-alcoholic fatty liver disease (NAFLD). Six-hundred-and-three patients from seven clinics in Yangpu district, Shanghai, China were recruited. Of them 115 individuals aged 50–65-year fulfilled the inclusion criteria (NAFLD with impaired fasting glucose or impaired glucose tolerance) and were randomly assigned into exercise (AEx n = 29), diet (Diet n = 28), exercise plus diet (AED n = 29), or no-intervention (NI n = 29) groups. Progressive supervised AEx training (60–75% VO2max intensity) was given 2-3 times/week in 30–60 min/sessions, and the diet intervention was provided as lunch with 38% carbohydrate and diet fibre of 12 g/day for 8.6-month. HFC was assessed by 1H MRS. We found that HFC was significantly reduced in the AEx (−24.4%), diet (−23.2%), and AED (−47.9%) groups by contrast to the 20.9% increase in the NI group (p = 0.001 for all) after intervention. However, only AED group significantly decreased HbA1c (−4.4%, p = 0.01) compared with the NI group (−0.6%). Aerobic exercise training combined with fibre-enriched diet can reduce HFC more effectively than either exercise or increased fibre-intake alone in pre-diabetic patients with NAFLD.

The prevalence of overweight and obesity has increased dramatically during last 3 decades with devastating consequences to public health. Recommended strategies to reduce obesity have focused on healthier diet and physical activity (PA). Clearly, these approaches have not been successful, but whether this is due to failure to restrict energy intake or to maintain high levels of energy expenditure has been the subject of great controversy. Consequently, there has been a great deal of confusion about the role of PA and exercise in obesity and weight management. In this article, the theoretical basis for considering reduced PA and energy expenditure as the cause of obesity is appraised. Further, the role of PA in food intake and weight control is examined. The idea that obesity is caused by consistent decline in daily energy expenditure is not supported either by objective measures of energy expenditure or physiological theory of weight gain alone. However, since voluntary exercise is the most important discretionary component of total daily energy expenditure, it can affect energy balance. Therefore, PA and exercise hold potential as part of the solution for the ongoing obesity epidemic.

SUMMARYThis cross-sectional study aimed to investigate whether body fat distribution, physical activity levels and dietary intakes are associated with insomnia and/or obstructive sleep apnea among overweight middleaged men. Participants were 211 Finnish men aged 30-65 years. Among the 163 overweight or obese participants, 40 had insomnia only, 23 had obstructive sleep apnea only, 24 had comorbid insomnia and obstructive sleep apnea and 76 were without sleep disorder. The remaining 48 participants had normal weight without sleep disorder. Fat mass, levels of physical activity and diet were assessed by dual-energy X-ray densitometry, physical activity questionnaire and 3-day food diary, respectively. Among the overweight participants, we found that: (i) groups with sleep disorders had higher fat mass in trunk and android regions than the group without sleep disorder (P = 0.048-0.004); (ii) the insomnia-only group showed a lower level of leisure-time physical activity (436.9 versus 986.5 MET min week À1 , P = 0.009) and higher intake of saturated fatty acids (14.8 versus 12.7 E%, P = 0.011) than the group without sleep disorder; and (iii) the comorbid group had a lower level of leisure-time physical activity (344.4 versus 986.5 MET min week À1 , P = 0.007) and lower folate intake (118.9 versus 152.1 lg, P = 0.002) than the group without sleep disorder, which were independent of body mass index. The results suggest that central obesity is associated with insomnia and/or obstructive sleep apnea. In addition, low levels of leisure-time physical activity and poor dietary intakes are related to insomnia or comorbid insomnia and obstructive sleep apnea among overweight men. IN TROD UCTI ONSleep disorders such as insomnia and obstructive sleep apnea (OSA) have become a significant health issue worldwide. The prevalence of insomnia has been estimated as 6-7% among the US and European populations (Ohayon, 2002;Wittchen et al., 2011), while more than 30% of the population may suffer at least one symptom related to insomnia (Ohayon, 2002). In Finland, the prevalence of diagnosed insomnia is 11.7%, which is 1.5-2 times higher than other European countries (Ohayon and Partinen, 2002). OSA is another sleep disorder with increasing prevalence, which affects 3-17% American adults in different age and gender groups, and is most observed commonly among men from middle to old age (Peppard et al., 2013). The prevalence of OSA is approximately 8% among Finnish population (Kronholm et al., 2009). Insomnia and OSA also often exist as comorbidity (Luyster et al., 2010).An increasing number of studies have shown the association between obesity and sleep disorders. One study Sleep and body fat suggests that obese individuals are 50% more likely to suffer insomnia than participants of normal weight, thus obesity is regarded as a risk factor for insomnia (Singareddy et al., 2012). The association between obesity and OSA is more widely recognized (Punjabi, 2008). More than two-thirds of individuals with OSA are obese (Punjabi, 2008;Vgontzas et...

Background Maternal smoking during pregnancy is associated with adverse offspring health outcomes across their life course. We hypothesize that DNA methylation is a potential mediator of this relationship. Methods We examined the association of prenatal maternal smoking with offspring blood DNA methylation in 2821 individuals (age 16 to 48 years) from five prospective birth cohort studies and perform Mendelian randomization and mediation analyses to assess whether methylation markers have causal effects on disease outcomes in the offspring. Results We identify 69 differentially methylated CpGs in 36 genomic regions ( P value < 1 × 10 −7 ) associated with exposure to maternal smoking in adolescents and adults. Mendelian randomization analyses provided evidence for a causal role of four maternal smoking-related CpG sites on an increased risk of inflammatory bowel disease or schizophrenia. Further mediation analyses showed some evidence of cg25189904 in GNG12 gene mediating the effect of exposure to maternal smoking on schizophrenia-related outcomes. Conclusions DNA methylation may represent a biological mechanism through which maternal smoking is associated with increased risk of psychiatric morbidity in the exposed offspring. Electronic supplementary material The online version of this article (10.1186/s13148-019-0683-4) contains supplementary material, which is available to authorized users.

The aim of this study was to investigate the association between cardiorespiratory fitness and gut microbiota composition in premenopausal women. The participants consisted of 71 premenopausal Finnish women (aged 19–49 years). Gut microbiota were analyzed using flow cytometry, 16S rRNA gene hybridization and DNA-staining. Maximum oxygen uptake (VO2max) was assessed by respiratory gas analyzer and body composition by Bioimpdance. We found that participants with low VO2max had lower Bacteroides, but higher Eubacterium rectale-Clostridium coccoides than the high VO2max group (p < 0.05 for all). VO2max was inversely associated with EreC (r = −0.309, p = 0.01) but not with other bacteria. VO2max also negatively correlated with fat% (r = −0.755, p < 0.001), triglycerides (r = −0.274, p = 0.021) and leptin (r = −0.574, p < 0.001). By contrast, EreC was positively associated with fat% (r = 0.382, p = 0.002), dietary fat intake (r = 0.258, p = 0.034), triglycerides (r = 0.390, p = 0.002) and leptin (r = 0.424, p = 0.001), but negatively with carbohydrate intake (r = −0.252, p = 0.034) and HDL (r = −0.26, p = 0.028). After adjusting for age and dietary intake, all the significant associations remained. However, after adjusting for fat%, the associations between VO2max and EreC disappeared. Our results suggest that cardiorespiratory fitness is associated with gut microbiota composition, independent of age and carbohydrate or fat intake. The association between VO2max and EreC, however, appears to be mediated by body fatness.

ObjectiveTo identify serum biomarkers through metabolomics approach that distinguishes physically inactive overweight/obese women with metabolic syndrome from those who are metabolically healthy, independent of body weight and fat mass.MethodsWe applied nuclear magnetic resonance spectroscopy-based profiling of fasting serum samples to examine the metabolic differences between 78 previously physically inactive, body weight and fat mass matched overweight/obese premenopausal women with and without MetS. MetS was defined as the presence of at least three of the following five criteria: waist circumference ≥88 cm, serum triacylglycerol ≥1.7 mmol/L, and high density lipoprotein cholesterol (HDL-C) <1.30 mmol/L, blood pressure ≥ 130/85 mmHg and fasting glucose ≥5.6 mmol/L). Principal component analysis was used to reduce the large number of correlated variables to fewer uncorrelated factors.ResultsTwo metabolic factors were associated with MetS independent of BMI, fat mass, waist circumference and physical activity/fitness. Factor comprising branched-chain amino acids (BCAA) and aromatic amino acids (AAA) and orosomucoid was associated with all clinical risk factors (p < 0.01 for all).ConclusionTwo metabolic factors distinguish overweight/obese women with metabolic syndrome from those who are metabolically healthy independent of body weight, fat mass and physical activity/fitness. In particular, factor comprising BCAA, AAA and orosomucoid seems auspicious biomarker determining metabolic health as it was associated with all clinical risk factors. Further research is needed to determine the public health and clinical significance of these results in terms of screening to identify those at greatest cardio-metabolic risk for whom appropriate intervention strategies should be developed.

Insulin resistance is associated adiposity, but the mechanisms are not fully understood. In this study, we aimed to identify early metabolic alterations associated with insulin resistance in normoglycemic women with varying degree of adiposity. One-hundred and ten young and middle-aged women were divided into low and high IR groups based on their median HOMA-IR (0.9 ± 0.4 vs. 2.8 ± 1.2). Body composition was assessed using DXA, skeletal muscle and liver fat by proton magnetic resonance spectroscopy, serum metabolites by nuclear magnetic resonance spectroscopy and adipose tissue and skeletal muscle gene expression by microarrays. High HOMA-IR subjects had higher serum branched-chain amino acid concentrations (BCAA) (p < 0.05 for both). Gene expression analysis of subcutaneous adipose tissue revealed significant down-regulation of genes related to BCAA catabolism and mitochondrial energy metabolism and up-regulation of several inflammation-related pathways in high HOMA-IR subjects (p < 0.05 for all), but no differentially expressed genes in skeletal muscle were found. In conclusion, in normoglycemic women insulin resistance was associated with increased serum BCAA concentrations, down-regulation of mitochondrial energy metabolism and increased expression of inflammation-related genes in the adipose tissue.