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Diet & Gastrointestinal Health
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DESCRIPTION
The Diet and Gastrointestinal Health Group aims to understand the molecular and cellular mechanisms that lead to non-communicable disorders of the gastrointestinal tract. Areas of expertise include inflammatory bowel disease, coeliac disease and irritable bowel syndrome, and the extent to which these are influenced by diet. A major focus is the role of the gastrointestinal microbiota in health and disease, and in particular their interaction with genetics and the immune system in inflammatory bowel disease and coeliac disease. We specialise in investigating how this interaction can be modified, for example, using pharmacogenetics and dietary approaches. Examples of dietary approaches include:
- Probiotics and prebiotics;
- Modification of fibre and fermentable carbohydrate consumption;
- Development of gluten-free dietary interventions.
In addition, we use proteomic techniques to study the effects of trauma and alcohol on protein turnover and tissue repair, and the effects of oxidative stress on these processes.
Research in the Diet and Gastrointestinal Health Group is funded by the European Union, the BBSRC, industry and various medical research charities.
Associated research programmes
Associated staff research interests
Interests:
My research interests are in the use of oral nutritional support interventions in the management of weight loss in patients with acute and chronic illness.
In 1999, I completed a postgraduate diploma in Systematic Reviews Methodology at University College London and subsequently completed a major systematic review of nutritional support in the management of weight loss, focusing particularly on food-based interventions. This is published in the Cochrane Library and is updated annually.
My PhD was completed in 2002-2006, and involved conducting a series of patient-focused studies examining aspects of nutritional support in the management of weight loss in patients with advanced cancers. The principal project during this period was a major intervention study, which necessitated recruitment, dietetic support and follow-up of more than 300 subjects.
My current research interests are split between using systematic review methodology to examine the role of interventions designed to enhance food intake in the management of patients with weight loss and, studies of the factors affecting patient compliance with oral nutritional interventions which focus on assessment of compliance and patient understanding of simple dietary interventions.
In 1999, I completed a postgraduate diploma in Systematic Reviews Methodology at University College London and subsequently completed a major systematic review of nutritional support in the management of weight loss, focusing particularly on food-based interventions. This is published in the Cochrane Library and is updated annually.
My PhD was completed in 2002-2006, and involved conducting a series of patient-focused studies examining aspects of nutritional support in the management of weight loss in patients with advanced cancers. The principal project during this period was a major intervention study, which necessitated recruitment, dietetic support and follow-up of more than 300 subjects.
My current research interests are split between using systematic review methodology to examine the role of interventions designed to enhance food intake in the management of patients with weight loss and, studies of the factors affecting patient compliance with oral nutritional interventions which focus on assessment of compliance and patient understanding of simple dietary interventions.
Tel:
020 7848 4318
Fax:
020 7848 4195
Email:
Website:
Interests:
Epidemiological data show calorie carbohydrate (CHO) intake has increased approx. 20% over the last 30 years, roughly in line with increases in the calories obtained from fat and protein. Epidemiological data also show calorie intake from ingested CHO has drifted away from complex CHO towards more refined, industry processed simple CHO. In particular, the ingestion of sweeteners such as HFCS has risen dramatically over the last 4 decades. These data suggests the forms in which CHOs are ingested, transported and sensed by the gut may be of critical importance in understanding the role dietary CHO plays in the development of diseases such as metabolic syndrome.
The gut mucosa is the first responder to ingested nutrients. During the digestive process complex CHO are broken down to simple sugars, which are then transported across the small intestine.
My research has been focussed on establishing the molecular mechanisms of intestinal sugar transport. Published data show sugar is transported across the small intestine via SGLT1, GLUT2 and GLUT5. In addition these transporters are subject to regulation by diet, drugs, hormones, and disease, such as diabetes. Recent data has also shown that following meal ingestion the gut senses luminal CHO levels, resulting in the release of hunger/satiety peptides which control energy (food) intake and expenditure.
Using tissue culture and in vivo models of the small intestine, I work on regulation of intestinal sugar transport by dietary CHOs; and the metabolic consequences of elevations in post-prandial flux of sugars. In addition, I study the molecular mechanisms by which dietary CHO, especially industry processed sugars and artificial sweeteners, are sensed by the gut, controlling the release of GI satiety peptides. These preclinical studies will pave the way towards human studies on dietary CHO in the gut and the development of metabolic syndrome.
The gut mucosa is the first responder to ingested nutrients. During the digestive process complex CHO are broken down to simple sugars, which are then transported across the small intestine.
My research has been focussed on establishing the molecular mechanisms of intestinal sugar transport. Published data show sugar is transported across the small intestine via SGLT1, GLUT2 and GLUT5. In addition these transporters are subject to regulation by diet, drugs, hormones, and disease, such as diabetes. Recent data has also shown that following meal ingestion the gut senses luminal CHO levels, resulting in the release of hunger/satiety peptides which control energy (food) intake and expenditure.
Using tissue culture and in vivo models of the small intestine, I work on regulation of intestinal sugar transport by dietary CHOs; and the metabolic consequences of elevations in post-prandial flux of sugars. In addition, I study the molecular mechanisms by which dietary CHO, especially industry processed sugars and artificial sweeteners, are sensed by the gut, controlling the release of GI satiety peptides. These preclinical studies will pave the way towards human studies on dietary CHO in the gut and the development of metabolic syndrome.
Tel:
+44 (0) 20 7848 4269
Fax:
+44 (0) 20 7848 4171
Email:
Website:
Interests:
The gastrointestinal (GI) microbiota play important roles in the maintenance of human health, including protection from enteropathogenic infection, stimulation of immune function and fermentation of otherwise non-digestible nutrients.
Numerous disorders of the GI tract are associated with alterations in the microbiota they harbour, a term called dysbiosis. Whether dysbiosis is a cause or consequence of disease is unclear, an issue we are currently investigating. The GI microbiota can be modified through dietary manipulation, including the use of probiotics (e.g. lactobacilli, bifidobacteria) and prebiotics (e.g. fructo-oligosaccharides). There is significant potential that such dietary substances may be therapeutic for GI disorders, an area we are keenly researching.
Our research translates findings from the basic sciences and tests them in the clinical environment, whilst our clinical trials always include endpoints for both efficacy and mechanistic evaluation. Our laboratory utilises molecular microbiological techniques such as fluorescent in situ hybridisation (FISH) and quantitative PCR in order to investigate various aspects of the GI microbiota.
In collaboration with both clinical researchers (e.g. gastroenterologists, dietitians) and basic scientists (e.g. immunologists, microbiologists) we have undertaken multi-centre investigations of the GI microbiota in patients with inflammatory bowel disease, irritable bowel syndrome and patients receiving artificial nutrition. Our findings indicate marked dysbiosis in such patients and further trials have investigated the efficacy of probiotics and prebiotics in these groups.
Further to this, many patients with GI disorders have disturbances across the spectrum of nutrition, including alterations in nutrient intake, digestion, absorption and metabolism. We are involved in investigating both the causes and consequences of these disturbances in order that malnutrition can be minimised. This involves research on barriers to food intake and the effect of disease on energy expenditure (indirect calorimetry), as well as the development and validation of clinical tools to assist in their detection.
Numerous disorders of the GI tract are associated with alterations in the microbiota they harbour, a term called dysbiosis. Whether dysbiosis is a cause or consequence of disease is unclear, an issue we are currently investigating. The GI microbiota can be modified through dietary manipulation, including the use of probiotics (e.g. lactobacilli, bifidobacteria) and prebiotics (e.g. fructo-oligosaccharides). There is significant potential that such dietary substances may be therapeutic for GI disorders, an area we are keenly researching.
Our research translates findings from the basic sciences and tests them in the clinical environment, whilst our clinical trials always include endpoints for both efficacy and mechanistic evaluation. Our laboratory utilises molecular microbiological techniques such as fluorescent in situ hybridisation (FISH) and quantitative PCR in order to investigate various aspects of the GI microbiota.
In collaboration with both clinical researchers (e.g. gastroenterologists, dietitians) and basic scientists (e.g. immunologists, microbiologists) we have undertaken multi-centre investigations of the GI microbiota in patients with inflammatory bowel disease, irritable bowel syndrome and patients receiving artificial nutrition. Our findings indicate marked dysbiosis in such patients and further trials have investigated the efficacy of probiotics and prebiotics in these groups.
Further to this, many patients with GI disorders have disturbances across the spectrum of nutrition, including alterations in nutrient intake, digestion, absorption and metabolism. We are involved in investigating both the causes and consequences of these disturbances in order that malnutrition can be minimised. This involves research on barriers to food intake and the effect of disease on energy expenditure (indirect calorimetry), as well as the development and validation of clinical tools to assist in their detection.
Tel:
+44 (0)20 7848 3858
Fax:
+44 (0)20 7848 4171
Email:
Website:
Interests:
Colorectal cancer is the second most common cancer in the UK, placing a high burden on healthcare resources. Nutritional and genetic factors are known to influence risk of developing the disease. Our work focuses on the role of the vitamin folic acid (folate) and common genetic mutations in enzymes that utilise folic acid (e.g. 5,10-methylenetetrahydrofolate reductase, MTHFR 677C→T) in determining colorectal cancer risk. We are currently investigating this relationship in individuals with and without colorectal neoplasia by using intermediary biomarkers of cancer risk such as DNA methylation and uracil misincorporation in DNA. These markers of DNA damage can influence the expression of genes involved in the cancer process and have been linked to low intakes of dietary folate in both animal and human studies.
Our previous work has shown a relationship between markers of folate status and genomic DNA methylation in the colon. A decrease in genomic DNA methylation in the colon was associated with lower serum and red cell folate and higher plasma homocysteine concentrations. We have also shown that supplementation with physiological intakes of folic acid can increase DNA methylation in the colon of individuals with colorectal neoplasms. We have extended this work to include analysis of gene-specific methylation, which is more important in the cancer process than genomic DNA methylation because it directly influences gene expression. Preliminary investigations in a panel of genes (including ER, MLH1, MGMT, MYOD1) have shown promising results. We have also investigated the role of folate in altering gene expression in the colon using Affymetrix GeneChips.
We are currently working on a project to determine whether individuals carrying the MTHFR 677C→T mutation have different patterns of DNA methylation and uracil misincorporation in the colon compared with those who do not carry the mutation. An intervention study will also be carried out to determine whether increasing folic acid intakes can alter markers of DNA damage in the colon and whether this response differs between individuals who carry the MTHFR 677C→T mutation and those who do not. An important aspect of our work is that we are recruiting subjects without colorectal neoplasia to participate in these studies and therefore investigating the relationship between diet and markers of damage before the disease develops.
Our previous work has shown a relationship between markers of folate status and genomic DNA methylation in the colon. A decrease in genomic DNA methylation in the colon was associated with lower serum and red cell folate and higher plasma homocysteine concentrations. We have also shown that supplementation with physiological intakes of folic acid can increase DNA methylation in the colon of individuals with colorectal neoplasms. We have extended this work to include analysis of gene-specific methylation, which is more important in the cancer process than genomic DNA methylation because it directly influences gene expression. Preliminary investigations in a panel of genes (including ER, MLH1, MGMT, MYOD1) have shown promising results. We have also investigated the role of folate in altering gene expression in the colon using Affymetrix GeneChips.
We are currently working on a project to determine whether individuals carrying the MTHFR 677C→T mutation have different patterns of DNA methylation and uracil misincorporation in the colon compared with those who do not carry the mutation. An intervention study will also be carried out to determine whether increasing folic acid intakes can alter markers of DNA damage in the colon and whether this response differs between individuals who carry the MTHFR 677C→T mutation and those who do not. An important aspect of our work is that we are recruiting subjects without colorectal neoplasia to participate in these studies and therefore investigating the relationship between diet and markers of damage before the disease develops.
Tel:
020 7848 4270
Email:
Website:
Interests:
The research undertaken is primarily involved with two conditions. These are coeliac disease (gluten sensitive enteropathy) that affects 1% of the European population and inflammatory bowel disease of the ileo-anal reservoir (pouchitis) following a total colectomy for either ulcerative colitis (UC) or familial adenomatous polyposis coli (FAP).
The aims of the research in coeliac disease are:
- To develop strains of wheat, rye and barley that retain the baking and nutritional qualities of the original cultivars but which do not exacerbate coeliac disease.
- To characterise epitopes within wheat and related cereals that exacerbate coeliac disease.
- To raise monoclonal antibodies to the toxic epitopes in order to
- Develop improved assays to quantify the gluten content of foods for individuals with coeliac disease and
-To improve our understanding the pathogenesis of the condition
- To Investigate the pathogenesis and genetics of coeliac disease, the latter of which may permit developing a cDNA diagnostic test kit
The work in pouchitis is to investigate the pathogenesis of this condition. This involves investigating the role of the antibiotics, metronidazole and ciprofloxacin which can be used to treat the condition. We are concomitantly studying the effect of the probiotics (VSL#3) which can be used to treat the condition. We are attempting to characterise the intestinal flora by 35S-DNA molecular fingerprinting and sequencing in collaboration with the Sanger Institute in Cambridge. This is as a prelude to developing improved treatment modalities to improve our understanding of the pathogenetic role that bacteria have in this condition. In parallel work we are studying the role of immune cells and cytokines in the pathogenesis of the condition with immunohistochemistry of mucosal biopsies.
The aims of the research in coeliac disease are:
- To develop strains of wheat, rye and barley that retain the baking and nutritional qualities of the original cultivars but which do not exacerbate coeliac disease.
- To characterise epitopes within wheat and related cereals that exacerbate coeliac disease.
- To raise monoclonal antibodies to the toxic epitopes in order to
- Develop improved assays to quantify the gluten content of foods for individuals with coeliac disease and
-To improve our understanding the pathogenesis of the condition
- To Investigate the pathogenesis and genetics of coeliac disease, the latter of which may permit developing a cDNA diagnostic test kit
The work in pouchitis is to investigate the pathogenesis of this condition. This involves investigating the role of the antibiotics, metronidazole and ciprofloxacin which can be used to treat the condition. We are concomitantly studying the effect of the probiotics (VSL#3) which can be used to treat the condition. We are attempting to characterise the intestinal flora by 35S-DNA molecular fingerprinting and sequencing in collaboration with the Sanger Institute in Cambridge. This is as a prelude to developing improved treatment modalities to improve our understanding of the pathogenetic role that bacteria have in this condition. In parallel work we are studying the role of immune cells and cytokines in the pathogenesis of the condition with immunohistochemistry of mucosal biopsies.
Tel:
020 7188 2494
Email:
Website:
Interests:
Our group is interested in the functionality of dietary polysaccharides (starch and non-starch polysaccharides or NSP) with respect to the bioaccessibility and bioavailability of nutrients and phytochemicals. Current studies focus on the rheological behaviour of water-soluble NSP in the gastrointestinal tract and also the properties of supramolecular structures such as starch and the plant cell wall matrix. We are particularly interested in the kinetics of starch digestion and glucose absorption and the so-called 'glycaemic index'.
An important part of this work is to perform structure-function studies in order to:
1. Understand the role of dietary NSP in the prevention and treatment of disease. More specifically, this has involved investigating polysaccharide function in relation to gastrointestinal (GI) events, especially the physico-chemical processes that influence carbohydrate digestion and absorption. This is of considerable importance in evaluating the role of starch and non-starch polysaccharides ('dietary fibre') in the aetiology and treatment of disease, such as diabetes and cardiovsacular disease.
2. Facilitate the development of 'functional foods' with enhanced medical or nutritional benefits.
An important part of this work is to perform structure-function studies in order to:
1. Understand the role of dietary NSP in the prevention and treatment of disease. More specifically, this has involved investigating polysaccharide function in relation to gastrointestinal (GI) events, especially the physico-chemical processes that influence carbohydrate digestion and absorption. This is of considerable importance in evaluating the role of starch and non-starch polysaccharides ('dietary fibre') in the aetiology and treatment of disease, such as diabetes and cardiovsacular disease.
2. Facilitate the development of 'functional foods' with enhanced medical or nutritional benefits.
Tel:
020 7848 4159, 020 7848 4238
Fax:
020 7848 4500
Email:
Website:
Interests:
Professor Emery's current research interests relate to the response of skeletal muscle and other tissues to various forms of injury, including surgical trauma and oxidative stress. The main focus is on protein metabolism, in particular the rates of protein synthesis and degradation, as well as the formation of protein adducts. Protein synthesis has been shown to increase during the healing of a surgical wound and this increase appears not to be affected by mild or moderate malnutrition, although severe malnutrition is known to inhibit wound healing. Further work remains to be done to define the interrelationships between nutritional status, wound healing and the metabolic response to trauma.
The main experimental approaches being used at present are proteomic techniques including 2-dimensional gel electrophoresis to separate proteins and mass spectrometry to identify the separated proteins. A method is currently being developed to measure the rate of synthesis of individual proteins in vivo.
The main experimental approaches being used at present are proteomic techniques including 2-dimensional gel electrophoresis to separate proteins and mass spectrometry to identify the separated proteins. A method is currently being developed to measure the rate of synthesis of individual proteins in vivo.
Tel:
020 7848 4191
Fax:
020 7848 4185
Email:
Website:
Interests:
Adverse effects of alcohol on muscle metabolism using a proteomic approach.
Tel:
020 7848 4255
Email:
Website:
CONTACTS FOR FURTHER INFORMATION
Dr Helen Wiseman, Research Degree Co-ordinator
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