Publications
348 results found
Violante IR, Anastasovska J, Sanchez-Canon GJ, et al., 2009, Cerebral Activation by Fasting Induces Lactate Accumulation in the Hypothalamus, MAGNETIC RESONANCE IN MEDICINE, Vol: 62, Pages: 279-283, ISSN: 0740-3194
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- Citations: 14
Modi N, Thomas EL, Uthaya SN, et al., 2009, Whole Body Magnetic Resonance Imaging of Healthy Newborn Infants Demonstrates Increased Central Adiposity in Asian Indians, PEDIATRIC RESEARCH, Vol: 65, Pages: 584-587, ISSN: 0031-3998
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- Citations: 77
Nunn AVW, Bell JD, Guy GW, 2009, Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe?, Nutrition and Metabolism, Vol: 6, Pages: 1-26, ISSN: 1743-7075
The metabolic syndrome may have its origins in thriftiness, insulin resistance and one of the most ancient of all signalling systems, redox. Thriftiness results from an evolutionarily-driven propensity to minimise energy expenditure. This has to be balanced with the need to resist the oxidative stress from cellular signalling and pathogen resistance, giving rise to something we call 'redox-thriftiness'. This is based on the notion that mitochondria may be able to both amplify membrane-derived redox growth signals as well as negatively regulate them, resulting in an increased ATP/ROS ratio. We suggest that 'redox-thriftiness' leads to insulin resistance, which has the effect of both protecting the individual cell from excessive growth/inflammatory stress, while ensuring energy is channelled to the brain, the immune system, and for storage. We also suggest that fine tuning of redox-thriftiness is achieved by hormetic (mild stress) signals that stimulate mitochondrial biogenesis and resistance to oxidative stress, which improves metabolic flexibility. However, in a non-hormetic environment with excessive calories, the protective nature of this system may lead to escalating insulin resistance and rising oxidative stress due to metabolic inflexibility and mitochondrial overload. Thus, the mitochondrially-associated resistance to oxidative stress (and metabolic flexibility) may determine insulin resistance. Genetically and environmentally determined mitochondrial function may define a 'tipping point' where protective insulin resistance tips over to inflammatory insulin resistance. Many hormetic factors may induce mild mitochondrial stress and biogenesis, including exercise, fasting, temperature extremes, unsaturated fats, polyphenols, alcohol, and even metformin and statins. Without hormesis, a proposed redox-thriftiness tipping point might lead to a feed forward insulin resistance cycle in the presence of excess calories. We therefore suggest that as oxidative stress det
Guy GW, Nunn AVW, Thomas LE, et al., 2009, Obesity, diabetes and longevity in the Gulf: Is there a Gulf Metabolic Syndrome?, International Journal of Diabetes Mellitus, Vol: 1, Pages: 43-54, ISSN: 1877-5934
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- Citations: 14
Kamaly N, Kalber T, Thanou M, et al., 2009, Folate Receptor Targeted Bimodal Liposomes for Tumor Magnetic Resonance Imaging, Bioconjugate Chem., Vol: 20, Pages: 648-655, ISSN: 1043-1802
Folate-targeted bimodal paramagnetic and fluorescent liposomes were developed and showed enhanced accumulation in a folate receptor expressing tumor model. These bimodal liposomes were composed of both a paramagnetic and a fluorescent lipid, and utilized a PEG-lipid amphiphile for prolonged in vivo circulation. The particles were formulated to ensure a size distribution of approximately 100 nm with a low polydispersity index. IGROV-1 cells were used to induce tumors in nude Balb/c mice, and the folate-targeted liposomes were injected intravenously. Rapid accumulation of the folate-targeted liposomes within the tumor tissue compared to nontargeted liposomes was observed. Furthermore, folate-labeled liposomes showed a 4-fold increase in tumor T-1 signal intensity at just 2 h postinjection with similar results being obtained for the nontargeted liposomes only 24 h postinjection. In addition, the folate-targeted liposomes were injected at half the nontargeted liposome dose, further demonstrating their effectiveness. Histological analysis of sectioned tumor slices revealed distinct fluorescence patterns between the targeted and nontargeted systems, with a more localized and hyperintense fluorescence signal observed from tumor sections post-folate-targeted liposome injections. These results demonstrate the effectiveness of folate targeting for dynamic real-time solid tumor MRI and provide insight into kinetics of targeted and nontargeted nanoparticles to solid tumors.
Protti A, Herlihy A, Tessier J, et al., 2009, Diagonal-SPRITE and Its Applications for In Vivo Imaging at High Field, The Open Magnetic Resonance Journal, Vol: 2, Pages: 1-7, ISSN: 1874-7698
Parkinson JRC, Chaudhri OB, Kuo Y-T, et al., 2009, Differential patterns of neuronal activation in the brainstem and hypothalamus following peripheral injection of GLP-1, oxyntomodulin and lithium chloride in mice detected by manganese-enhanced magnetic resonance imaging (MEMRI), NEUROIMAGE, Vol: 44, Pages: 1022-1031, ISSN: 1053-8119
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- Citations: 69
Goldstone AP, de Hernandez CG, Beaver JD, et al., 2009, Fasting biases brain reward systems towards high-calorie foods, Vol: 30, Pages: 1625-1635, ISSN: 1460-9568
Parkinson JRC, Chaudhri OB, Bell JD, 2009, Imaging Appetite-Regulating Pathways in the Central Nervous System Using Manganese-Enhanced Magnetic Resonance Imaging, NEUROENDOCRINOLOGY, Vol: 89, Pages: 121-130, ISSN: 0028-3835
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- Citations: 20
Knapp S, Hosie AM, Anstee QM, et al., 2008, IDENTIFICATION OF A MODEL OF ALCOHOL PREFERENCE AND ITS SIMILARITY TO HUMAN ALCOHOLISM, 59th Annual Meeting of the American-Association-for-the-Study-of-Liver-Diseases, Publisher: JOHN WILEY & SONS INC, Pages: 398A-399A, ISSN: 0270-9139
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- Citations: 1
Thomas EL, Uthaya S, Vasu V, et al., 2008, Neonatal intrahepatocellular lipid, ARCHIVES OF DISEASE IN CHILDHOOD-FETAL AND NEONATAL EDITION, Vol: 93, Pages: F382-F383, ISSN: 1359-2998
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- Citations: 18
Mehta SR, Thomas EL, Bell JD, et al., 2008, Non-invasive means of measuring hepatic fat content, WORLD JOURNAL OF GASTROENTEROLOGY, Vol: 14, Pages: 3476-3483, ISSN: 1007-9327
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- Citations: 181
Mehta SR, Godsland IF, Barton N, et al., 2008, Intra-hepatic insulin exposure but not percent extraction of newly-secreted insulin is increased in subjects with non-alcoholic fatty liver disease (NAFLD), Publisher: WILEY, ISSN: 0742-3071
, 2008, Author index, Diabetic Medicine, Vol: 25, Pages: 163-172, ISSN: 0742-3071
Kamaly N, Kalber T, Ahmad A, et al., 2008, Bimodal paramagnetic and fluorescent liposomes for cellular and tumor magnetic resonance imaging., Bioconjugate Chem., Vol: 19, Pages: 118-129, ISSN: 1043-1802
A novel bimodal fluorescent and paramagnetic liposome is described for cellular labeling. In this study, we show the synthesis of a novel gadolinium lipid, Gd.DOTA.DSA, designed for liposomal cell labeling and tumor imaging. Liposome formulations consisting of this lipid were optimized in order to allow for maximum cellular entry, and the optimized formulation was used to label HeLa cells in vitro. The efficiency of this novel bimodal Gd-liposome formulation for cell labeling was demonstrated using both fluorescence microscopy and magnetic resonance imaging (MRI). The uptake of Gd-liposomes into cells induced a marked reduction in their MRI T 1 relaxation times. Fluorescence microscopy provided concomitant proof of uptake and revealed liposome internalization into the cell cytosol. The optimized formulation was also found to exhibit minimal cytotoxicity and was shown to have capacity for plasmid DNA (pDNA) transfection. A further second novel neutral bimodal Gd-liposome is described for the labeling of xenograft tumors in vivo utilizing the enhanced permeation and retention effect (EPR). Balb/c nude mice were inoculated with IGROV-1 cells, and the resulting tumor was imaged by MRI using these in vivo Gd-liposomes formulated with low charge and a poly(ethylene glycol) (PEG) calyx for long systemic circulation. These Gd-liposomes which were less than 100 nm in size were shown to accumulate in tumor tissue by MRI, and this was also verified by fluorescence microscopy of histology samples. Our in vivo tumor imaging results demonstrate the effectiveness of MRI to observe passive targeting of long-term circulating liposomes to tumors in real time, and allow for MRI directed therapy, wherein the delivery of therapeutic genes and drugs to tumor sites can be monitored while therapeutic effects on tumor mass and/or size may be simultaneously observed, quantitated, and correlated.
So P-W, Yu W-S, Kuo Y-T, et al., 2007, Impact of Resistant Starch on Body Fat Patterning and Central Appetite Regulation, PLOS ONE, Vol: 2, ISSN: 1932-6203
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- Citations: 95
Kuo Y-T, Parkinson JRC, Chaudhri OB, et al., 2007, The temporal sequence of gut Peptide-CNS interactions tracked <i>in vivo</i> by magnetic resonance Imaging, JOURNAL OF NEUROSCIENCE, Vol: 27, Pages: 12341-12348, ISSN: 0270-6474
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- Citations: 27
Thomas EL, Potter E, Tosi I, et al., 2007, Pioglitazone added to conventional lipid-lowering treatment in familial combined hyperlipidaemia improves parameters of metabolic control: relation to liver, muscle and regional body fat content., Atherosclerosis, Vol: 195, Pages: e181-e190
Familial combined hyperlipidaemia (FCHL) is a complex genetic disorder conferring high risk of premature atherosclerosis, characterized by high cholesterol and/or triglyceride, low high density lipoprotein (HDL) cholesterol and insulin resistance. We examined whether pioglitazone, added to conventional lipid-lowering therapy, would favourably affect metabolic parameters and alter body fat content. We undertook a randomized, double blind, placebo-controlled study in 22 male patients with FCHL treated with pioglitazone or matching placebo 30 mg daily for 4 weeks, increasing to 45 mg for 12 weeks. Magnetic resonance imaging and proton magnetic resonance spectroscopy were performed to measure adipose tissue (AT) body content as well as intrahepatocellular lipids (IHCL) and intramyocellular lipids (IMCL) at baseline and after treatment. Significantly improved in the pioglitazone group were: triglyceride/HDL (atherogenic index of plasma) -32.3% (p=0.002), plasma glucose -4.4% (p=0.03), alanine-aminotransferase (ALT) -7.7% (p=0.005) and adiponectin 130.1% (p=0.001). Pioglitazone treatment resulted in a significant increase in total (5.3%, p=0.02) and subcutaneous (7.1%, p=0.003) adipose tissue as well as in soleus-IMCL levels (47.4%, p=0.02) without alteration in intra-abdominal AT or IHCL. Changes in ALT and AST and IHCL were strongly correlated (r=0.72, p<0.01; r=.0.86, p<0.01, respectively). In patients with FCHL on conventional lipid-lowering therapy, the addition of pioglitazone acts favourably on several metabolic parameters.
Yajnik C, Umranikar S, Lubree H, et al., 2007, Increased abdominal and visceral adiposity is manifest in Indian babies at birth, EARLY HUMAN DEVELOPMENT, Vol: 83, Pages: S66-S67, ISSN: 0378-3782
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- Citations: 1
, 2007, Abstracts of the 43rd European Association for the Study of Diabetes (EASD) annual meeting, 18-21 September 2007, Amsterdam, The Netherlands., Diabetologia, Vol: 50 Suppl 1, Pages: S7-515, ISSN: 0012-186X
So P-W, Parkes HG, Bell JD, 2007, Application of magnetic resonance methods to studies of gene therapy, PROGRESS IN NUCLEAR MAGNETIC RESONANCE SPECTROSCOPY, Vol: 51, Pages: 49-62, ISSN: 0079-6565
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- Citations: 2
So PW, Bell JD, 2007, The Application of In Vivo MRI and MRS in Phenomic Studies of Murine Models of Disease, Modern Magnetic Resonance, Editors: Webb
Wardle NJ, Herlihy AH, So P-W, et al., 2007, Synthesis of a novel 'smart' bifunctional chelating agent 1-(2-[β,D-galactopyranosyloxylethyl)-7-(1-carboxy-3-[4-aminophenyllpropyl)-4,10-bis(carboxymethyl)-1,4,7,10-tetraazacyclododecane (Gal-PA-DO3A-NH<sub>2</sub>) and its Gd(III) complex, BIOORGANIC & MEDICINAL CHEMISTRY, Vol: 15, Pages: 4714-4721, ISSN: 0968-0896
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- Citations: 10
Nunn AVW, Bell J, Barter P, 2007, The integration of lipid-sensing and anti-inflammatory effects: how the PPARs play a role in metabolic balance., Nucl Recept, Vol: 5
The peroxisomal proliferating-activated receptors (PPARs) are lipid-sensing transcription factors that have a role in embryonic development, but are primarily known for modulating energy metabolism, lipid storage, and transport, as well as inflammation and wound healing. Currently, there is no consensus as to the overall combined function of PPARs and why they evolved. We hypothesize that the PPARs had to evolve to integrate lipid storage and burning with the ability to reduce oxidative stress, as energy storage is essential for survival and resistance to injury/infection, but the latter increases oxidative stress and may reduce median survival (functional longevity). In a sense, PPARs may be an evolutionary solution to something we call the 'hypoxia-lipid' conundrum, where the ability to store and burn fat is essential for survival, but is a 'double-edged sword', as fats are potentially highly toxic. Ways in which PPARs may reduce oxidative stress involve modulation of mitochondrial uncoupling protein (UCP) expression (thus reducing reactive oxygen species, ROS), optimising forkhead box class O factor (FOXO) activity (by improving whole body insulin sensitivity) and suppressing NFkB (at the transcriptional level). In light of this, we therefore postulate that inflammation-induced PPAR downregulation engenders many of the signs and symptoms of the metabolic syndrome, which shares many features with the acute phase response (APR) and is the opposite of the phenotype associated with calorie restriction and high FOXO activity. In genetically susceptible individuals (displaying the naturally mildly insulin resistant 'thrifty genotype'), suboptimal PPAR activity may follow an exaggerated but natural adipose tissue-related inflammatory signal induced by excessive calories and reduced physical activity, which normally couples energy storage with the ability to mount an immune response. This is further worsened when pancreatic decompensation occurs, resulting in gluco-oxida
Chung Y-L, Alexanderson H, Pipitone N, et al., 2007, Creatine supplements in patients with idiopathic inflammatory myopathies who are clinically weak after conventional pharmacologic treatment:: Six-month, double-blind, randomized, placebo-controlled trial, ARTHRITIS & RHEUMATISM-ARTHRITIS CARE & RESEARCH, Vol: 57, Pages: 694-702, ISSN: 0004-3591
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- Citations: 85
Shojaee-Moradie F, Baynes KCR, Pentecost C, et al., 2007, Exercise training reduces fatty acid availability and improves the insulin sensitivity of glucose metabolism, DIABETOLOGIA, Vol: 50, Pages: 404-413, ISSN: 0012-186X
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- Citations: 141
Kuo Y-T, Herlihy AH, So P-W, et al., 2006, Manganese-enhanced magnetic resonance imaging (MEMRI) without compromise of the blood-brain barrier detects hypothalamic neuronal activity <i>in vivo</i>, NMR IN BIOMEDICINE, Vol: 19, Pages: 1028-1034, ISSN: 0952-3480
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- Citations: 56
Chaudhri OB, Parkinson JRC, Kuo Y-T, et al., 2006, Differential hypothalamic neuronal activation following peripheral injection of GLP-1 and oxyntomodulin in mice detected by manganese-enhanced magnetic resonance imaging, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol: 350, Pages: 298-306, ISSN: 0006-291X
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- Citations: 71
Thomas EL, Brynes AE, Hamilton G, et al., 2006, Effect of nutritional counselling on hepatic, muscle and adipose tissue fat content and distribution in non-alcoholic fatty liver disease, WORLD JOURNAL OF GASTROENTEROLOGY, Vol: 12, Pages: 5813-5819, ISSN: 1007-9327
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- Citations: 88
Batterham RL, Heffron H, Kapoor S, et al., 2006, Critical role for peptide YY in protein-mediated satiation and body-weight regulation, CELL METABOLISM, Vol: 4, Pages: 223-233, ISSN: 1550-4131
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- Citations: 434
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