1.
Unveiling the Correlation between Inadequate Energy/Macronutrient Intake and Clinical Alterations in Volunteers at Risk of Metabolic Syndrome by a Predictive Model.
Danesi, F, Mengucci, C, Vita, S, Bub, A, Seifert, S, Malpuech-Brugère, C, Richard, R, Orfila, C, Sutulic, S, Ricciardiello, L, et al
Nutrients. 2021;(4)
Abstract
Although lifestyle-based interventions are the most effective to prevent metabolic syndrome (MetS), there is no definitive agreement on which nutritional approach is the best. The aim of the present retrospective analysis was to identify a multivariate model linking energy and macronutrient intake to the clinical features of MetS. Volunteers at risk of MetS (F = 77, M = 80) were recruited in four European centres and finally eligible for analysis. For each subject, the daily energy and nutrient intake was estimated using the EPIC questionnaire and a 24-h dietary recall, and it was compared with the dietary reference values. Then we built a predictive model for a set of clinical outcomes computing shifts from recommended intake thresholds. The use of the ridge regression, which optimises prediction performances while retaining information about the role of all the nutritional variables, allowed us to assess if a clinical outcome was manly dependent on a single nutritional variable, or if its prediction was characterised by more complex interactions between the variables. The model appeared suitable for shedding light on the complexity of nutritional variables, which effects could be not evident with univariate analysis and must be considered in the framework of the reciprocal influence of the other variables.
2.
Effects of Nutrients on Platelet Function: A Modifiable Link between Metabolic Syndrome and Neurodegeneration?
Arnoldussen, IAC, Witkamp, RF
Biomolecules. 2021;(10)
Abstract
Metabolic syndrome increases the risk of vascular dementia and other neurodegenerative disorders. Recent studies underline that platelets play an important role in linking peripheral with central metabolic and inflammatory mechanisms. In this narrative review, we address the activation of platelets in metabolic syndrome, their effects on neuronal processes and the role of the mediators (e.g., serotonin, platelet-derived growth factor). Emerging evidence shows that nutritional compounds and their metabolites modulate these interactions-specifically, long chain fatty acids, endocannabinoids and phenolic compounds. We reviewed the role of activated platelets in neurovascular processes and nutritional compounds in platelet activation.
3.
Oxidative Stress in NAFLD: Role of Nutrients and Food Contaminants.
Rives, C, Fougerat, A, Ellero-Simatos, S, Loiseau, N, Guillou, H, Gamet-Payrastre, L, Wahli, W
Biomolecules. 2020;(12)
Abstract
Non-alcoholic fatty liver disease (NAFLD) is often the hepatic expression of metabolic syndrome and its comorbidities that comprise, among others, obesity and insulin-resistance. NAFLD involves a large spectrum of clinical conditions. These range from steatosis, a benign liver disorder characterized by the accumulation of fat in hepatocytes, to non-alcoholic steatohepatitis (NASH), which is characterized by inflammation, hepatocyte damage, and liver fibrosis. NASH can further progress to cirrhosis and hepatocellular carcinoma. The etiology of NAFLD involves both genetic and environmental factors, including an unhealthy lifestyle. Of note, unhealthy eating is clearly associated with NAFLD development and progression to NASH. Both macronutrients (sugars, lipids, proteins) and micronutrients (vitamins, phytoingredients, antioxidants) affect NAFLD pathogenesis. Furthermore, some evidence indicates disruption of metabolic homeostasis by food contaminants, some of which are risk factor candidates in NAFLD. At the molecular level, several models have been proposed for the pathogenesis of NAFLD. Most importantly, oxidative stress and mitochondrial damage have been reported to be causative in NAFLD initiation and progression. The aim of this review is to provide an overview of the contribution of nutrients and food contaminants, especially pesticides, to oxidative stress and how they may influence NAFLD pathogenesis.
4.
The SWI/SNF chromatin-remodeling factors BAF60a, b, and c in nutrient signaling and metabolic control.
Wang, RR, Pan, R, Zhang, W, Fu, J, Lin, JD, Meng, ZX
Protein & cell. 2018;(2):207-215
Abstract
Metabolic syndrome has become a global epidemic that adversely affects human health. Both genetic and environmental factors contribute to the pathogenesis of metabolic disorders; however, the mechanisms that integrate these cues to regulate metabolic physiology and the development of metabolic disorders remain incompletely defined. Emerging evidence suggests that SWI/SNF chromatin-remodeling complexes are critical for directing metabolic reprogramming and adaptation in response to nutritional and other physiological signals. The ATP-dependent SWI/SNF chromatin-remodeling complexes comprise up to 11 subunits, among which the BAF60 subunit serves as a key link between the core complexes and specific transcriptional factors. The BAF60 subunit has three members, BAF60a, b, and c. The distinct tissue distribution patterns and regulatory mechanisms of BAF60 proteins confer each isoform with specialized functions in different metabolic cell types. In this review, we summarize the emerging roles and mechanisms of BAF60 proteins in the regulation of nutrient sensing and energy metabolism under physiological and disease conditions.