Annals of Nutrition and Metabolism

Thông tin nền: Chúng tôi chưa biết đến nghiên cứu nào chỉ ra tác động của việc tiêu thụ hàng ngày các thực phẩm bổ sung probiotics đa loài đối với các chỉ số chuyển hóa, protein phản ứng C nhạy cảm cao (hs-CRP) và stress oxy hóa ở bệnh nhân tiểu đường. Mục tiêu: Nghiên cứu này nhằm xác định tác động của các thực phẩm bổ sung probiotics đa loài đến các chỉ số chuyển hóa, hs-CRP và stress oxy hóa ở bệnh nhân tiểu đường. Phương pháp: Nghiên cứu thử nghiệm lâm sàng ngẫu nhiên, mù đôi, có kiểm soát giả dược này được thực hiện trên 54 bệnh nhân tiểu đường từ 35 đến 70 tuổi. Các đối tượng được phân bổ ngẫu nhiên để sử dụng hoặc một thực phẩm bổ sung probiotics đa loài (n = 27) hoặc giả dược (n = 27) trong 8 tuần. Thực phẩm bổ sung probiotics đa loài gồm 7 chủng vi khuẩn còn sống và đã được sấy khô: Lactobacillus acidophilus (2 × 109 CFU), L. casei (7 × 109 CFU), L. rhamnosus (1.5 × 109 CFU), L. bulgaricus (2 × 108 CFU), Bifidobacterium breve (2 × 1010 CFU), B. longum (7 × 109 CFU), Streptococcus thermophilus (1.5 × 109 CFU), và 100 mg fructo-oligosaccharide. Mẫu máu lúc nhịn ăn được lấy tại thời điểm cơ bản và sau can thiệp để đo các chỉ số chuyển hóa, hs-CRP và các chỉ số sinh học về stress oxy hóa bao gồm khả năng chống oxy hóa tổng thể trong huyết tương và tổng glutathione (GSH). Kết quả: So sánh giữa các nhóm về glucose huyết tương lúc nhịn ăn (FPG) cho thấy việc tiêu thụ các thực phẩm bổ sung probiotics ngăn ngừa sự gia tăng FPG (+28.8 ± 8.5 đối với giả dược so với +1.6 ± 6 mg/dl đối với nhóm probiotics, p = 0.01). Mặc dù sự gia tăng đáng kể trong insulin huyết thanh và nồng độ cholesterol lipoprotein mật độ thấp được tìm thấy ở cả nhóm probiotics và nhóm giả dược, nhưng những thay đổi này tương tự nhau giữa hai nhóm. Chúng tôi ghi nhận sự gia tăng đáng kể trong HOMA-IR (mô hình đánh giá nhà ở - kháng insulin) ở cả nhóm probiotics (p = 0.02) và nhóm giả dược (p = 0.001); tuy nhiên, sự gia tăng ở nhóm giả dược cao hơn đáng kể so với nhóm probiotics (+2.38 so với +0.78, p = 0.03). Những thay đổi trung bình trong hs-CRP huyết thanh có sự khác biệt đáng kể giữa hai nhóm (-777.57 đối với nhóm probiotics so với +878.72 ng/ml đối với nhóm giả dược, p = 0.02). Việc bổ sung probiotics dẫn đến sự gia tăng đáng kể nồng độ GSH trong huyết tương so với giả dược (240.63 so với -33.46 µmol/l, p = 0.03). Kết luận: Tóm lại, việc bổ sung probiotics đa loài, so với giả dược, trong 8 tuần ở bệnh nhân tiểu đường đã ngăn ngừa sự gia tăng FPG và dẫn đến giảm hs-CRP huyết thanh và tăng GSH tổng thể trong huyết tương.

Non-communicable diseases (NCDs), such as cardiovascular disease and type 2 diabetes, constitute the main cause of death worldwide. Eighty percent of these deaths occur in low- and middle-income countries, especially as these countries undergo socio-economic improvement following reductions in the burden of infectious disease. The World Health Organization predicts a substantial increase in the incidence of NCDs over the next decade globally. NCDs are generally preventable, but current approaches are clearly inadequate. New initiatives are needed to implement such prevention, and there needs to be greater recognition that early-life interventions are likely to be the most efficacious. Devising appropriate prevention strategies necessitates an understanding of how the developmental environment influences risk. Progress in this field has been slow due to an excessive emphasis on fixed genomic variations (hard inheritance) as the major determinants of disease susceptibility. However, new evidence demonstrates the much greater importance of early-life developmental factors, involving epigenetic processes and ‘soft’ inheritance in modulating an individual’s vulnerability to NCD. This also offers opportunities for novel epigenetic biomarkers of risk or interventions targeting epigenetic pathways to be devised for use in early life. This may pave the way to much more effective, customised interventions to promote health across the life course.

The German, Austrian, and Swiss nutrition societies are the editors of the ‘reference values for nutrient intake'. They have revised the reference values for the intake of vitamin C and published them in February 2015. The average vitamin C requirement in healthy adults is considered to be the vitamin C amount that compensates for the metabolic losses of vitamin C, and ensures a fasting ascorbate plasma level of 50 µmol/l. Based on the present data from studies with non-smoking men, metabolic losses of 50 mg/day are assumed, as well as an absorption rate of 80% and an urinary excretion of 25% of the vitamin C intake. Taking this into account, the calculated average requirement in men is 91 mg/day. Considering a coefficient of variation of 10%, a reference value (recommended intake) of 110 mg/day for men is derived. The vitamin C requirement in women as well as in children and adolescents is extrapolated from the requirement in men and in relation to their body weight. This results in a recommended intake of about 95 mg/day for adult women. Because the requirement in pregnant and lactating women is increased, higher recommended intakes are derived for them, 105 mg/day for pregnant women from the fourth month on and 125 mg/day for lactating women, respectively. For boys and girls at the age of 1 to under 15 years, there are increasing recommended intake values from 20 to 85 mg/day. For male and female adolescents, at the age of 15 to under 19 years, the recommended intake is 105 and 90 mg, respectively. As smokers have higher metabolic losses and lower plasma levels of vitamin C than non-smokers (turnover is 40% higher), the reference value for vitamin C intake is set to 135 mg/day for female smokers and 155 mg/day for male smokers. For infants in their first year of life, the reference value (estimated value) is set to 20 mg vitamin C/ day, based upon the lowest observed vitamin C intake for infants in the United Kingdom and the United States, that obviously meets the requirement in infants and that is 3 times higher than the amount necessary to prevent scurvy (7 mg/day).

<b><i>Background/Aims:</i></b> Diabetes mellitus and pre-diabetes are closely associated with visceral obesity. Visceral adiposity index (VAI) is a novel sex-specific index, indirectly expressing visceral adipose function. Our aim was to determine the associations of VAI with dysglycemia (the combination of diabetes and pre-diabetes) and to compare the predictive ability for dysglycemia between VAI and traditional obesity indices. <b><i>Methods:</i></b> We performed a cross-sectional analysis of the data of 2,754 Chinese community-dwelling people who participated in the health checkup. Sex-specific VAI tertile cut-off points were used as follows: 1.70, 2.77 in males and 0.98, 1.75 in females. Binary logistic regression models were performed to estimate the association of the higher values of all the obesity indices with pre-diabetes and diabetes. The area under the curve (AUC) of the receiver operating characteristic (ROC) curve was applied to compare the predictive potential for dysglycemia among the obesity indices. <b><i>Results:</i></b> VAI was the only index significantly associated with both pre-diabetes and diabetes in both sexes after adjusting for potential confounders. The results of ROC analysis and AUC showed that VAI possessed the largest AUC, followed by other obesity indices. <b><i>Conclusions:</i></b> Higher VAI values are positively associated with the presence of pre-diabetes and diabetes in Chinese adults.

The prevalence of obesity is increasing at an alarming rate in many parts of the world. About 2 billion people are overweight and one third of them obese. The plight of the most affected populations, like those in high-income countries in North America, Australasia and Europe, has been well publicized. However, the more recent increases in population obesity in low- and middle-income countries that are now increasingly being observed have been less recognized. Based on the existing prevalence and trend data and the epidemiological evidence linking obesity with a range of physical and psychosocial health conditions, it is reasonable to describe obesity as a public health crisis that severely impairs the health and quality of life of people and adds considerably to national health-care budgets. Intersectoral action to manage and prevent obesity is urgently required to reverse current trends.

Plasma lipoprotein abnormalities in maturity onset diabetes (MOD) reflect both enhanced production and impaired removal of triglyceride-rich lipoproteins. Hyper-glycemia and hyperinsulinemia lead to overproduction of very-low-density lipoproteins by the liver. Fat tolerance is reduced in MOD patients: this might be due to low lipoprotein lipase activity (LLA) and/or to low incorporation of LLA-released fatty acids into adipose tissue glyceride. The finding of abnormal low-density lipoprotein composition, with relative enrichment in triglyceride, suggests remnant particle accumulation.

Vitamin D (vitD) deficiency is associated with a wide range of chronic diseases and conditions, including obesity, and with an increasing severity of metabolic dysregulation, such as insulin resistance, hyperlipidemia, liver disease, and hypertension, both in children and adults. However, the nature of the association between low vitD status and obesity remains unclear. This fact has motivated the scientific community to conduct genetic association analyses between 25-hydroxyvitamin D (25[OH]D)-related genes and obesity traits. In this line, the variation in the vitD receptor (<i>VDR</i>) gene represents the bulk of the findings. Specifically, polymorphisms in the <i>VDR</i> gene have been associated with obesity traits in some but not all, studies. Thus, results regarding this matter remain inconclusive. Other genes aside from <i>VDR</i> have also been investigated in relation to obesity-related traits. However, again, findings have been inconsistent. In general, results point to the fact that the <i>DBP/GC</i> gene could be an important protein-linking obesity and vitD status. On the other hand, several studies have attempted to determine the molecular mechanism of the relationship between 25(OH)-D levels and obesity. Some of these studies suggest that vitD, due to its fat-soluble characteristic, is retained by the adipose tissue and has the capacity to metabolize 25(OH)-D locally, and this can be altered during obesity. Additionally, vitD is capable of regulating the gene expression related to adipogenesis process, inflammation, oxidative stress, and metabolism in mature adipocytes. Therefore, the aim of the present review was to evaluate the association between obesity and vitD deficiency describing the main molecular mechanism of the relationship and the link with genetic factors. <b><i>Key Messages:</i></b> Low serum 25(OH)-D is positively associated with obesity or BMI in adults and children. Circulating vitD concentrations are, at least, partially determined by genetic factors. VitD plays an important role in the adipogenesis process and inflammation status in adipocytes and adipose tissue.

<b><i>Background:</i></b> The obesity pandemic has been paralleled by a high prevalence of vitamin D deficiency (VDD). There is growing epidemiological evidence linking low vitamin D status with obesity events. In addition, observational studies also show that obesity may increase the risk of VDD. However, there is insufficient knowledge to understand whether there is a causality between the two. Moreover, the impact of vitamin D supplementation on obesity indices has shown inconsistent outcomes. <b><i>Objective:</i></b> This meta-analysis aimed to assess whether vitamin D supplementation modified general and central obesity indices in apparently healthy populations. <b><i>Methods:</i></b> A systematic retrieval of relevant randomized controlled trials (RCTs) was undertaken using Pubmed, Embase, Web of Knowledge and Chinese National Knowledge Infrastructure databases. The pooled weighted mean difference (WMD) and 95% confidence intervals (CI) were used to assess the changes in body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR) and 25-hydroxyvitamin D (25[OH]D) from baseline. <b><i>Results:</i></b> Twenty RCTs involving 3,153 participants reporting either BMI, WC, WHR or 25(OH)D met the inclusion criteria. When compared with placebo, vitamin D supplementation had no significant decreases in BMI (WMD = –0.09 kg/m², 95% CI –0.19 to 0.01, <i>p</i> = 0.08), WC (WMD = –0.71 cm, 95% CI –1.58 to 0.16, <i>p</i> = 0.112) or WHR (WMD = 0.00, 95% CI –0.01 to 0.01, <i>p</i> = 0.749). However, in the subgroups of females, Asia region studies and intervention duration ≥6 months, a beneficial and significant reduction in BMI and WC was noted (all <i>p</i> &#x3c; 0.026). On the other hand, pooled results showed that there was a significant increase in serum 25(OH)D levels (WMD = 13.20 ng/mL, 95% CI 9.83–16.58, <i>p</i> &#x3c; 0.001) after vitamin D intervention. No publication bias was found in our study. <b><i>Conclusions:</i></b> Overall, supplementation with vitamin D produced no significant effect on the BMI, WC or WHR of healthy adults.

<b><i>Background:</i></b> In phenylketonuria (PKU), phenylalanine-free <smlcap>L</smlcap>-amino acid supplements are the major source of dietary micronutrients. <b><i>Methods:</i></b> Four hundred fifty-two retrospective annual/bi-annual non-fasting blood samples for nutritional markers (plasma zinc, selenium, and serum folate) from 78 subjects aged 1-16 years (median number of blood samples: 6, range 1-14) were analysed over 12 years. Longitudinal blood result data were available for 51 subjects (65%). The dietary intake from supplements was calculated. <b><i>Results:</i></b> The median intakes of all of the micronutrients studied were >200% of the reference nutrient intakes (RNI). There was no statistical correlation between dietary intake and nutritional markers outside of the normal reference range (RR) except for selenium, but there was a correlation between a lower plasma zinc, plasma selenium and haemoglobin status and better blood phenylalanine control in 1- to 4-year-old children. On at least one occasion, the individual plasma concentrations of zinc (71%, n = 54/76) and selenium (21%, n = 16/75) were below the RR; however, the concentrations of selenium (41%, n = 31/75) and serum folate (83%, n = 34/41) were also above the RR. Dietary intakes exceeded the upper tolerable intakes for zinc and copper (32%, n = 25) and folate (65%, n = 51). Individual longitudinal data demonstrated little change in micronutrient status over time. <b><i>Conclusions:</i></b> In PKU, biochemical micronutrient deficiencies are common despite micronutrient intakes above the RNI. Further study of the nutritional profiling of <smlcap>L</smlcap>-amino acid supplements in PKU is needed.