ORCID Profile
0000-0002-4740-4307
Current Organisation
King's College London
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Publisher: Georg Thieme Verlag KG
Date: 03-2021
DOI: 10.1055/A-1377-6583
Abstract: Currently, we are experiencing a true pandemic of a communicable disease by the virus SARS-CoV-2 holding the whole world firmly in its grasp. Amazingly and unfortunately, this virus uses a metabolic and endocrine pathway via ACE2 to enter our cells causing damage and disease. Our international research training programme funded by the German Research Foundation has a clear mission to train the best students wherever they may come from to learn to tackle the enormous challenges of diabetes and its complications for our society. A modern training programme in diabetes and metabolism does not only involve a thorough understanding of classical physiology, biology and clinical diabetology but has to bring together an interdisciplinary team. With the arrival of the coronavirus pandemic, this prestigious and unique metabolic training programme is facing new challenges but also new opportunities. The consortium of the training programme has recognized early on the need for a guidance and for practical recommendations to cope with the COVID-19 pandemic for the community of patients with metabolic disease, obesity and diabetes. This involves the optimal management from surgical obesity programmes to medications and insulin replacement. We also established a global registry analyzing the dimension and role of metabolic disease including new onset diabetes potentially triggered by the virus. We have involved experts of infectious disease and virology to our faculty with this metabolic training programme to offer the full breadth and scope of expertise needed to meet these scientific challenges. We have all learned that this pandemic does not respect or heed any national borders and that we have to work together as a global community. We believe that this transC us metabolic training programme provides a prime ex le how an international team of established experts in the field of metabolism can work together with students from all over the world to address a new pandemic.
Publisher: Elsevier BV
Date: 03-2016
DOI: 10.1016/J.BBR.2015.12.027
Abstract: Perinatal junk food exposure increases the preference for palatable diets in juvenile and adult rat offspring. Previous studies have implicated reduced sensitivity of the opioid pathway in the programming of food preferences however it is not known when during development these changes in opioid signalling first emerge. This study aimed to determine the impact of a maternal junk food (JF) diet on mu-opioid receptor (MuR) expression and ligand binding in two key regions of the reward pathway, the nucleus accumbens (NAc) and the ventral tegmental area (VTA) in rats during the early suckling (postnatal day (PND) 1 and 7) and late suckling/early post-weaning (PND 21 and 28) periods. Female rats were fed either a JF or a control diet for two weeks prior to mating and throughout pregnancy and lactation. MuR expression in the VTA was significantly reduced in female JF offspring on PND 21 and 28 (by 32% and 57% respectively, P<0.05), but not at earlier time points (PND 1 and 7). MuR ligand binding was also reduced (by 22%, P<0.05) in the VTA of female JF offspring on PND 28. No effects of perinatal junk food exposure on MuR mRNA expression or binding were detected at these time points in male offspring. These findings provide evidence that the opioid signalling system is a target of developmental programming by the end of the third postnatal week in females, but not in males.
Publisher: Springer Science and Business Media LLC
Date: 12-10-2022
DOI: 10.1038/S41366-022-01210-3
Abstract: Obesity in pregnancy has been associated with increased childhood cardiometabolic risk and reduced life expectancy. The UK UPBEAT multicentre randomised control trial was a lifestyle intervention of diet and physical activity in pregnant women with obesity. We hypothesised that the 3-year-old children of women with obesity would have heightened cardiovascular risk compared to children of normal BMI women, and that the UPBEAT intervention would mitigate this risk. Children were recruited from one UPBEAT trial centre. Cardiovascular measures included blood pressure, echocardiographic assessment of cardiac function and dimensions, carotid intima-media thickness and heart rate variability (HRV) by electrocardiogram. Compared to offspring of normal BMI women ( n = 51), children of women with obesity from the trial standard care arm ( n = 39) had evidence of cardiac remodelling including increased interventricular septum (IVS mean difference 0.04 cm 95% CI: 0.018 to 0.067), posterior wall (PW 0.03 cm 0.006 to 0.062) and relative wall thicknesses (RWT 0.03 cm 0.01 to 0.05) following adjustment. Randomisation of women with obesity to the intervention arm ( n = 31) prevented this cardiac remodelling (intervention effect mean difference IVS −0.03 cm (−0.05 to −0.008) PW −0.03 cm (−0.05 to −0.01) RWT −0.02 cm (−0.04 to −0.005)). Children of women with obesity (standard care arm) compared to women of normal BMI also had elevated minimum heart rate (7 bpm 1.41 to 13.34) evidence of early diastolic dysfunction (e prime) and increased sympathetic nerve activity index by HRV analysis. Maternal obesity was associated with left ventricular concentric remodelling in 3-year-old offspring. Absence of remodelling following the maternal intervention infers in utero origins of cardiac remodelling. The UPBEAT trial is registered with Current Controlled Trials, ISRCTN89971375.
Publisher: KARGER
Date: 2008
DOI: 10.1159/000115355
Abstract: Obesity and its sequelae may prove to be the greatest threat to human lifestyle and health in the developed world this century. The so called obesity epidemic has seen the incidence of obesity and overweight almost double in Western societies and the trend is mirrored in nations that are transitioning to first world economies. There is no doubt that much of the rise in obesity can be attributed to lifestyle factors such as the excess consumption of energy-dense foods and the decline in physical activity. However, the 'fetal origins'hypothesis, first proposed by Barker and colleagues and elaborated by several groups over the past 15 years to be termed the 'Developmental Origins of Adult Health and Disease' (DOHaD), provides an alternative explanation for the rising rates of obesity. The DOHaD hypothesis states that exposure to an unfavourable environment during development (either in utero or in the early postnatal period) programmes changes in fetal or neonatal development such that the in idual is then at greater risk of developing adulthood disease. This chapter discusses the effects of maternal obesity on fetal development and birth outcomes as well as the manner in which DOHaD may contribute to the obesity epidemic.
Publisher: Wiley
Date: 12-04-2007
DOI: 10.1113/EXPPHYSIOL.2006.036202
Abstract: We have previously reported that male and female offspring of Sprague-Dawley rats fed a diet rich (approximately 50% of caloric intake from fat) in animal fat (lard) during pregnancy and suckling (OHF) demonstrate cardiovascular dysfunction, including blunted endothelium-dependent vasodilatation in the aorta as well as reduced renal Na(+),K(+)-ATPase activity. Cardiovascular dysfunction has been reported in other models of developmental programming and some researchers describe transmission from F(1) to F(2) generations. Here we report a study of vascular function, as assessed in isolated rings of aorta mounted in an organ bath, and renal Na(+),K(+)-ATPase activity in 6-month-old male and female F(2) offspring of lard-fed and control-fed (OC) dams (n = 13 per diet group). An increase in brain (OC 0.61 +/- 0.01% versus OHF 0.66 +/- 0.02% of bodyweight) and kidney weights (OC 0.32 +/- 0.01% versus OHF 0.37 +/- 0.01% of bodyweight) was observed in female F(2) offspring of lard-fed dams compared with F(2) controls (P < 0.03). Constrictor responses to phenylephrine in the aorta were not different from F(2) controls (repeated measures ANOVA, P = 0.85). Also, endothelium-dependent dilator function, as assessed by responses to acetylcholine (repeated measures ANOVA, P = 0.96) and passive distensibility in the absence of extracellular calcium (repeated measures ANOVA, P = 0.68), was similar. Additionally, renal Na(+),K(+)-ATPase activity was not statistically different from that observed in control animals (ANOVA, P = 0.89). Although a maternal diet rich in animal fat has deleterious effects on parameters of cardiovascular risk in F(1) animals, it does not appear that disorders previously reported in the F(1) generation are transmitted to the F(2) generation.
Publisher: Wiley
Date: 14-10-2008
Publisher: Wiley
Date: 05-2005
Publisher: Wiley
Date: 17-02-2006
Publisher: BMJ
Date: 17-11-2021
DOI: 10.1136/ARCHDISCHILD-2021-322860
Abstract: Maternal obesity may increase offspring risk of cardiovascular disease. We assessed the impact of maternal obesity on cardiac structure and function in newborns as a marker of fetal cardiac growth. Neonates born to mothers of healthy weight (body mass index (BMI) 20–25 kg/m 2 , n=56) and to mothers who were obese (BMI ≥30 kg/m 2 , n=31) underwent 25-minute continuous ECG recording and non-sedated, free-breathing cardiac MRI within 72 hours of birth. Mean (SD) heart rate during sleep was higher in infants born to mothers who were versus were not obese (123 (12.6) vs 114 (9.8) beats/min, p=0.002). Heart rate variability during sleep was lower in infants born to mothers who were versus were not obese (SD of normal-to-normal R-R interval 34.6 (16.8) vs 43.9 (16.5) ms, p=0.05). Similar heart rate changes were seen during wakefulness. Left ventricular end-diastolic volume (2.35 (0.14) vs 2.54 (0.29) mL/kg, p=0.03) and stroke volume (1.50 (0.09) vs 1.60 (0.14), p=0.04) were decreased in infants born to mothers who were versus were not obese. There were no differences in left ventricular end-systolic volume, ejection fraction, output or myocardial mass between the groups. Maternal obesity was associated with increased heart rate, decreased heart rate variability and decreased left ventricular volumes in newborns. If persistent, these changes may provide a causal mechanism for the increased cardiovascular risk in adult offspring of mothers with obesity. In turn, modifying antenatal and perinatal maternal health may have the potential to optimise long-term cardiovascular health in offspring.
Publisher: Wiley
Date: 26-11-2004
Publisher: Wiley
Date: 05-2005
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Paul David Taylor.