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The gut microbiota and their metabolites, e.g., short-chain fatty acids (SCFA), are associated with obesity. The primary aims were to study faecal SCFA levels and the changes in SCFA levels after weight-loss interventions in subjects with obesity, and secondarily, to study factors associated with the faecal SCFA levels. In total, 90 subjects (men / women 15/75) with a mean age of 44.4 (SD 8.4) years, BMI 41.7 (SD 3.7) kg/m2 and morbid obesity (BMI > 40 or > 35 kg/m2 with obesity-related complications) were included. Faecal SCFA and other variables were measured at inclusion and after a six-month conservative weight-loss intervention followed by bariatric surgery (RouxenY gastric bypass or gastric sleeve). Six months after surgery, the total amount of SCFA was reduced, the total and relative amounts of the main straight SCFA (acetic-, propionic-, and butyric- acids) were reduced, and the total and relative amounts of branched SCFA (isobutyric-, isovaleric-, and isocaproic- acids) were increased. The changes indicate a shift toward a proteolytic fermentation pattern with unfavorable health effects. The amount of SCFA was associated with the diet but not with metabolic markers or makers of the faecal microbiota composition. Dietary interventions could counteract the unfavorable effects.Depression symptoms and lower health-related quality of life (HRQoL) are associated with inflammation. This multicenter dietary intervention was shown to reduce inflammation in older people. This was the main outcome. Here, we describe the effects on HRQoL, anxiety, and depressive symptoms according to inflammation status. Overall, 125 healthy older subjects (65-80 year) were recruited (Italy, France, and Germany) and randomized into four arms (A, Healthy diet (HD); B, HD plus De Simone Formulation probiotic blend; C, HD plus AISA d-Limonene; D, HD plus Argan oil). NSC 737664 The HD was weight maintaining, rich in antioxidant vitamins, polyphenols, polyunsaturated fatty acids (n6 n3 ratio = 31), and fiber. Data on inflammatory parameters, mental (MCS) and physical (PCS) component summaries of HRQoL (SF-36), anxiety symptoms (STAI state), and depressive symptoms (CES-D) were collected before and after 56 days of intervention. Body fat mass proportion (BFM) was considered a co-variable. A decrease of CES-D score was seen in the four arms (A -40.0%, p = 0.001; B -32.5%, p = 0.023; C -42.8%, p = 0.004; and D -33.3%, p = 0.21). Within the subgroups of subjects with medium/high inflammation a similar decrease in CES-D score occurred in all groups (A -44.8%, p = 0.021; B, -46.7%, p = 0.024; C, -52.2%, p = 0.039; D, -43.8%, p = 0.037). The effect of interventions on CES-D was not related to baseline inflammation. MCS-HRQoL improved in A and C. There was no change in anxiety or PCS-HRQoL. In this trial with no control group, a decrease in depressive symptoms in healthy older volunteers was observed after a 2-month healthy diet intervention, independently of inflammation but with possible limitations due to participation.We examined whether energy and macronutrient intake from different meals was associated with changes in cardiometabolic risk (CMR) factors in children. CMR score (CMRS) was computed by summing Z-scores of waist circumference, the average of systolic and diastolic blood pressure, fasting glucose, high-density lipoprotein cholesterol (multiplying by -1), and triglycerides. We included 5517 children aged 6-13 years from six major cities in China. Five meal patterns were identified according to energy intake balanced, breakfast dominant, lunch dominant, dinner dominant, and snack dominant patterns. These patterns were not significantly associated with changes in CMR factors. Carbohydrate intake (% energy) at lunch was positively associated with the change in CMRS (beta coefficient (95% CI) (0.777 (0.509, 1.046) in quintile 5 versus quintile 1). A positive association between carbohydrate intake at dinner and change in CMRS was observed. High protein intake at both lunch and dinner was associated with a favorable change in CMRS. Moderate fat intake at lunch was associated with a lower increase in CMRS. Meal patterns driven by energy were not significantly associated with CMR factors; however, a low carbohydrate-high protein-moderate fat lunch and low carbohydrate-high protein dinner were associated with favorable changes in CMRS in children.The transfer of Microcystis aeruginosa from freshwater to estuaries has been described worldwide and salinity is reported as the main factor controlling the expansion of M. aeruginosa to coastal environments. Analyzing the expression levels of targeted genes and employing both targeted and non-targeted metabolomic approaches, this study investigated the effect of a sudden salt increase on the physiological and metabolic responses of two toxic M. aeruginosa strains separately isolated from fresh and brackish waters, respectively, PCC 7820 and 7806. Supported by differences in gene expressions and metabolic profiles, salt tolerance was found to be strain specific. An increase in salinity decreased the growth of M. aeruginosa with a lesser impact on the brackish strain. The production of intracellular microcystin variants in response to salt stress correlated well to the growth rate for both strains. Furthermore, the release of microcystins into the surrounding medium only occurred at the highest salinity treatment when cell lysis occurred. This study suggests that the physiological responses of M. aeruginosa involve the accumulation of common metabolites but that the intraspecific salt tolerance is based on the accumulation of specific metabolites. While one of these was determined to be sucrose, many others remain to be identified. Taken together, these results provide evidence that M. aeruginosa is relatively salt tolerant in the mesohaline zone and microcystin (MC) release only occurs when the capacity of the cells to deal with salt increase is exceeded.Type 2 deiodinase (D2), the principal activator of thyroid hormone (TH) signaling in target tissues, is expressed in cutaneous squamous cell carcinomas (SCCs) during late tumorigenesis, and its repression attenuates the invasiveness and metastatic spread of SCC. Although D2 plays multiple roles in cancer progression, nothing is known about the mechanisms regulating D2 in cancer. To address this issue, we investigated putative upstream regulators of D2 in keratinocyte carcinomas. We found that the expression of D2 in SCC cells is positively regulated by the NANOG transcription factor, whose expression, besides being causally linked to embryonic stemness, is associated with many human cancers. We also found that NANOG binds to the D2 promoter and enhances D2 transcription. Notably, blockage of D2 activity reduced NANOG-induced cell migration as well as the expression of key genes involved in epithelial-mesenchymal transition in SCC cells. In conclusion, our study reveals a link among endogenous endocrine regulators of cancer, thyroid hormone and its activating enzyme, and the NANOG regulator of cancer biology.
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