Accumulating literature is providing evidence that the gut microbiota is involved in metabolic disorders, but the question of how to effectively modulate it to restore homeostasis, especially in the elderly, is still under debate. In this study, we profiled the intestinal microbiota of 20 elderly obese women (EO) at the baseline (T0), after 15 days of hypocaloric Mediterranean diet administered as part of a nutritional-metabolic rehabilitation program for obesity (T1), and after a further 15 days of the same diet supplemented with a probiotic mix (T2). Fecal samples were characterized by Illumina MiSeq sequencing of the 16S rRNA gene. The EO microbiota showed the typical alterations found in obesity, namely, an increase in potential pro-inflammatory components (i.e., Collinsella) and a decrease in health-promoting, short-chain fatty acid producers (i.e., Lachnospiraceae and Ruminococcaceae members), with a tendency to reduced biodiversity. After 15 days of the rehabilitation program, weight decreased by (2.7 ± 1.5)% and the gut microbiota dysbiosis was partially reversed, with a decline of Collinsella and an increase in leanness-related taxa. During the next 15 days of diet and probiotics, weight dropped further by (1.2 ± 1.1)%, markers of oxidative stress improved, and Akkermansia, a mucin degrader with beneficial effects on host metabolism, increased significantly. These findings support the relevant role of a correct dietetic approach, even in the short term, to modulate the EO gut microbiota towards a metabolic health-related configuration, counteracting the increased risk of morbidity in these patients.

irisin is conventionally regarded as a myokine involved in the browning of white adipose tissue, energy expenditure and glucose tolerance. its potential link to fat accumulation and metabolic dysfunction is debated. We sought to explore the relationship between circulating irisin and components of body composition in two different phenotypes of severe obesity. For this purpose, 30 obese adults with Prader-Will syndrome (PWS) (age 35.7 ± 1.5 y, BMI 45.5 ± 1.5 kg/m 2) and 30 adult controls with common obesity (age 34.9 ± 1.7 y, BMI 46.8 ± 1.4 kg/m 2) underwent analysis of irisin levels, metabolic profile, body composition and resting energy expenditure (REE). Normal irisin levels were obtained from a group of 20 lean donors (age 32.4 ± 1.5 y, BMI 23.8 ± 0.8 kg/m 2). Expected differences in body composition and metabolic profile existed between study groups. PWS exhibited lower muscle mass (p < 0.001), FFM (p < 0.001), REE (p < 0.001), as well as insulin (p < 0.05), HOMA-IR (p < 0.05) and triglycerides levels (p < 0.05) than controls with common obesity. In PWS, irisin levels were significantly lower and overall less dispersed than in controls with common obesity (p < 0.05), while being similar to values recorded in lean subjects. to explore the relation between irisin and body composition in obesity, univariate correlation analysis in the obese populations as a whole showed positive associations between irisin and muscle mass (p = 0.03) as well as REE (p = 0.01), which disappeared when controlled for the pWS status. noticeably, a positive association became evident between irisin and %fM after controlling for the pWS status (p = 0.02). Also positive were associations between irisin and insulin (p = 0.02), HOMA-IR (p = 0.02) and triglycerides (p = 0.04). In stepwise multivariable regression analysis, irisin levels were independently predicted by the pWS status (p = 0.001), %FM (p = 0.004) and triglycerides (p = 0.008). Current results suggest that obese adults with PWS harbor lower irisin levels than individuals with common obesity. the divergent models of obesity herein studied suggest a potential link between circulating irisin and muscle mass and metabolic dysfunction relating to adiposity. Prader-Willi syndrome (PWS) is a rare genetic disorder characterized by neonatal hypotonia associated with poor suck, followed by the lack of a sense of satiety with obsessive craving for food in childhood and gradual development of morbid obesity in adulthood unless eating is externally controlled 1-4. Further clinical features include body dysmorphisms, developmental disability, cognitive and behavioral disorders, endocrine dysfunctions leading to short stature, hypogonadism and hypothyroidism 1. PWS occurs because of the lack of expression of genes located on the paternal chromosome 15q11.2-q13. Three main genetic mechanisms have been recognized in determining PWS: deletion of the paternal chromosome 15 (del15q11-q13), maternal uniparental disomy of chromosome 15 (UPD15), and imprinting defects 2 .

Objective: To investigate the relationship between oxytocin, menopause and obesity. Methods: A cross-sectional analysis on 56 obese (OB; 28 premenopausal) and 53 normal-weight women (NW; 27 premenopausal) was performed by measurement of oxytocin, leptin, adiponectin, gonadotropins, sex steroids, glucose, and lipid homeostasis as well as DXA assessment of fat mass (%FM) and fat-free mass (FFM). Results: Women from NW and OB groups were comparable for age but differed in anthropometric measures. In our cohorts, menopause was not associated with changes in gluco-lipid homeostasis and %FM, while FFM was lower in postmenopausal women from both study groups (p < 0.05). In each group, leptin was unaltered, and adiponectin only marginally changed across menopause, while oxytocin levels were lower in post- than in premenopausal women (NW: p < 0.05; OB: p < 0.005), and lower in OB than NW women, either when assessed as whole groups or if stratified by menopause (p < 0.001). In correlation analysis, inverse associations related oxytocin to menopause, obesity, and adiposity-related measures. BMI (p < 0.0001) and menopause independently predicted oxytocin levels (p < 0.001), but their interaction was null (p = 0.5). Conclusions: Obesity and menopause are independent negative predictors of plasma oxytocin. Longitudinal studies should clarify the role of oxytocin on weight modifications experienced around and after menopause.