Dr Isaac Ampong

Former PhD student (completed)
Msc Chemical Pathology(KNUST-Gh), Bsc Molecular Biology & Biotec(UCC-Gh)
Monday- Friday, 09:00-17:00


After completing an undergraduate degree in Molecular Biology and Biotechnology (1st Class Hon.) and a further MSc in Chemical Pathology, University of Cape Coast and Kwame Nkrumah University of Science & Technology, respectively in Ghana, Isaac started his PhD at  Aston University, UK in October, 2016 before transferring to the University of Surrey, UK in April, 2017. He had already in his masters studies, researched on the role of diet(i.e Ghanaian locally consumed vegetable oils) in glucose and cholesterol metabolism using in vivo model of diabetes before awarded the prestigious commonwealth scholarship by the Commonwealth Scholarship Commission, UK to pursue a PhD research to understand how certain gut microbiota affect specific odd chain fatty acids metabolism which have been found to reduce diabetes and cardio-metabolic risk. Isaac is employing a range of different approaches such as PCR, HOMA-IR/oral glucose challenge studies, GC-FID/GC-MS, cell culture, dietary intervention, Next generation sequencing, stereology. He is part of a cross-multidisciplinary team researching to find solutions to the increasing rate of obesity and related metabolic diseases and translate them for better health of millions affected. Isaac overall goal is to understand the mechanisms underlying the risk of type 2 diabetes and obesity and develop interventions to avert them through the use of dietary model of these conditions.


Research interests

My publications


Ampong Isaac, Watkins Adam, Gutierrez Jorge, Ikwuobe John, Griffiths Helen (2019) Dietary protein insufficiency ? an important consideration in fatty liver disease?,British Journal of Nutrition Cambridge
Dietary protein insufficiency has been linked to excessive triglyceride storage (TG) and non-alcoholic fatty liver disease (NAFLD) in developing countries. Hepatic TG accumulation following a low-protein diet may be due to altered peroxisomal, mitochondrial and gut microbiota function. Hepatic peroxisomes and mitochondria normally mediate metabolism of nutrients to provide energy and substrates for lipogenesis. Peroxisome biogenesis and activities can be modulated by odd (OCFA) and short-chain (SCFA) fatty acids that are derived from gut bacteria e.g. propionate and butyrate. Also produced during amino acid metabolism by peroxisomes and mitochondria, propionate and butyrate correlate with reduced risk of obesity, insulin resistance and NAFLD.
In this horizon-scanning review, we have compiled available evidence on the effects of protein malnutrition on OCFA production, arising from loss in mitochondrial, peroxisomal and gut microbiota function, and its association with lipid accumulation in the liver. The methyl donor amino acid composition of dietary protein is an important contributor to liver function and lipid storage; the presence and abundance of dietary branched chain amino acids can modulate the composition and metabolic activity of the gut microbiome and on the other hand, can affect protective OCFA and SCFA production in the liver. In preclinical animal models fed with low protein diets, specific amino acid supplementation can ameliorate fatty liver disease. The association between low dietary protein intake and fatty liver disease is underexplored and merits further investigation, particularly in vulnerable groups with dietary protein restriction in developing countries.