Prof. Dr. Peter R Flatt
School of Biomedical Sciences, University of Ulster, Coleraine, UK
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Academic Career Length
52Years (1975-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications1 August 1990 in Diabetologia
Journal Article
SSS. K. Swanston-Flatt
S. K. Swanston-Flatt
CDC. Day
C. Day
CBC. J. Bailey
C. J. Bailey
Peter R Flatt1 March 2007 in British Journal of Nutrition
Journal Article
JHJ. M. A. Hannan
J. M. A. Hannan
LAL. Ali
L. Ali
BRB. Rokeya
B. Rokeya
JKJ. Khaleque
J. Khaleque
MAM. Akhter
M. Akhter
Yasser Abdel-Wahab +1
Trigonella foenum-graecum(fenugreek) seeds have been documented as a traditional plant treatment for diabetes. In the present study, the antidiabetic properties of a soluble dietary fibre (SDF) fraction ofT. foenum-graecumwere evaluated. Administration of SDF fraction (0·5 g/kg body weight) to normal, type 1 or type 2 diabetic rats significantly improved oral glucose tolerance. Total remaining unabsorbed sucrose in the gastrointestinal tract of non-diabetic and type 2 diabetic rats, following oral sucrose loading (2·5 g/kg body weight) was significantly increased byT. foenum-graecum(0·5 g/kg body weight). The SDF fraction suppressed the elevation of blood glucose after oral sucrose ingestion in both non-diabetic and type 2 diabetic rats. Intestinal disaccharidase activity and glucose absorption were decreased and gastrointestinal motility increased by the SDF fraction. Daily oral administration of SDF to type 2 diabetic rats for 28 d decreased serum glucose, increased liver glycogen content and enhanced total antioxidant status. Serum insulin and insulin secretion were not affected by the SDF fraction. Glucose transport in 3T3-L1 adipocytes and insulin action were increased byT. foenum-graecum.The present findings indicate that the SDF fraction ofT. foenum-graecumseeds exerts antidiabetic effects mediated through inhibition of carbohydrate digestion and absorption, and enhancement of peripheral insulin action.
1 December 2007 in American Journal of Physiology-Endocrinology and Metabolism
Journal Article
PMPaula L. McClean
Paula L. McClean
NINigel Irwin
Nigel IrwinRCRoslyn S. Cassidy
Roslyn S. Cassidy
Jens Holst
Victor GaultPeter R FlattThe gut hormone gastric inhibitory polypeptide (GIP) plays a key role in glucose homeostasis and lipid metabolism. This study investigated the effects of administration of a stable and specific GIP receptor antagonist, (Pro3)GIP, in mice previously fed a high-fat diet for 160 days to induce obesity and related diabetes. Daily intraperitoneal injection of (Pro3)GIP over 50 days significantly decreased body weight compared with saline-treated controls, with a modest increase in locomotor activity but no change of high-fat diet intake. Plasma glucose, glycated hemoglobin, and pancreatic insulin were restored to levels of chow-fed mice, and circulating triglyceride and cholesterol were significantly decreased. (Pro3)GIP treatment also significantly decreased circulating glucagon and corticosterone, but concentrations of GLP-1, GIP, resistin, and adiponectin were unchanged. Adipose tissue mass, adipocyte hypertrophy, and deposition of triglyceride in liver and muscle were significantly decreased. These changes were accompanied by significant improvement of insulin sensitivity, meal tolerance, and normalization of glucose tolerance in (Pro3)GIP-treated high-fat-fed mice. (Pro3)GIP concentrations peaked rapidly and remained elevated 24 h after injection. These data indicate that GIP receptor antagonism using (Pro3)GIP provides an effective means of countering obesity and related diabetes induced by consumption of a high-fat, energy-rich diet.
1 July 2014 in Peptides
Journal Article
JCJ. Michael Conlon
J. Michael Conlon
Milena MechkarskaMLMiodrag Lukic
Miodrag LukicPeter R Flatt1 December 2006 in Diabetes & Vascular Disease Research
Journal Article
Inhibitors of the enzyme dipeptidyl peptidase IV (DPP IV) provide a strategy for the treatment of type 2 diabetes. DPP IV rapidly inactivates the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Inhibition of DPP IV prolongs and enhances the activity of endogenous GLP-1 and GIP, which serve as important prandial stimulators of insulin secretion and regulators of blood glucose control. In clinical trials DPP IV inhibitors (or ‘gliptins’) have shown efficacy and tolerability in the management of hyperglycaemia in type 2 diabetes, without causing weight gain or hypoglycaemia.
About Me
Prof. Peter R. Flatt holds a DSc from Ulster University and a BSc Hons and PhD from Aston University. He was a Research Fellow at the University of Uppsala, Sweden (1978-80) before taking up an academic appointment at Surrey University in 1980. He is currently Professor of Biomedical Sciences at Ulster University, a position that he has held since 1989. Prof. Flatt is Head of the Diabetes Research Centre, having served as Director of the Biomedical Sciences Research Centre (1992-94), Head of the School of Biomedical Sciences (1994-97), and Director of the Biomedical Sciences research Institute (2016-23). Prof. Flatt is the founding Chairman (1991-) of the Islet Study Group of the European Association for the Study of Diabetes (EASD), member of the EASD Council (1997-01), Scientific Secretary & Committee Member of Diabetes UK (1991-97; 2001-04), Member of European Incretin Study Group (2022-), and a member of the Grants Review Board of the Juvenile Diabetes Federation International (1996-99). He is recipient of the Mary Jane Kugal Award (1999) of the Juvenile Diabetes Federation International, Biochemical Society Medal (2005), and was elected to membership of the Royal Irish Academy (2006), University Distinguished Senior Research Fellowship (2006) and Diabetes UK Dorothy Hodgkin Award Lecturer (2008). Patent holder, Academic co-founder, and Chief Scientific Officer/Director of Diabetica Ltd and academic founder of DiaBeta Labs. He was awarded MBE by KIng Charles IIII in 2025.
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