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Medical nutritional therapy is the first-line approach in managing gestational diabetes mellitus (GDM). Diet is also a powerful modulator of the gut microbiota, whose impact on insulin resistance and the inflammatory response in the host are well known. Changes in the gut microbiota composition have been described in pregnancies either before the onset of GDM or after its diagnosis. The possible modulation of the gut microbiota by dietary interventions in pregnancy is a topic of emerging interest, in consideration of the potential effects on maternal and consequently neonatal health. To date, very few data from observational studies are available about the associations between diet and the gut microbiota in pregnancy complicated by GDM. In this review, we analyzed the available data and discussed the current knowledge about diet manipulation in order to shape the gut microbiota in pregnancy.

It has been hypothesized that assuming most of the caloric intake later in the day leads to metabolic disadvantages, but few studies are available on this topic. Aim of our study was to prospectively examine whether eating more of the daily caloric intake at dinner leads to an increased risk of obesity, hyperglycemia, metabolic syndrome, and non-alcoholic fatty liver disease (NAFLD). 1245 non-obese, non-diabetic middle-aged adults from a population-based cohort underwent a 3-day food record questionnaire at enrollment. Anthropometric values, blood pressure, blood metabolic variables, and estimated liver fat were measured at baseline and at 6-year follow-up. Prospective cohort study. Subjects were divided according to tertiles of percent daily caloric intake at dinner. A significant increase in the incidence rate of obesity (from 4.7 to 11.4%), metabolic syndrome (from 11.1 to 16.1%), and estimated NAFLD (from 16.5 to 23.8%) was observed from the lower to higher tertile. In a multiple logistic regression model adjusted for multiple covariates, subjects in the highest tertile showed an increased risk of developing obesity (OR = 2.33; 95% CI 1.17-4.65; p = 0.02), metabolic syndrome (OR = 1.52; 95% CI 1.01-2.30; p = 0.04), and NAFLD (OR = 1.56; 95% CI 1.10-2.22; p = 0.01). Consuming more of the daily energy intake at dinner is associated with an increased risk of obesity, metabolic syndrome, and NAFLD.

Natriuretic peptides are not only involved in cardiovascular adaption to various conditions, but also in metabolic diseases. We performed this study to assess the effect of a very short time of lifestyle inpatient intervention on NTproBNP values in normotensive subjects with severe obesity and normal cardiac function. We recruited 14 consecutive obese normotensive subjects with normal cardiac function who were aged 30 years and more and were referred to inpatient rehabilitation in an academic clinic over a two months period. They were examined at baseline and after a 3-weeks program including dietary intervention with hypocaloric diet and assisted personalized physical aerobic and anaerobic activities and compared to age, sex and BMI-matched control subjects under usual care. BMI significantly decreased (40.8 ±1.6 vs 42.3 ± 1.6 kg/m2, p <0.0001). Median reduction in body weight was 4.9 kg (interquartile range 2.4-5.2 kg). After diet and exercise-induced weight loss, plasma NTproBNP levels showed an almost two-fold increase, which was statistically significant (28.2 ± 12.3 vs 17.2 ± 13.2 ng/L, p = 0.01), and particularly relevant in the subgroup with NT-proBNP values below median values compared to those with higher values (p = 0.02). No significant variations were found in control subjects (18.0 ± 13.0 vs 16.5 ± 11.2 ng/L, p = 0.18). The lipid profile was significantly ameliorated, and both HbA1c and insulin levels showed a marginally non-significant decrease after treatment. An almost two-fold increase in NTproBNP levels was evident after a very short time period of lifestyle intervention in normotensive severe obese patients without cardiac disease. This finding might have clinical relevance, considering the role of NT-proBNP as risk factor of impaired glucose tolerance.

Background and aims NTproBNP and BNP levels are reduced in obese subjects, but population-based data comparing the pattern of this relationship in the full spectrum of insulin-resistance mediated conditions, overweight/obesity, metabolic syndrome and diabetes, are limited. Methods The study-base were 3244 individuals aged 45–74 years, none of whom had heart failure, 1880 without diabetes and 1364 with diabetes, identified as part of two surveys of the population-based Casale Monferrato Study. All measurements were centralized. We examined with multiple linear regression and cubic regression splines the relationship between NTproBNP and BMI, independently of known risk factors and confounders. A logistic regression analysis was also performed to assess the effect of overweight/obesity (BMI ≥ 25 kg/m 2 ), diabetes and metabolic syndrome on NTproBNP values. Results Out of the overall cohort of 3244 people, overweight/obesity was observed in 1118 (59.4%) non-diabetic and 917 (67.2%) diabetic subjects, respectively. In logistic regression, compared to normal weight individuals, those with a BMI ≥ 25 kg/m 2 had a OR of 0.70 (95% CI 0.56–0.87) of having high NTproBNP values, independently of diabetes. As interaction between diabetes and NTproBNP was evident (p < 0.001), stratified analyses were performed. Diabetes either alone or combined with overweight/obesity or metabolic syndrome enhanced fourfold and over the OR of having high NTproBNP levels, while the presence of metabolic syndrome alone had a more modest effect (OR 1.54, 1.18–2.01) even after having excluded individuals with CVD. In the non-diabetic cohort, obesity/overweight and HOMA-IR ≥ 2.0 decreased to a similar extent the ORs of high NTproBNP [0.76 (0.60–0.95) and 0.74 (0.59–0.93)], but the association between overweight/obesity and NTproBNP was no longer significant after the inclusion into the model of HOMA-IR, whereas CRP > 3 mg/dl conferred a fully adjusted OR of 0.65 (0.49–0.86). Conclusions NT-proBNP levels are lower in overweight/obesity, even in those with diabetes. Both insulin-resistance and chronic low-grade inflammation are involved in this relationship. Further intervention studies are required to clarify the potential role of drugs affecting the natriuretic peptides system on body weight and risk of diabetes.

The world is currently facing the coronavirus disease (COVID-19) pandemic which places great pressure on health care systems and workers, often presents with severe clinical features, and sometimes requires admission into intensive care units. Derangements in nutritional status, both for obesity and malnutrition, are relevant for the clinical outcome in acute illness. Systemic inflammation, immune system impairment, sarcopenia, and preexisting associated conditions, such as respiratory, cardiovascular, and metabolic diseases related to obesity, could act as crucial factors linking nutritional status and the course and outcome of COVID-19. Nevertheless, vitamins and trace elements play an essential role in modulating immune response and inflammatory status. Overall, evaluation of the patient's nutritional status is not negligible for its implications on susceptibility, course, severity, and responsiveness to therapies, in order to perform a tailored nutritional intervention as an integral part of the treatment of patients with COVID-19. The aim of this study was to review the current data on the relevance of nutritional status, including trace elements and vitamin status, in influencing the course and outcome of the disease 3 mo after the World Health Organization's declaration of COVID-19 as a pandemic. •Derangements in nutritional status can influence the course of coronavirus disease (COVID-19).•Obesity may worsen the outcome of COVID-19, requiring the most intensive care.•Vitamins and trace elements have a crucial role in immunomodulation.

The mass media has increasingly frequently suggested to the general population that specific foods or nutritional schemes are able to affect both human metabolism and energy expenditure, thus facilitating weight loss. This critical review is aimed at assessing available evidence on the roles of nutrients, food and dietary regimens in energy intake and energy expenditure. We queried the National Library of Medicine, the Cochrane Library, Excerpta Medica dataBASEand the Cumulative Index to Nursing and Allied Health Literature database, and a search strategy was performed by using database-specific subject headings and keywords. We found that available scientific evidence on these topics is scarce, and that the limited number of available studies often have poor methodological quality. Only a few foods show beneficial effects on metabolism and energy expenditure, as the human energy balance is complex and multifactorial. Finally, microbiota may interfere with the intake, use and expenditure of energy in the human body. Conclusive evidence is still lacking, and, at present, it is not possible to identify a food or a diet with a significant impact on human energy expenditure.

Background Timing of food intake impacts on metabolic diseases. Few data are available about post-meal changes in epinephrine (E), norepinephrine (NE), and acylated ghrelin (AG) at different times of the day. Subjects and methods This randomized cross-over trial investigated E/NE/AG concentrations after identical meals consumed at 0800 or 2000 hours in 20 healthy volunteers, by standardizing diet, exercise, duration of fast, and resting. Participants randomly received the test meal at 0800 or 2000 hours, and vice versa after 1 week. Blood samples were collected before and up to 180-min post-meal, every 30 min, with participants supine, motionless, but awake. Results Median E levels increased at 30–60 min, then declined and rose again at 150 min; values at 60 min (19.0 vs. 15.0 ng/l, p  = 0.03) and 180 min (25.0 vs. 11.0 ng/l, p  < 0.001) were higher after the morning meals. NE rose at 30–60 min and then progressively declined; median values at 60 min (235.3 vs. 206.3 ng/l, p  = 0.02) and 120 min (208.8 vs. 142.0 ng/l, p  = 0.04) increased more after morning meals. AG progressively declined to increase again at 90 min after meal; median AG area-under-the-curve (AUC) values were lower at morning (7206.8 vs. 8828.3 pg/mL×h). AG-AUC was inversely associated with diet-induced thermogenesis ( β  = −121.6; 95% CI −201.0 to 42.2; p  = 0.009 for each unit increase), while log NE-AUC was inversely associated with log-triglyceride AUC ( β  = −0.57; 95% CI −0.98 to 0.16; p  = 0.015) in a multiple regression model, after multiple adjustments. Conclusions In conclusion, E/NE concentrations were higher after the morning meal, while AG showed an opposite behavior. These data, although requiring confirmation in larger samples, suggest an adjunctive possible mechanism explaining the unfavorable effects of evening eating on metabolic risk

Background/Objectives It has been hypothesized that assuming most of the caloric intake later in the day leads to metabolic disadvantages, but few studies are available on this topic. Aim of our study was to prospectively examine whether eating more of the daily caloric intake at dinner leads to an increased risk of obesity, hyperglycemia, metabolic syndrome, and non-alcoholic fatty liver disease (NAFLD). Subjects/Methods 1245 non-obese, non-diabetic middle-aged adults from a population-based cohort underwent a 3-day food record questionnaire at enrollment. Anthropometric values, blood pressure, blood metabolic variables, and estimated liver fat were measured at baseline and at 6-year follow-up. Design Prospective cohort study. Results Subjects were divided according to tertiles of percent daily caloric intake at dinner. A significant increase in the incidence rate of obesity (from 4.7 to 11.4%), metabolic syndrome (from 11.1 to 16.1%), and estimated NAFLD (from 16.5 to 23.8%) was observed from the lower to higher tertile. In a multiple logistic regression model adjusted for multiple covariates, subjects in the highest tertile showed an increased risk of developing obesity (OR = 2.33; 95% CI 1.17-4.65; p = 0.02), metabolic syndrome (OR = 1.52; 95% CI 1.01-2.30; p = 0.04), and NAFLD (OR = 1.56; 95% CI 1.10-2.22; p = 0.01). Conclusions Consuming more of the daily energy intake at dinner is associated with an increased risk of obesity, metabolic syndrome, and NAFLD.

Diet and lifestyle factors greatly affect health and susceptibility to diseases, including cancer. Stem cells’ functions, including their ability to divide asymmetrically, set the rules for tissue homeostasis, contribute to health maintenance, and represent the entry point of cancer occurrence. Stem cell properties result from the complex integration of intrinsic, extrinsic, and systemic factors. In this context, diet-induced metabolic changes can have a profound impact on stem cell fate determination, lineage specification and differentiation. The purpose of this review is to provide a comprehensive description of the multiple “non-metabolic” effects of diet on stem cell functions, including little-known effects such as those on liquid-liquid phase separation and on non-random chromosome segregation (asymmetric division). A deep understanding of the specific dietetic requirements of normal and cancer stem cells may pave the way for the development of nutrition-based targeted therapeutic approaches to improve regenerative and anticancer therapies.

PurposeLow mitochondrial DNA (mtDNA) content in oocytes and in cumulus cells is an indicator of poor oocyte quality. Moreover, initial evidence showed a correlation between mtDNA content in cumulus cells and mtDNA copy number in peripheral blood cells. On these bases, we deemed of interest investigating the correlation between mtDNA copy number in peripheral blood and natural fecundity.MethodsThis is a nested case–control study drawn from a prospective cohort of pregnant women referred for routine first trimester screening for aneuploidies (from 11 + 0 to 12 + 6 weeks of gestation) between January 2012 and March 2013 at the “Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico” of Milan, Italy. Cases were subfertile women who attempted to become pregnant for 12–24 months. Controls were the two subsequently age-matched women who became pregnant in less than 1 year. MtDNA was quantified using real-time PCR and normalized to nuclear DNA.ResultsOne hundred and four subfertile women and 208 controls were selected. The median (IQR) mtDNA copy number was 95 (73–124) and 145 (106–198), respectively (p < 0.001). The area under the ROC curve was 0.73 (95% CI 0.67–0.79) (p < 0.001). The Youden index was 105 mtDNA copy number. The crude OR for subfertility in women with mtDNA copy number below this threshold was 5.72 (95% CI 3.43–9.55). The accuracy of mtDNA copy number assessment in peripheral blood progressively decreased with increasing female age.ConclusionsLow mtDNA copy number in peripheral blood is associated with an increased risk of subfertility and may represent a biomarker of natural fecundity.