J. A. Tredger
University of Surrey
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Featured researches published by J. A. Tredger.
British Journal of Nutrition | 1990
Linda M. Morgan; J. A. Tredger; J. Wright; Vincent Marks
Six healthy non-obese male subjects were given three test meals containing 100 g carbohydrate and 1.5 g soluble paracetamol, supplemented on one occasion with 10 g guar gum and on another with 10 g sugarbeet fiber. A further six subjects were given the same test meal supplemented on one occasion with 10 g soya-bean-cotyledon fibre and on another, 5 g glucomannan. Venous blood samples were taken before, and at intervals for 180 min following the meal, and analysed for insulin, gastric inhibitory polypeptide (GIP) and paracetamol (as an index of gastric emptying). Arterialized blood samples were taken and analysed for glucose. Meal supplementation with both guar gum and sugar-beet fibre improved glucose tolerance, but circulating glucose levels were unaffected by the addition of either soya-bean-cotyledon fibre or glucomannan to the meals. Supplementation with guar gum and glucomannan lowered post-prandial insulin levels. Insulin levels were enhanced by addition of soya-bean-cotyledon fibre to the meal and unaffected by sugar-beet fibre. Post-prandial GIP levels were lowered in the guar-gum-supplemented meal and augmented with sugar-beet fibre supplementation. Addition of glucomannan and soya-bean-cotyledon fibre did not affect circulating GIP levels. The study failed to confirm previous reports of improved glucose tolerance following glucomannan and soya-bean-cotyledon fibre supplementation. The failure of sugar-beet fibre to reduce post-prandial insulin secretion despite improved glucose tolerance may be due to the observed increased secretion of GIP. The increased insulin levels seen following soya-bean-cotyledon fibre supplementation cannot be attributed either to changes in glucose tolerance, GIP secretion or gastric emptying.(ABSTRACT TRUNCATED AT 250 WORDS)
British Journal of Nutrition | 1989
Susan M. Shutler; Gemma M. Bircher; J. A. Tredger; Linda M. Morgan; Ann F. Walker; A. G. Low
1. Thirteen normo-cholesterolaemic male students consumed one 450 g can of baked beans (Phaseolus vulgaris) in tomato sauce, daily, for 14 d as part of their normal diet. After a 14 d washout period, eleven of the students went on to consume one 440 g can of spaghetti in tomato sauce, daily, for 14 d. 2. Fasting blood samples were taken frequently for measurement of plasma cholesterol, high-density lipoprotein (HDL)-cholesterol, triacylglycerols, glucose, insulin and C-peptide. Diet diaries (3 d) were completed by the subjects during each period. 3. Consumption of beans and spaghetti led to a significant reduction in the amount of fat eaten daily (P less than 0.05). Bean consumption also resulted in significant increases in protein, fibre and sugar intakes (P less than 0.02, P less than 0.001 and P less than 0.05 respectively). 4. During the bean-eating period the mean total plasma cholesterol level of the students fell significantly from 5.1 to 4.5 mmol/l (P less than 0.02). No reduction in plasma cholesterol occurred during the spaghetti-eating period. 5. HDL-cholesterol levels fell significantly during both periods (P less than 0.001), but HDL:total cholesterol ratio was significantly reduced only during the spaghetti-eating period (P less than 0.001). Neither beans nor spaghetti affected triacylglycerol, insulin or C-peptide levels. 6. The benefits of a legume-rich diet are discussed.
British Journal of Nutrition | 1988
Linda M. Morgan; J. A. Tredger; Shelagh M. Hampton; A. P. French; J. C. F. Peake; Vincent Marks
1. Five healthy volunteers whose usual fat and energy intakes were moderately high (fat intake 155 (SE 11) g/d; energy intake 13683 (SE 909) kJ/d) were given on two separate occasions (a) 96 g fat and (b) 96 g fat and intravenous (IV) glucose (250 g glucose/l; 100 ml followed by a 2 ml/min infusion for 180 min). 2. Subjects continued on a low-fat diet for 35 d (fat intake 25 (SE 4) g/d; energy intake 6976 (SE 539) kJ/d) and the tests repeated. 3. The gastric inhibitory polypeptide (GIP) response to oral fat was significantly attenuated by IV glucose whilst subjects were consuming their normal diets and the GIP response to fat alone was significantly diminished during the low-fat diet. Post-prandial plasma triglycerides, light scattering indices (LSI; an index of post-prandial chylomicronaemia) and paracetamol levels paralleled the integrated GIP responses on both normal and low-fat diets. 4. The study of oral fat with or without glucose was repeated on seven further volunteers consuming their usual diet, substituting 10 MBq 99Tcm-labelled tin colloid for the paracetamol to investigate the rate of gastric emptying by radionuclide imaging. 5. Plasma GIP, insulin, triglyceride and LSI levels were similar to those found in the first study. IV glucose almost doubled the gastric emptying time of the oral fat load (half emptying time (t1/2) 148 (SE 11) min after fat alone and 224 (SE 18) min after fat and IV glucose). Post-prandial plasma motilin levels were significantly depressed by IV glucose.(ABSTRACT TRUNCATED AT 250 WORDS)
British Journal of Nutrition | 1988
Linda M. Morgan; Shelagh M. Hampton; J. A. Tredger; R. Cramb; Vincent Marks
1. Five healthy volunteers (usual fat intake 103 (SE 9) g/d and energy intake 9855 (SE 937) kJ/d were given on two separate occasions (a) 100 g oral glucose and (b) sufficient intravenous (IV) glucose to obtain similar arterialized plasma glucose levels to those after oral glucose. 2. Subjects increased their fat intake by 68 (SE 9.6)% for 28 d by supplementing their diet with 146 ml double cream/d (fat intake on high-fat diet (HFD) 170 (SE 8) g/d; energy intake 12347 (SE 770)). 3. The 100 g oral glucose load was repeated and IV glucose again given in quantities sufficient to obtain similar arterialized blood glucose levels. Immunoreactive plasma insulin, C-peptide and gastric inhibitory polypeptide (GIP) were measured. 4. Plasma GIP levels were higher following oral glucose after the HFD (area under plasma GIP curve 0-180 min 1660 (SE 592) v. 2642 (SE 750) ng/l.h for control and HFD respectively; P less than 0.05). Both insulin and C-peptide levels were significantly higher after oral than after IV glucose (P less than 0.01) but neither were affected by the HFD. Glucose levels were lower following the HFD after both oral and IV glucose (area under plasma glucose curve 0-180 min, following oral glucose 6.7 (SE 0.3) mmol/l.h for control and 4.2 (SE 0.6) mmol/l.h for HFD; P less than 0.01). 5. Glucose-stimulated GIP secretion was thus enhanced by the HFD. Insulin secretion in response to oral glucose was unchanged, in spite of an improvement in glucose tolerance. 6. The improvement in glucose tolerance post-HFD could possibly be due to a GIP-mediated inhibition of hepatic glycogenolysis, or a decreased rate of glucose uptake from the small intestine.
British Journal of Nutrition | 1994
P. D. Overton; Nigel P. Furlonger; J. M Beety; J. Chakraborty; J. A. Tredger; Linda M. Morgan
This study investigates the mechanisms of action for the hypocholesterolaemic effects of sugar-beet fibre (SBF) and guar gum. Four groups of ten male Wistar rats were fed ad lib. on test diets containing either 100 g SBF or guar/kg, or control diets containing 100 g cellulose or wheat bran/kg for 28 d. Food intake, weight gain and food consumption ratios were unaffected by the diets. Circulating cholesterol and hepatic cholesterol concentrations were significantly lower in both SBF- and guar-fed groups compared with either cellulose- or bran-fed animals. Circulating triacylglycerol concentrations were significantly lower in SBF- and guar-fed animals, but total hepatic lipid concentrations and hepatic and adipose tissue lipogenesis rates were unaffected by the diets. Hepatic cholesterol-7 alpha-hydroxylase (EC 1.14.13.17) activities were significantly higher in the guar-fed animals compared with cellulose or bran control groups. Hepatic 3-hydroxy-3-methylglutaryl-CoA reductase (EC 1.1.1.88) activities were unaffected. Circulating bile acid concentrations were significantly lower in SBF- and guar-fed animals and faecal bile acid output was significantly higher in the guar-fed group compared with bran- or cellulose-fed groups. This study supports the hypothesis that guar exerts its hypocholesterolaemic effect via intraluminal bile acid binding and loss of cholesterol from increased faecal bile acid excretion. The mechanism of action for the hypocholesterolaemic effect of SBF is less clear; the results of the present study point to a mechanism involving disruption of the enterohepatic bile acid circulation, possibly via changes in the rate of absorption of dietary lipid.
British Journal of Nutrition | 1985
Linda M. Morgan; J. A. Tredger; A. Madden; P. Kwasowski; Vincent Marks
The effect of incorporating guar gum into predominantly single-component meals of carbohydrate, fat or protein on liquid gastric emptying and on the secretion of gastric inhibitory polypeptide (GIP), gastrin and motilin, was studied in healthy human volunteers. Volunteers were given either 80 ml Hycal (carbohydrate meal), 150 g cooked lean minced beef (protein meal) or 200 ml double cream (fat meal) either with or without 5 or 6 g guar gum. Liquid gastric emptying was monitored in the fat and protein meals by taking 1.5 g paracetamol, consumed in water, with the meals and monitoring its appearance in circulation. Postprandial insulin and GIP levels were both significantly reduced by addition of guar gum to the carbohydrate meal. Postprandial GIP secretion was also reduced by addition of guar gum to the protein meal, but protein-stimulated gastrin secretion was enhanced by guar gum. There was a significant negative correlation between peak circulating gastrin levels and the corresponding GIP levels. Postprandial GIP secretion and plasma motilin levels were unaffected by addition of guar gum to the fat meal. 5 and 10 g guar gum/l solutions in water possessed buffering capacities between pH 2.75 and 5.5. Guar gum at 5 g/l caused no detectable change in liquid gastric-emptying time. The observed augmentation of gastrin secretion by guar gum following a protein meal could be due either to the buffering capacity of guar gum or to the attenuation of GIP secretion. It is possible that the chronic use of guar gum could be associated with changes in gastric acid secretion.
British Journal of Nutrition | 1993
Linda M. Morgan; J. A. Tredger; Y. Shavila; J.S. Travis; J. Wright
The effects of guar gum, sugar-beet fibre (SBF) and wheat bran supplementation of a high-fat test meal were compared with an NSP-free control meal and a meal containing an equivalent amount of the ion-exchange resin cholestyramine in healthy non-obese human volunteers. Their effects on gastric emptying, postprandial circulating bile acids, triacylglycerols and gastrointestinal hormone levels were studied. The in vitro binding of NSP and cholestyramine to [1-14C]glycocholic acid was measured and compared with their in vivo effect. Guar gum and cholestyramine supplementation significantly lowered circulating postprandial bile acid, triacylglycerol and gastric inhibitory polypeptide concentrations, but sugar-beet fibre and wheat bran were without effect. Liquid gastric emptying, as assessed by circulating paracetamol levels, was slightly accelerated in the guar gum-supplemented meal. Glycocholic acid bound strongly to the insoluble fraction of cholestyramine and the soluble fraction of guar gum. The insoluble fractions of SBF and wheat bran bound only small quantities of glycocholate; no bile acid binding was detected in the soluble fractions of these NSP. The study demonstrates that measurement of postprandial bile acids enables an indirect measurement to be made of bile acid binding to NSP in vivo. The results support the hypothesis that the hypocholesterolaemic action of guar gum is largely mediated via interruption of the enterohepatic bile acid circulation, but indicate that the hypocholesterolaemic action of SBF is mediated by another mechanism.
British Journal of Nutrition | 1999
Christine M. Williams; J. A. Francis-Knapper; Diane H. Webb; C. A. Brookes; Antonis Zampelas; J. A. Tredger; J. Wright; Gert W. Meijer; Philip C. Calder; Parveen Yaqoob; Helen M. Roche; M. J. Gibney
Journal of Human Nutrition and Dietetics | 1991
J. A. Tredger; Linda M. Morgan; J.S. Travis; Vincent Marks
Digestion | 1993
Linda M. Morgan; Ruan Elliott; J. A. Tredger; J. Nightingale; Vincent Marks