Cagampang, Felino - University of Southampton

个人简介

Dr Felino Cagampang is currently Associate Professor in Integrative Physiology within Medicine at the University of Southampton. He obtained his undergraduate degree at the University of the Philippines, and graduate degrees (MSc & PhD) at Nagoya University (Japan). He did his post-doctoral research work at the Mitsubishi Kasei Institute of Life Sciences (Japan), at King’s College London, and at the University of Manchester, in the field of circadian clock biology. In 2002, he joined the University of Southampton.

研究领域

Dr Cagampang’s research focuses on developmental programming of obesity and the metabolic syndrome, and the role of the biological clock system in disease pathologies and treatment. Developmental programming of obesity and the metabolic syndrome In collaboration with clinical colleagues, Dr Cagampang has developed a unique mouse model where offspring of obese mothers develop a phenotype similar to the human metabolic syndrome (i.e. a clustering of cardiometabolic risk factors that include obesity and having fatty liver, elevated blood pressure, insulin resistance and glucose intolerance, dyslipidemia, being in a proinflammatory and prothrombic state). We found that maternal obesity during pregnancy, as a consequence of too much fat in the mother’s diet, can affect the developing liver of the fetus, making them more susceptible to developing fatty liver in later life. Eating an unhealthy fat-enriched diet in postnatal life can cause the fatty liver condition rapidly progressing to non-alcoholic fatty liver disease with ageing. We are currently investigating various mechanisms that may be involved in the developmental programming of this metabolic disorder, including mitochondrial dysfunction, telomere and epigenetic modifications, and altered circadian clock function. We are also exploring various intervention strategies to protect the offspring from developing metabolic syndrome in adulthood. We have shown previously in this mouse model that by giving the cholesterol lowering drug statin to obese pregnant mothers, it not only improves the mother’s cardiometabolic health but was also able to give some post weaning protection to the offspring fed an unhealthy fat-enriched diet. Currently we are investigating in this mouse model whether improving glycaemic control of the obese pregnant mothers with the anti-diabetic drug metformin will also reduce future risk of the offspring to obesity and the metabolic syndrome. With colleagues from Clinical Neurosciences, we are exploring the possibility of whether obesity-induced high fat feeding during pregnancy increase susceptibility of the offspring to Alzheimer disease and eye damage with ageing. In collaboration with clinical colleagues in Obstetrics & Gynaecology, we are examining follicular development in the ovaries of female offspring from the high-fat fed mothers. Other collaborative work using this mouse model includes the investigation of placental function in obese pregnancy, and muscle function, bone development, brown adipose tissue function and thermogenesis, and changes in gut microflora and physiology in offspring from these obese mothers. Circadian clock system and developmental programming of diseases Most physiological processes exhibit rhythmic changes with a period of around 24h (termed 'circadian'), and are regulated within cells by endogenous timing systems involving a set of 'clock' genes. The involvement of the circadian clock system in the pathogenesis of diseases remains unclear. Dr Cagampang is interested in the role of the clock system in developmental programming of the metabolic syndrome. Using the mouse model of maternal high fat feeding leading to metabolic syndrome susceptibility in the offspring, Dr Cagampang’s group has been investigating whether there are alterations in circadian rhythms of genes involved in regulating appetite, energy expenditure and clock function in various tissues and organs of the offspring. His group is examining whether these changes are brought about by epigenetic modifications. In collaboration with clinical colleagues from Obstetrics & Gynaecology, Dr Cagampang is also investigating sleep and clock function in gynaecological pathologies.

近期论文

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Endogenous reference genes for gene expression studies on bicuspid aortic valve associated aortopathy in humans - Harrison, Oliver, Moorjani, Narain, Torrens, Christopher, Ohri, Sunil and Cagampang, Felino Published:2016Publication:PLoS OneVolume:11, (10)Page Range:1-9doi:10.1371/journal.pone.0164329PMID:27727313 MNK1 and MNK2 mediate adverse effects of high-fat feeding in distinct ways - Moore, C.E.J., Pickford, J, Cagampang, F.R., Stead, R.S., Tian, S., Zhao, X., Tang , X., Byrne, C. and Proud, C. Published:2016Publication:Scientific ReportsVolume:6, (23476)doi:10.1038/srep23476 Altered cellular redox status, sirtuin abundance and clock gene expression in a mouse model of developmentally primed NASH - Bruce, K.D., Szczepankiewicz, D, Sihota, K.K., Ravindraanandan, M., Thomas, H., Lillycrop, K.A., Burdge, G.C., Hanson, M.A., Byrne, C.D. and Cagampang, F.R. Published:2016Publication:Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of LipidsVolume:1861, (7)Page Range:584-593PMID:27040510 Altered cellular redox status, sirtuin abundance and 1 clock gene expression in a mouse model of developmentally primed NASH - Bruce, Kimberley, Szczepankiewicz, Dawid, Sihota, Kiran K., Ravindraanandan, Manoj, Thomas, Hugh, Lillycrop, Karen A., Burdge, Graham C., Hanson, Mark A., Byrne, Christopher D. and Cagampang, Felino R. Published:2016Publication:Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of LipidsPage Range:1-29doi:10.1016/j.bbalip.2016.03.026PMID:27040510