Effect of guar on second-meal glucose tolerance in normal man

1986 ◽  
Vol 71 (1) ◽  
pp. 49-55 ◽  
Author(s):  
T. R. Trinick ◽  
M. F. Laker ◽  
D. G. Johnston ◽  
M. Keir ◽  
K. D. Buchanan ◽  
...  

1. Whole body glucose turnover and absorption of a 50 g glucose drink was studied in six healthy volunteers on two occasions, 4 h after a ‘breakfast’ of 50 g of glucose, mixed on one occasion with 20 g of guar gum. 2. Plasma glucose concentrations were significantly reduced with guar gum compared with those obtained without guar gum (P < 0.0001). 3. Whole body glucose turnover studied by an intravenous primed dose constant infusion technique using d-[3-3H]glucose showed no significant difference between the two groups: 353 ± 15 mmol with guar and 350 ± 9 mmol without guar. 4. Total oral glucose absorption, followed with a D-[1-14C]glucose tracer, was significantly decreased by guar treatment, being 219 ± 3 mmol with guar and 239 ± 5 mmol without guar (P < 0.05). 5. Serum insulin levels were lowered by guar treatment (P<0.05) while those of C-peptide, gastric inhibitory polypeptide, glucagon, Cortisol and pancreatic polypeptide did not differ significantly. 6. Blood lactate concentrations were raised in the guar treated group (P < 0.05) whereas pyruvate, alanine, glycerol and 3-hydroxybutyrate concentrations did not differ significantly. 7. These results support the suggestion that guar improves second-meal tolerance to glucose by decreasing absorption.

1998 ◽  
Vol 83 (2) ◽  
pp. 626-631 ◽  
Author(s):  
Jaswinder S. Samra ◽  
Mo L. Clark ◽  
Sandy M. Humphreys ◽  
Ian A. MacDonald ◽  
Peter A. Bannister ◽  
...  

Cortisol is known to increase whole body lipolysis, yet chronic hypercortisolemia results in increased fat mass. The main aim of the study was to explain these two apparently opposed observations by examining the acute effects of hypercortisolemia on lipolysis in subcutaneous adipose tissue and in the whole body. Six healthy subjects were studied on two occasions. On one occasion hydrocortisone sodium succinate was infused iv to induce hypercortisolemia (mean plasma cortisol concentrations, 1500 ± 100 vs. 335± 25 nmol/L; P &lt; 0.001); on the other occasion (control study) no intervention was made. Lipolysis in the sc adipose tissue of the anterior abdominal wall was studied by measurement of arterio-venous differences, and lipolysis in the whole body was studied by constant infusion of[ 1,2,3-2H5]glycerol for measurement of the systemic glycerol appearance rate. Hypercortisolemia led to significantly increased arterialized plasma nonesterified fatty acid (NEFA; P &lt; 0.01) and blood glycerol concentrations (P &lt; 0.05), with an increase in systemic glycerol appearance (P &lt; 0.05). However, in sc abdominal adipose tissue, hypercortisolemia decreased veno-arterialized differences for NEFA (P &lt; 0.05) and reduced NEFA efflux (P &lt; 0.05). This reduction was attributable to decreased intracellular lipolysis (P &lt; 0.05), reflecting decreased hormone-sensitive lipase action in this adipose depot. Hypercortisolemia caused a reduction in arterialized plasma TAG concentrations (P &lt; 0.05), but without a significant change in the local extraction of TAG (presumed to reflect the action of adipose tissue lipoprotein lipase). There was no significant difference in plasma insulin concentrations between the control and hypercortisolemia study. Site-specific regulation of the enzymes of intracellular lipolysis (hormone-sensitive lipase) and intravascular lipolysis (lipoprotein lipase) may explain the ability of acute cortisol treatment to increase systemic glycerol and NEFA appearance rates while chronically promoting net central fat deposition.


1985 ◽  
Vol 54 (2) ◽  
pp. 449-458 ◽  
Author(s):  
A. N. Janes ◽  
T. E. C. Weekes ◽  
D. G. Armstrong

1. Sheep fitted with re-entrant canulas in the proximal duodenum and terminal ileum were used to determine the amount of α-glucoside entering, and apparently disappearing from, the small intestine when either dried-grass or ground maize-based diets were fed. The fate of any α-glucoside entering the small intestine was studied by comparing the net disappearance of such a-glucoside from the small intestine with the absorption of glucose into the mesenteric venous blood.2. Glucose absorption from the small intestine was measured in sheep equipped with catheters in the mesenteric vein and carotid artery. A continuous infusion of [6-3H]glucose was used to determine glucose utilization by the mesenteric-drained viscera and the whole-body glucose turnover rate (GTR).3. The amounts of α-glucoside entering the small intestine when the dried-grass and maize-based diets were given were 13.9 (SE 1.5) and 95.4 (SE 16.2) g/24 h respectively; apparent digestibilities of such α-glucoside in the small intestine were 60 and 90% respectively.4. The net absorption of glucose into the mesenteric venous blood was —2.03 (SE 1.20) and 19.28 (SE 0.75) mmol/h for the dried-grass and maize-based diets respectively. Similarly, total glucose absorption amounted to 1.52 (SE 1.35) and 23.33 (SE 1.86) mmol/h (equivalent to 7 and 101 g/24 h respectively). These values represented 83 and 11 1% of the a-glucoside apparently disappearing from the small intestine, determined using the re-entrant cannulated sheep.5. Total glucose absorption represented 8 and 61% of the whole-body GTR for the dried-grass and maize-based diets respectively. Endogenous glucose production was significantly lower when the sheep were fed on the maize-based diet compared with the dried-grass diet.6. The mesenteric-drained viscera metabolized a small amount of glucose, equivalent to 234 and 17% of the total glucose absorbed for the dried-grass and maize-based diets respectively.7. It is concluded that a large proportion of the starch entering the small intestine of sheep given a maize-based diet is digested and absorbed as glucose, and thus contributes to the whole-body GTR.


1995 ◽  
Vol 74 (4) ◽  
pp. 539-556 ◽  
Author(s):  
P. R. Ellis ◽  
F. G. Roberts ◽  
A. G. Low ◽  
L. M. Morgan

The present study was designed to determine the quantitative effects of starchy meals containing guar gum on rates of net apparent glucose absorption and net apparent insulin and gastric inhibitory polypeptide (GIP) production in growing pigs. The effects of these meals on the viscosity of jejunal digesta were also examined and correlated to changes in glucose absorption. Four growing pigs were each given either a low-fat semi-purified diet (control) or the same diet supplemented with a high-molecular-weight guar gum at concentrations in the diet of 20 or 40 g/kg. Blood samples were removed simultaneously via indwelling catheters from the mesenteric artery and the hepatic portal vein. Samples of jejunal digesta were removed via a T-piece cannula and used immediately for viscosity measurements at 39°. The ‘zero-shear’ viscosity of each sample was then calculated. Blood-flow measurements were made using an ultrasonic flow probe fitted to the hepatic portal vein. All measurements were made at intervals of 10 or 30 min during a 4 h postprandial period. Meals containing guar gum significantly increased (P < 0·05) the viscosity of jejunal digesta, an effect that was strongly dependent on the concentration of guar gum in the original diet. No significant differences in blood-flow rates were found between the control and guar-containing diets. Both concentrations of guar gum significantly reduced (P < 0·05) glucose absorption and insulin and GIP secretion rates over the 4 h postprandial period. An inverse relationship between the rate of glucose absorption and the ‘zero-shear’ viscosity of jejunal digesta was found. This study also provides direct evidence for the important role played by the entero-insular axis in modifying the glycaemic response to a meal containing guar gum.


1991 ◽  
Vol 261 (4) ◽  
pp. E473-E478
Author(s):  
A. Katz ◽  
M. K. Spencer ◽  
S. Lillioja ◽  
Z. Yan ◽  
D. M. Mott ◽  
...  

Biopsies were obtained from the quadriceps femoris muscle of two male patients deficient in phosphofructokinase (PFK) 1. In the basal state the patients had markedly higher contents of UDP-glucose (approximately 5-fold), hexose monophosphates (approximately 7- to 13-fold), inosine monophosphate (IMP) (approximately 15-fold), and fructose 2,6-bisphosphate (F-2,6-P2; approximately 6-fold) than controls. Fructose 1,6-bisphosphate was not detectable, and phosphocreatine was lower (33 and 54 mmol/kg dry wt) than in controls [72 +/- 4 (SD)]. Patients had normal fasting plasma glucose and insulin levels and basal glucose turnover rates and responded normally to a 75-g oral glucose challenge. Patients were also studied during euglycemic hyperinsulinemia (approximately 95 mg/dl; 40 and 400 mU.m-2.min-1). Whole body glucose disposal rates were normal during both insulin infusion rates. Biopsies taken after the 400 mU insulin infusion showed decreases in acetylcarnitine and citrate and increases in the fractional activity of glycogen synthase. It is suggested that the high basal levels of F-2,6-P2 are, at least partly, a consequence of the high levels of fructose 6-phosphate, which will stimulate flux through PFK-2 and inhibit fructose-2,6-bisphosphatase. The low phosphocreatine and high IMP contents indicate that carbohydrate availability is important for control of high-energy phosphate metabolism, even in the basal state. The insulin-mediated decreases in acetylcarnitine and citrate suggest an activation of the tricarboxylic acid cycle in skeletal muscle but an absence of the normal response to replenish these intermediates.


1984 ◽  
Vol 66 (3) ◽  
pp. 329-336 ◽  
Author(s):  
N. A. Blackburn ◽  
J. S. Redfern ◽  
H. Jarjis ◽  
A. M. Holgate ◽  
I. Hanning ◽  
...  

1. Experiments were carried out in human volunteers to investigate the mechanism by which guar gum improves glucose tolerance. 2. Guar reduced both plasma glucose and insulin responses to an oral glucose load, and delayed gastric emptying. However, there was no correlation between changes in individual blood glucose responses and changes in gastric emptying rates induced by guar. 3. With a steady-state perfusion technique, glucose absorption was found to be significantly reduced during perfusion of the jejunum with solutions containing guar, but returned to control values during subsequent guar-free perfusions. 4. Preperfusing the intestine with guar did not affect electrical measurements of unstirred layer thickness in the human jejunum in vivo.. 5. Experiments in vitro established that glucose diffusion out of a guar/glucose mixture was delayed under conditions of constant stirring. 6. We conclude that guar improves glucose tolerance predominantly by reducing glucose absorption in the small intestine. It probably does this by inhibiting the effects of intestinal motility on fluid convection.


2007 ◽  
Vol 92 (1) ◽  
pp. 229-234 ◽  
Author(s):  
Won Hah Park ◽  
Yoo Joung Oh ◽  
Gae Young Kim ◽  
Sang Eun Kim ◽  
Kyung-Hoon Paik ◽  
...  

Abstract Context: Obestatin is a peptide hormone derived from the proteolytic cleavage of ghrelin preprohormone. In Prader-Willi syndrome (PWS), the levels of total ghrelin (TG) and acylated ghrelin (AG) are increased, and these hormones are regulated by insulin. Objective: Our objective was to analyze the changes in the obestatin levels after glucose loading and to characterize the correlations of obestatin with TG, AG, and insulin. Design: Plasma obestatin, TG, AG, and insulin levels were measured in PWS children (n = 15) and controls (n = 18) during an oral glucose tolerance test. Setting: All subjects were admitted to the Samsung Medical Center. Interventions: An oral glucose tolerance test was performed after an overnight fast. Main Outcome Measures: The plasma levels of obestatin, TG, AG, and serum insulin were measured at 0, 30, 60, 90, and 120 min after glucose challenge, and areas under the curves (AUCs) were calculated. Results: No significant difference in AUC of the plasma obestatin was found between the PWS children and normal obese controls (P = 0.885), although AUC of AG (P = 0.002) and TG (P = 0.003) were increased in the PWS children. Moreover, There was a negative correlation between the AUC of AG and AUC of insulin both in PWS (r = −0.432; P = 0.049) and in controls (r = −0.507; P = 0.016). However, AUC of obestatin was not significantly correlated with AUC of insulin (in PWS, r = 0.168 and P = 0.275; in controls, r = −0.331 and P = 0.09). Conclusions: Our results indicate that plasma obestatin is not elevated in PWS children and is not regulated by insulin both in PWS children and in obese controls.


1994 ◽  
Vol 140 (2) ◽  
pp. 309-312 ◽  
Author(s):  
J H Hays ◽  
E Silverman ◽  
B B Potter ◽  
K M M Shakir

Abstract Although the action of gastric inhibitory polypeptide (GIP) on the β cells of the pancreas is well documented, the effect of this hormone on insulin secretion in patients who are hypothyroid has not been studied. Hypothyroid patients demonstrate increased serum immunoreactive insulin levels in response to oral glucose when compared with euthyroid subjects. We postulated that a delayed and exaggerated response of GIP could account for the hyperinsulinaemic response. Nine thyroidectomized patients (aged 44·9 ± 3·6 years) who were otherwise healthy but undergoing re-evaluation for recurrence of thyroid carcinoma, were given a 75 g oral glucose tolerance test (OGTT). These subjects were studied 6 weeks after thyroid hormone replacement had been stopped and while on hormone treatment. The serum glucose and plasma GIP responses to oral glucose were similar in the euthyroid and hypothyroid states. The serum insulin response as well as the areas under the curve for insulin following OGTT were significantly elevated (P<0·01) during hypothyroidism. Solid-phase gastric emptying times studied in six patients who were euthyroid and hypothyroid were not different (35 ± 12 versus 36 ± 14 min respectively). None of the subjects had detectable levels of serum thyroglobulin, microsomal or parietal cell antibodies. In summary, we have confirmed a hyperinsulinaemic response to an OGTT and normal solid-phase gastric emptying rates in this form of hypothyroidism. We did not find significant differences in serum glucose or GIP responses and postulate this as evidence of resistance to the effects of endogenous insulin. The mechanism of alterations in carbohydrate tolerance in the hypothyroid state continue to remain unknown. Journal of Endocrinology (1994) 140, 309–312


1999 ◽  
Vol 86 (6) ◽  
pp. 1770-1777 ◽  
Author(s):  
J. L. Bowtell ◽  
K. Gelly ◽  
M. L. Jackman ◽  
A. Patel ◽  
M. Simeoni ◽  
...  

The purpose of this study was to determine the efficacy of glutamine in promoting whole body carbohydrate storage and muscle glycogen resynthesis during recovery from exhaustive exercise. Postabsorptive subjects completed a glycogen-depleting exercise protocol, then consumed 330 ml of one of three drinks, 18.5% (wt/vol) glucose polymer solution, 8 g glutamine in 330 ml glucose polymer solution, or 8 g glutamine in 330 ml placebo, and also received a primed constant infusion of [1-13C]glucose for 2 h. Plasma glutamine concentration was increased after consumption of the glutamine drinks (0.7–1.1 mM, P < 0.05). In the second hour of recovery, whole body nonoxidative glucose disposal was increased by 25% after consumption of glutamine in addition to the glucose polymer (4.48 ± 0.61 vs. 3.59 ± 0.18 mmol/kg, P < 0.05). Oral glutamine alone promoted storage of muscle glycogen to an extent similar to oral glucose polymer. Ingestion of glutamine and glucose polymer together promoted the storage of carbohydrate outside of skeletal muscle, the most feasible site being the liver.


1981 ◽  
Vol 46 (2) ◽  
pp. 267-276 ◽  
Author(s):  
P. R. Ellis ◽  
E. C. Apling ◽  
A. R. Leeds ◽  
N. R. Bolster

1. Bread alone and supplemented with guar gum at three levels (50, 100 and 150 g/kg) was given to eleven non-diabetic subjects, and blood glucose and serum insulin were determined preprandialy, and at 30 min and 60 min after commencement of the meal. The satiating effect, up to 120 min, of the guar bread and its acceptability to the same group of normal volunteers was also studied.2. No significant differences in blood glucose were observed between control and guar breads at 30 min and 60 min, apart from 100 g guar/kg bread at 30 min (P < 0·05). A significant difference in serum insulin was indicated between: control and 50 (P < 0·02) and 150 (P < 0·02) guar/kg breads at 30 min; control and 50 (P < 0·05), 100 (P < 0·001) and 150 (P < 0·05) guar/ke breads at 60 min.3. There were no significant differences in the satiety scores for control and guar breads. Significant increases in satiety attributed to 150 g guar/kg bread were found when compared to: 50 g guar/kg bread immediately after eating (P < 0·05), 100 g guar/kg bread at 60 min (P < 0·02) and 50 and 100 g guar/kg breads at 120min (both P < 0·05).4. There was a positive correlation between hedonic score and relative replacement of guar (r 0·62, P < 0·001, n 44) and from the regression line it was found that 50 and 100 g guar/kg breads produced hedonic scores close to a neutral response of 5, whereas 150 g guar/kg bread at a predictive score of 6·3 appeared to be unacceptable to our subjects.5. Guar bread at the 100 g/kg level (59 g guar/kg bread) reduced the serum insulin by 48% at 60 min and is found to be an acceptable food product at this level of incorporation. However, more information is required to demonstrate the possible satiating potential of guar bread.


2019 ◽  
Vol 241 (3) ◽  
pp. 189-199 ◽  
Author(s):  
Holly M Johnson ◽  
Erin Stanfield ◽  
Grace J Campbell ◽  
Erica E Eberl ◽  
Gregory J Cooney ◽  
...  

Poor nutrition plays a fundamental role in the development of insulin resistance, an underlying characteristic of type 2 diabetes. We have previously shown that high-fat diet-induced insulin resistance in rats can be ameliorated by a single glucose meal, but the mechanisms for this observation remain unresolved. To determine if this phenomenon is mediated by gut or hepatoportal factors, male Wistar rats were fed a high-fat diet for 3 weeks before receiving one of five interventions: high-fat meal, glucose gavage, high-glucose meal, systemic glucose infusion or portal glucose infusion. Insulin sensitivity was assessed the following day in conscious animals by a hyperinsulinaemic-euglycaemic clamp. An oral glucose load consistently improved insulin sensitivity in high-fat-fed rats, establishing the reproducibility of this model. A systemic infusion of a glucose load did not affect insulin sensitivity, indicating that the physiological response to oral glucose was not due solely to increased glucose turnover or withdrawal of dietary lipid. A portal infusion of glucose produced the largest improvement in insulin sensitivity, implicating a role for the hepatoportal region rather than the gastrointestinal tract in mediating the effect of glucose to improve lipid-induced insulin resistance. These results further deepen our understanding of the mechanism of glucose-mediated regulation of insulin sensitivity and provide new insight into the role of nutrition in whole body metabolism.


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