Nutrition During Pregnancy and the Effect of Carbohydrates on the Offspring’s Metabolic Profile: In Search of the “Perfect Maternal Diet”

Fetal growth and development is primarily dependent upon the nutritional, hormonal and metabolic environment provided by the mother. A wartime famine study in Holland first showed that a low food intake reduces the glucose offered to the fetus and thus produces smaller size infants at birth. Maternal glucose regulation is however affected by numerous factors including physiological changes of pregnancy (e.g. insulin resistance [IR]), pathological conditions (e.g. gestational diabetes mellitus) and maternal nutrition. Maternal glucose is substantially influenced by the type of carbohydrates in the diet through its direct effect on glycemia. The rate at which each carbohydrate raises blood glucose levels after ingestion, can be measured via the dietary glycemic index (GI). Carbohydrate type and the GI of the diet enhance or inhibit abnormal hyperglycemia during pregnancy caused by either pathological conditions or the inability of the mother to cope with the physiological IR of pregnancy. In turn, maternal gestational hyperglycemia may be involved in the pathogenesis of IR, impaired glucose tolerance, type 2 diabetes mellitus, the Metabolic Syndrome and subsequent cardiovascular diseases in adult offspring. A low GI maternal diet has been associated with measurable benefits to the offspring. These include a positive effect on altering maternal blood glucose production, insulinemia and reduced adiposity as well as fetal and placental insulin and glucose regulation, fetal growth, birth weight and offspring adiposity. We review the possible links between dietary carbohydrate in health during pregnancy and the effect of maternal carbohydrate ingestion on programming the offspring’s metabolic profile

Correlation between mesenteric fat thickness and serum apolipoproteins in patients with peripheral arterial occlusive disease

BACKGROUND: Visceral fat possesses the most detrimental potential for cardiovascular morbidity through the release of adipokines, as well as metabolic and proinflammatory mediators, which adversely affect metabolic and vascular homeostasis. Among the different types of visceral adipose tissue, mesenteric fat is considered particularly detrimental, due to its close proximity to the portal circulation, affecting directly the liver, which is the main regulator of body metabolic homeostasis. Mesenteric fat can be reliably estimated using abdominal ultrasonography, the only available imaging method able to depict individual mesenteric leaves. Aim of the present study was to investigate the correlation of mesenteric fat thickness (MFT) with serum apolipoprotein levels in patients undergoing digital subtraction angiography in a single center. METHODS: 35 male patients with peripheral arterial disease were examined. After careful examination of the periumbilical area, the mesenteric leaves were identified. The maximal distance between each pair of sequential leaves was measured, and the mean value of the three thickest leaves was determined as the mesenteric fat thickness. Six apolipoprotein fasting serum concentrations were measured using a Luminex proteomics platform (xMAP Multiplex immunoassay): apolipoprotein A-I (apoAI), apolipoprotein A-II (apoAII), apolipoprotein B (apoB), apolipoprotein C-II (apoCII), apolipoprotein C-III (apoCIII) and apolipoprotein E (apoE). RESULTS: MFT correlated with apoAII and apoB serum concentrations. The correlations with apoAII and apoB remained significant following correction for BMI. No correlations were noted between MFT and serum apoAI, apoCII, apoCIII or apoE levels before or after adjustment for BMI. CONCLUSIONS: Our study indicates that MFT is significantly correlated with the concentration of atherogenic low density lipoproteins particles, as well as with apoAII, a determinant of free fatty acids levels. No correlation was observed between mesenteric fat thickness and very low density lipoprotein or chylomicron particles concentration

Preterm Birth and Its Association with Maternal Diet, and Placental and Neonatal Telomere Length

Preterm birth (PTB), a multi-causal syndrome, is one of the global epidemics. Maternal nutrition, but also neonatal and placental telomere length (TL), are among the factors affecting PTB risk. However, the exact relationship between these factors and the PTB outcome, remains obscure. The aim of this review was to investigate the association between PTB, maternal nutrition, and placental-infant TL. Observational studies were sought with the keywords: maternal nutrition, placental TL, newborn, TL, and PTB. No studies were found that included all of the keywords simultaneously, and thus, the keywords were searched in dyads, to reach assumptive conclusions. The findings show that maternal nutrition affects PTB risk, through its influence on maternal TL. On the other hand, maternal TL independently affects PTB risk, and at the same time PTB is a major determinant of offspring TL regulation. The strength of the associations, and the extent of the influence from covariates, remains to be elucidated in future research. Furthermore, the question of whether maternal TL is simply a biomarker of maternal nutritional status and PTB risk, or a causative factor of PTB, to date, remains to be answered

“Is obesity linked to aging?” Adipose tissue and the role of telomeres

Obesity is a condition in which excess or abnormal fat accumulation may present with adverse effects on health and decreased life expectancy. Increased body weight and adipose tissue accumulation amplifies the risk of developing various age-related diseases, such as cardiovascular disease. Type 2 Diabetes Mellitus, musculoskeletal disorders, respiratory diseases and certain types of cancer. This imbalance in body composition and body weight is now recognized as a state of increased oxidative stress and inflammation for the organism. Increasing oxidative stress and inflammation affect telomeres. Telomeres are specialized DNA-protein structures found at the ends of eukaryotic chromosomes and serve as markers of biological aging rate. They also play a critical role in maintaining genomic integrity and are involved in age-related metabolic dysfunction. Erosion of telomeres is hazardous to healthy cells, as it is a known mechanism of premature cellular senescence and loss of longevity. The association of telomeres and oxidative stress is evident in cultured somatic cells in vitro, where oxidative stress enhances the process of erosion with each cycle of replication. Shorter telomeres have been associated with increasing body mass index, increased adiposity, and more recently with increasing waist to hip ratio and visceral excess fat accumulation. Furthermore, many of the metabolic imbalances of obesity (e.g. glycemic, lipidemic, etc.) give rise to organ dysfunction in a way that resembles the accelerated aging process. This article is a non-systematic review of the evidence linking obesity and accelerated aging processes as they are regulated by telomeres. (C) 2011 Elsevier B.V. All rights reserved

Knowledge of Blood Transfusion in Medical And Biology Student

Introduction: Blood transfusion (hemotherapy) is a therapeutic intervention used in treatment strategies of multiple diseases, thus, proper education is of utmost importance. Since currently there are no specified educational programs, undergraduate students were evaluated for the knowledge gained during university courses. Purpose: To evaluate and compare the level of knowledge of students of the faculty of Health Science, Department of Medicine (DM), and Department of Molecular Biology-Genetics (DMB&Gs) on issues related to the transfusion of blood products. Methods: A cross-sectional observational study was carried out with 123 students from the aforementioned departments of the Democritus University of Thrace, from the third year to the last year of study. A questionnaire was used, weighted, and was based on the European Commission’s Guide to the Preparation, Use and Quality Assurance for Blood Components. Statistical tests such as chi-square (chi 2), t-test, analysis of variance (ANOVA), and linear regression were used to investigate the factors that affect the overall score. Results: The mean score of the students was 42.55 while the standard deviation (SD) was 12.27. The difference in the scores between the students of the DM (M = 44.63, SD = 13.2) and those of the DMB&Gs (mean = 38.25, SD = 9.05) was statistically significant in the univariable analysis (t= 3.1, p = 0.0), but in the multivariable analysis, it was not statistically significant (beta = -4.1, p = 0.1.). The results of the multiple regression model indicated that the year of study, the professional status of the father, and the grade in the hematology course were associated with the total score. Conclusions: The level of knowledge regarding blood product transfusion among students of the faculty of Health Science is insufficient

Ageing, longevity, exceptional longevity and related genetic and non genetics markers: panel statement

In May 2012, a group of scientists and clinicians met in Athens (Greece) to consider the relevance of ageing, longevity, exceptional longevity and related genetic and non genetic markers. During this meeting, we firstly reviewed recent epidemiological and clinical studies on ageing, longevity and exceptional longevity, briefly analyzed the ageing theories and discussed successful and unsuccessful ageing also taking into account the evolutionary perspective. Secondly, we considered the three phenotypes based on the definition of ageing, longevity and exceptional longevity and the associated biomarkers. Third, we discussed proposed treatments suitable to counteract or slow down ageing. Finally, this panel produced a consensus statement to highlight the importance of ageing, longevity and exceptional longevity, since this is a rapidly increasing phenotype worldwide. We acknowledge that not all experts in this field may completely agree with this statement

Correlation between mesenteric fat thickness and serum apolipoproteins in patients with peripheral arterial occlusive disease

Abstract Background Visceral fat possesses the most detrimental potential for cardiovascular morbidity through the release of adipokines, as well as metabolic and proinflammatory mediators, which adversely affect metabolic and vascular homeostasis. Among the different types of visceral adipose tissue, mesenteric fat is considered particularly detrimental, due to its close proximity to the portal circulation, affecting directly the liver, which is the main regulator of body metabolic homeostasis. Mesenteric fat can be reliably estimated using abdominal ultrasonography, the only available imaging method able to depict individual mesenteric leaves. Aim of the present study was to investigate the correlation of mesenteric fat thickness (MFT) with serum apolipoprotein levels in patients undergoing digital subtraction angiography in a single center. Methods 35 male patients with peripheral arterial disease were examined. After careful examination of the periumbilical area, the mesenteric leaves were identified. The maximal distance between each pair of sequential leaves was measured, and the mean value of the three thickest leaves was determined as the mesenteric fat thickness. Six apolipoprotein fasting serum concentrations were measured using a Luminex proteomics platform (xMAP Multiplex immunoassay): apolipoprotein A-I (apoAI), apolipoprotein A-II (apoAII), apolipoprotein B (apoB), apolipoprotein C-II (apoCII), apolipoprotein C-III (apoCIII) and apolipoprotein E (apoE). Results MFT correlated with apoAII and apoB serum concentrations. The correlations with apoAII and apoB remained significant following correction for BMI. No correlations were noted between MFT and serum apoAI, apoCII, apoCIII or apoE levels before or after adjustment for BMI. Conclusions Our study indicates that MFT is significantly correlated with the concentration of atherogenic low density lipoproteins particles, as well as with apoAII, a determinant of free fatty acids levels. No correlation was observed between mesenteric fat thickness and very low density lipoprotein or chylomicron particles concentration.</p

The challenges in moving from ageing to successful longevity

During the last decades survival has significantly improved and centenarians are becoming a fast-growing group of the population. Human life span is mainly dependent on environmental and genetic factors. Favourable modifications of lifestyle factors (e.g. physical activity, diet and not smoking) and healthcare (e.g. effective vascular disease prevention) have also increased human life span. Genetic factors contribute to the variation of human life span by around 25%, which is believed to be more profound after 85 years of age. It is likely that multiple factors influence life span and we need answers to questions such as: 1) What does it take to reach 100?, 2) Do centenarians have better health during their lifespan compared with contemporaries who died at a younger age?, 3) Do centenarians have protective modifications of body composition, fat distribution and energy expenditure, maintain high physical and cognitive function, and sustained engagement in social and productive activities?, 4) Do centenarians have genes which contribute to longevity?, 5) Do centenarians benefit from epigenetic phenomena?, 6) Is it possible to influence the transgenerational epigenetic inheritance (epigenetic memory) which leads to longevity?, 7) Is the influence of nutrigenomics important for longevity?, 8) Do centenarians benefit more from drug treatment, particularly in primary prevention?, and, 9) Are there any potential goals for drug research? Many definitions of successful ageing have been proposed, but at present there is no consensus definition. Such definitions may need to differentiate between "Longevity Syndrome" and "Exceptional Longevity"