In a few weeks time we will be joined by new PhD student Fiona Sach, who is funded through a NERC Envision Doctoral Training Programme, the Hermes Trust and Royal Society International Exchange scheme. Her project is supervised through Lisa Yon in the Vet School at Nottingham, Martin Broadley and myself in the School of Biosciences and is linked to the British Geological Survey with Michael Watts and Melanie Leng. Fiona will be focusing on mineral nutrition in captive and wild elephants.
Fiona has posted her own blog about the project here.
Our paper on the effect of maternal protein restriction on the rodent placental transcriptome has been accepted for publication in Genes and Nutrition. This work stems from studies originally performed by Angie Swali six years ago, with more recent RNA Sequencing analysis identifying differential regulation of genes involved in placental cholesterol transport as one of the possible mediators of developmental programming. The most recent elements of this project were funded by the Rosetrees Trust.
The effect of maternal undernutrition on the rat placental transcriptome: protein restriction up-regulates cholesterol transport.
Zoe Daniel, Angelina Swali, Richard Emes, Simon Langley-Evans
Fetal exposure to a maternal low protein diet during rat pregnancy is associated with hypertension, renal dysfunction and metabolic disturbance in adult life. These effects are present when dietary manipulations target only the first half of pregnancy. It was hypothesised that early gestation protein restriction would impact upon placental gene expression and that this may give clues to the mechanism which links maternal diet to later consequences. Pregnant rats were fed control or a low protein diet from conception to day 13 gestation. Placentas were collected and RNA Sequencing performed using the Illumina platform. Protein restriction down-regulated 67 genes and up-regulated 24 genes in the placenta. Ingenuity pathway analysis showed significant enrichment in pathways related to cholesterol and lipoprotein transport and metabolism, including atherosclerosis signalling, clathrin-mediated endocytosis, LXR/RXR and FXR/RXR activation. Genes at the centre of these processes included the apolipoproteins ApoB, ApoA2 and ApoC2, microsomal triglyceride transfer protein (Mttp), the clathrin-endocytosis receptor cubilin, the transcription factor retinol binding protein 4 (Rbp4) and transerythrin (Ttr; a retinol and thyroid hormone transporter). Real-time PCR measurements largely confirmed the findings of RNASeq and indicated that the impact of protein restriction was often striking (cubilin up-regulated 32-fold, apoC2 up-regulated 17.6-fold). The findings show that gene expression in specific pathways is modulated by maternal protein restriction in the day-13 rat placenta. Changes in cholesterol transport may contribute to altered tissue development in the fetus and hence programme risk of disease in later life.
Our paper on setting weight loss targets in a commercial weight management group has been accepted for publication in the Journal of Human Nutrition and Dietetics. It will be available through the journal website within 6 weeks- see Early View.
Setting targets leads to greater long-term weight losses and ‘unrealistic’ targets increase the effect in a large community-based commercial weight management group.
Amanda Avery, Michaela Carrington, Simon Langley-Evans and Judy Swift
Background. Setting personal targets is an important behavioural component in weight management programmes. Normal practice is to encourage ‘realistic’ weight loss but the under-pinning evidence base for this is limited and controversial. This study investigates the effect of number and size of weight loss targets on long-term weight loss in a large community sample of adults.
Methods. Weight change, attendance and target weight data for all new UK members, joining January to March 2012 was extracted from a commercial slimming organisation’s electronic database.
Results. Of the 35 380 members who had weight data available at 12 months after joining, 69.1% (n=24 447) had a starting BMI≥30kg/m2. Their mean weight loss was 12.9±7.8% and for both sexes, weight loss at 12 months was greater for those who set targets (p<0.001). Those that set ≥ 4 targets achieved the greatest loss (p<0.001). OR for weight loss ≥10% at 12 months was 10.3 (CI 9.7- 11.1, p<0.001) where targets had been set compared to none. At the highest quintile of target size, the size of the first target explained 47.2% (p<0.001) of the variance in weight loss achieved at 12 months. The mean BMI reduction in those with a target >25% was 7.6±4.0 kg/m2. A higher percentage of obese members did not set targets (p<0.001) compared to those with a BMI below 30kg/m2.
Conclusions. Much of the variance in achieved weight loss in this population was explained by the number of targets set and the size of the first target. Whilst obese people were less likely to set targets, doing so increased the likelihood of achieving clinically significant weight loss and for some ‘unrealistic’ targets improved results.
Our paper entitled Maternal high-fat feeding in pregnancy programmes atherosclerotic lesion size in the ApoE*3 Leiden mouse has been accepted for publication by the Journal of the Developmental Origins of Health and Disease. Study authors are Liz Tarling, Ruth Austin, Kevin Ryan, Susanne Kugler, Simon Langley-Evans and Andy Salter.
The paper describes the impact of feeding a high fat diet during pregnancy upon development of atherosclerosis in the adult ApoE*3 Leiden offspring of wild type mice. ApoE*3 Leiden mice are mice carrying a human mutation of the ApoE gene. This gene predisposes to atherosclerosis in mice that are fed a high cholesterol diet. In our study transgenic males were mated with wild type females and the pregnant mice were either fed a low fat or a high fat ‘Western’ type diet. Atherosclerosis prone ApoE*3 Leiden female offspring were then fed either low fat, low cholesterol diet or a high cholesterol atherogenic diet.
All mice fed the atherogenic diet developed atherosclerotic plaques, but those whose mothers were fed the high fat diet developed significantly larger plaques. This study confirms our earlier work that showed that maternal diet during pregnancy can programme atherosclerosis in the offspring, but importantly showed that a typical high fat Western diet is as effective in this programming as is undernutrition (our previous work showed programming by feeding a low protein diet). The data are consistent with the hypothesis that maternal fat intake may result in the development of atherosclerotic plaques during fetal development, but other mechanisms may be at work, including programming of inflammatory processes.
We are very pleased to welcome Nagehan Ertugrul Bilgili to the lab. Nagehan will be working under the supervision of myself and Simon Welham to investigate the role of amino acids in renal development.
The University of Nottingham has formed a new partnership with the University of Adelaide and as part of this the universities have created some new PhD studentships. Our lab has been fortunate enough to secure one of these studentships and we have now appointed Sally Draycott to be our student. Sally, a recent graduate from the School of Biosciences (Animal Science) will spend 2 years of her project here at Sutton Bonington and 2 years in Adelaide. Her supervisor in Australia will be Professor Robert Gibson. The project will examine the effect of fatty acids in the maternal diet upon fetal development and later health.
Calling course leaders and module organisers everywhere. Although it may be August and you are maybe sitting with your feet up listening to England destroy Australia in the cricket (as am I), climbing a mountain, walking the Pennine Way, perhaps lazing on a beach or paddling in the surf, you just know that it will soon be over and the students will be returning to campus hungry for your wisdom. It. Is. Going. To. Happen.
I am aware that many courses will be teaching lifespan nutrition at various stages of their degrees. Many of those courses make use of my book, Nutrition: A lifespan approach. I have extensively updated that first edition now and the second edition, entitled Nutrition Health and Disease: A lifespan approach will be available in a couple of weeks. If your libraries are now updating their stock, or you are renewing your reading lists then now might be a good time to take the details (ISBN:978-1-118-90709-2) and get some orders in.
As well as an updated text which will refer students to the current state-of-the-art in the subject, buying the book will give lecturers access to pre-prepared lecture slides which can be used in teaching.