Rate Of Glucose Absorption Research Articles

Nasogastric Aspiration as an Indicator for Feed Absorption in Model-Based Glycemic Control in Neonatal Intensive Care

STAR (stochastic targeted) is a glycemic control model-based framework for critically ill neonates that has shown benefits in reducing hypoglycemia and hyperglycemia. STAR uses a stochastic matrix method to forecast future changes in a patient's insulin sensitivity and then applies this result to a physiological model to select an optimal insulin treatment. Nasogastric aspiration may be used as an indicator to suggest periods of care when enteral feed absorption is compromised, improving the performance of glycemic control. An analysis has been carried out to investigate the effect of poorly absorbed feeds on glycemic control. Clinical data were collected from eight patients on insulin therapy and enteral feed, which included large or significantly milky aspirates. Patients had a median gestational age of 25 weeks and postnatal age of 5.5 days. Virtual patients were created using the NICING model, and insulin sensitivity (SI) profiles were fit. Alternative feed profiles were generated whereby enteral feed absorption was redistributed with time to account for poor feed absorption. The effect of poor feed absorption, as indicated by aspirates, is investigated. The average percentage change of SI 4 h before a significant aspirate was 1.16%, and 1.49% in the 4 h following the aspirate. No distinct relationship was found between the fractional change in SI and the volume of the aspirate. Accounting for aspirates had a clinically negligible impact on glycemic control in virtual trials. Accounting for aspirates by manipulating enteral feed profiles had a minimal influence on both modeling and controlling glycemia in neonates. The impact of this method is clinically insignificant, suggesting that a population constant for the rate of glucose absorption in the gut adequately models feed absorption within the STAR framework.

The kinetics of starch and nitrogen digestion regulate growth performance and nutrient utilisation of broilers fed coarsely ground, sorghum-based diets

A study was conducted to examine the effect of starch and nitrogen digestion kinetics on broiler performance using sorghum-based diets as a model. Three sorghum varieties with red, white and yellow pericarps and three feed forms, mash, intact pellets and reground pellets, constituted a 3 × 3 factorial array of dietary treatments. Starch and nitrogen digestion kinetics were determined using an exponential mathematical model to relate digestion coefficients in the proximal jejunum, proximal ileum and distal ileum with mean retention times in each segment. There were interactions between sorghum variety and feed form for starch and nitrogen digestion kinetics. Steam-pelleting at a conditioning temperature of 90°C (unprocessed mash versus reground pellets) substantially influenced starch digestion rate in red and yellow sorghum-based diets, but not in white sorghum-based diets. Alternatively, with nitrogen digestion rate, there were no significant differences in yellow sorghum-based diets between feed forms but there were in red and white sorghum-based diets. The digestion rate of starch was more rapid than nitrogen, especially in the proximal jejunum. Starch digestion rates were significantly correlated with nitrogen retention but this was not the case with nitrogen digestion rates. The rate of glucose absorption from predicted glycaemic indices was highly correlated with enhanced feed efficiency. Thus this study demonstrates that even under ad libitum feeding regimes, kinetics of starch and protein digestion regulated feed efficiency and nitrogen retention in broiler chickens. The dynamics of starch and protein digestion were more accurate indicators of feed efficiency and nitrogen retention than apparent ileal starch and nitrogen digestibility.

Interaction of insulin with prokinetic drugs in STZ-induced diabetic mice

To study the possible interactions of metoclopramide, domperidone and erythromycin in streptozotocin-induced diabetic mice treated with insulin by various parameters. Effects of the individual as well as combined drugs were studied in diabetic mice via estimation of the blood glucose and serum insulin levels, small intestinal transit (SIT), gastric emptying (GE), xylose absorption and glucose tolerance tests. Groups were given insulin 2 IU/kg s.c., metoclopramide 20 mg/kg p.o., domperidone 20 mg/kg p.o. and erythromycin 6 mg/kg p.o. individually and in combination. There were also normal and diabetic control groups. The first set of experiments was carried out to investigate the subchronic effect on blood glucose and serum insulin levels in diabetic mice of one week of daily dose administration of the tested drugs individually as well as the combination of insulin with each prokinetic drug. The other five sets of experiments were carried out to investigate the acute effect of a single dose of each drug individually and in combination on blood glucose and serum insulin levels, SIT, GE, oral xylose absorption and glucose tolerance tests. The study included the prokinetic drugs metoclopramide (20 mg/kg), domperidone (20 mg/kg) and erythromycin (6 mg/kg), as well as insulin (2 IU/kg), which was individually effective in decreasing SIT, enhancing GE and increasing xylose absorption significantly in diabetic mice. Erythromycin tended to decrease blood glucose level and increase serum insulin level after 1 wk of daily administration in diabetic mice. Erythromycin potentiated the effect of insulin on blood glucose level and serum insulin level whereas other prokinetic agents failed to do so after repeated dose administration in diabetic mice. Metoclopramide or erythromycin in combination with insulin significantly decreased SIT, in diabetic mice, to lower levels than with insulin alone. Administration of prokinetic drugs along with insulin antagonized the action of insulin on xylose absorption. These combinations also increased the rate of glucose absorption from the gut. The present study suggests that prokinetic drugs could potentially improve glycemic control in diabetic gastroparesis by allowing a more predictable absorption of nutrients, matched to the action of exogenous insulin. The use of prokinetics, such as erythromycin, may be interesting in the clinic in decreasing the need for insulin in diabetic patients. The dose of insulin may be safely decreased with erythromycin in chronic treatments.

Effects on cognitive performance of modulating the postprandial blood glucose profile at breakfast

Considering the importance of glucose as a brain substrate, the postprandial rate of glucose delivery to the blood could be expected to affect cognitive functions. The purpose was to evaluate to what extent the rate of glucose absorption affected measures of cognitive performance in the postprandial period. In addition, cognitive performance was evaluated in relation to individual glucoregulation. A white wheat bread (WWB) enriched with guar gum (G-WWB) with the capacity to produce a low but sustained blood glucose net increment was developed. The G-WWB was evaluated in the postprandial period after breakfast with respect to effects on cognitive function (working memory and selective attention (SA)) in 40 healthy adults (49-71 years, body mass index 20-29 kg/m(2)), using a high glycaemic index WWB for comparison in a randomised crossover design. The G-WWB improved outcome in the cognitive tests (SA test) in the later postprandial period (75-225 min) in comparison with the WWB (P<0.01). Subjects with better glucoregulation performed superior in cognitive tests compared with subjects with worse glucoregulation (P<0.05). Beneficial effects on cognitive performance were observed with the G-WWB in the late postprandial period. The positive effect is suggested to emanate from improved insulin sensitivity, possibly in a combination with an enhanced neural energy supply. The results highlight the importance of carbohydrate foods that induces a low but sustained blood glucose profile in enhancing postprandial cognitive functions.

Non-Nutritive Sweeteners and their Role in the Gastrointestinal Tract

Non-nutritive sweeteners can bind to sweet-taste receptors present not only in the oral cavity, but also on enteroendocrine and pancreatic islet cells. Thus, these sweeteners may have biological activity by eliciting or inhibiting hormone secretion. Because consumption of non-nutritive sweeteners is common in the United States, understanding the physiological effects of these substances is of interest and importance. A PubMed (1960-2012) search was performed to identify articles examining the effects of non-nutritive sweeteners on gastrointestinal physiology and hormone secretion. The majority of in vitro studies showed that non-nutritive sweeteners can elicit secretion of gut hormones such as glucagon-like peptide 1 and glucose-dependent insulinotropic peptide in enteroendocrine or islet cells. In rodents, non-nutritive sweeteners increased the rate of intestinal glucose absorption, but did not alter gut hormone secretion in the absence of glucose. Most studies in humans have not detected effects of non-nutritive sweeteners on gut hormones or glucose absorption. Of eight human studies, one showed increased glucose-stimulated glucagon-like peptide 1 secretion after diet soda consumption, and one showed decreased glucagon secretion after stevia ingestion. In humans, few studies have examined the hormonal effects of non-nutritive sweeteners, and inconsistent results have been reported, with the majority not recapitulating in vitro data. Further research is needed to determine whether non-nutritive sweeteners have physiologically significant biological activity in humans.

Mechanism-based population modelling for assessment of L-cell function based on total GLP-1 response following an oral glucose tolerance test

GLP-1 is an insulinotropic hormone that synergistically with glucose gives rise to an increased insulin response. Its secretion is increased following a meal and it is thus of interest to describe the secretion of this hormone following an oral glucose tolerance test (OGTT). The aim of this study was to build a mechanism-based population model that describes the time course of total GLP-1 and provides indices for capability of secretion in each subject. The goal was thus to model the secretion of GLP-1, and not its effect on insulin production. Single 75 g doses of glucose were administered orally to a mixed group of subjects ranging from healthy volunteers to patients with type 2 diabetes (T2D). Glucose, insulin, and total GLP-1 concentrations were measured. Prior population data analysis on measurements of glucose and insulin were performed in order to estimate the glucose absorption rate. The individual estimates of absorption rate constants were used in the model for GLP-1 secretion. Estimation of parameters was performed using the FOCE method with interaction implemented in NONMEM VI. The final transit/indirect-response model obtained for GLP-1 production following an OGTT included two stimulation components (fast, slow) for the zero-order production rate. The fast stimulation was estimated to be faster than the glucose absorption rate, supporting the presence of a proximal-distal loop for fast secretion from L: -cells. The fast component (st₃) = 8.64·10⁻⁵ [mg⁻¹]) was estimated to peak around 25 min after glucose ingestion, whereas the slower component (st₄ = 26.2·10⁻⁵ [mg⁻¹]) was estimated to peak around 100 min. Elimination of total GLP-1 was characterised by a first-order loss. The individual values of the early phase GLP-1 secretion parameter (st₃) were correlated (r = 0.52) with the AUC(0-60 min.) for GLP-1. A mechanistic population model was successfully developed to describe total GLP-1 concentrations over time observed after an OGTT. The model provides indices related to different mechanisms of subject abilities to secrete GLP-1. The model provides a good basis to study influence of different demographic factors on these components, presented mainly by indices of the fast- and slow phases of GLP-1 response.

The Effect of a Dietary Carbohydrase Enzyme System on Blood Glucose Levels When Combined with Foods of Varying Glycemic Index in Male Sprague–Dawley Rats

Extensive research has shown that physical performance and recovery can be improved by maintaining or enhancing glucose availability. Carbogen(®) (Triarco Industries, Wayne, NJ, USA), a patented dietary fungal carbohydrase enzyme system, converts complex carbohydrates and fiber into simpler carbohydrates when ingested. Supplementing the enzymatic digestion of complex carbohydrates and fiber that may be digested very slowly or not at all in vivo may increase the availability of glucose. This may be reflected by increased absorption rates and higher measurable levels of whole blood glucose (WBG) that may be bioavailable for extended energy production. These preliminary investigations evaluate the ability of Carbogen to produce a rapid and more sustained increase in WBG levels when combined with a variety of food substrates commonly used by athletes and non-athletes to increase levels of physical activity. To investigate this, food substrates having a low, moderate, or high glycemic index (GI) with various amounts of total carbohydrates and dietary fiber were used. The individually tested substrates include soy nuts, cooked pasta, meal replacement bars, a nutrition shake, and a carbohydrate sports supplement. The investigations presented here consist of seven separate preclinical rat feasibility studies conducted over a period of approximately 12 months. The collective results presented here identify specific attributes of a category of food substrates common to sports nutrition enthusiasts that may significantly increase WBG levels over an extended time when dosed with Carbogen. Specifically, using Carbogen with a food substrate having a low or moderate GI and containing dietary fiber may increase the rate of glucose absorption and maintain significant increases in WBG levels.

Glucose Absorption in Gestational Diabetes Mellitus During an Oral Glucose Tolerance Test

OBJECTIVEWomen with gestational diabetes mellitus (GDM) show reduced insulin sensitivity and markedly elevated glucose excursions. After delivery, GDM mostly reverts to normal glucose tolerance (NGT), although leaving an increased risk of type 2 diabetes. Because gastrointestinal function changes during pregnancy causing vomiting, constipation, or reduced motility, we thought that gut glucose absorption in GDM or pregnancy might be altered to affect circulating glucose excursions.RESEARCH DESIGN AND METHODSBy undergoing 180-min oral glucose tolerance tests (OGTTs), pregnant women with GDM (GDMpreg; n = 15, BMI = 32 ± 2 kg/m2, aged 33 ± 1 years) were compared with NGT women (NGTpreg; n = 7, BMI = 28 ± 1 kg/m2, aged 34 ± 2 years), matching for major anthropometric characteristics (each P > 0.2). After delivery (6–7 months later), both groups were studied the same way. We computed and mathematically modeled gut glucose absorption from insulin-mediated glucose disappearance and endogenous glucose production (EGP). Whole-body insulin sensitivity was calculated using the Clamp-like Index.RESULTSGDMpreg showed 16–25% higher plasma glucose concentrations (P < 0.04) during the final 2 h of OGTT, similar EGP, but lower (P < 0.01) insulin sensitivity (2.7 ± 0.2 mg · kg−1 · min−1 vs. NGTpreg: 4.5 ± 0.8 mg · kg−1 · min−1). In GDMpreg, gut glucose absorption rates were ≤52% lower from 30 to 120 min (P < 0.03 vs. conditions after delivery or NGTpreg). In contrast, glucose absorption rates in NGTpreg were comparable during and after pregnancy. None of the studied women developed diabetes after delivery.CONCLUSIONSIn GDMpreg, OGTT gut glucose absorption is markedly lower during hyperglycemia, whereas both glycemia and glucose absorption in NGTpreg are comparable between pregnant and postpartum states. Thus, hyperglycemia in GDM does not seem to result from too rapid or increased glucose absorption.

Increased Jejunal Absorption of Glucose in Rats Submitted to Blockade of GABAA Receptors in the Hypothalamic Paraventricular Nucleus

In this study we investigated the status of jejunal absorption and peripheral metabolism of glucose following disinhibition of paraventricular nucleus (PVN) induced by the GABAA antagonist bicuculline methiodide (BMI). Adult male Wistar rats (270-300g) were anesthetized to implant unilateral guide cannula targeted to PVN for later microinjec- tion of BMI (10 pmol/100 nl, n=6) or vehicle (NaCl 0.9 % /100 nl, n=5). The jejunal loop was isolated and perfused (0.5 mL/min) with Tyrode solution containing twice the normal concentrations of glucose, sodium, and potassium. After mi- croinjections into PVN, perfusate and blood samples were taken every 10 min over a 40 min period. In comparison with vehicle, BMI into PVN increased glucose absorption at 30 min (1.2 ± 0.1 vs. 1.8 ± 0.1 � mol/min; *P<0.05) and at 40 min (1.3 ± 0.2 vs. 2.4 ± 0.3 � mol/min; *P<0.05), whereas plasma insulin was significantly reduced (0.5 ± 0.04 vs. 0.3 ± 0.04 ng/ml, *P<0.01). At the end of the experiment, samples from the liver and gastrocnemius muscle were taken to measure levels of glycogen, intermediate metabolites of the glycolytic pathway and ATP. Compared to control, muscle glucose-6- phosphate (0.380 ± 0.063 vs. 0.253 ± 0.020 � mol/g; P<0.05) and ATP (0.166 ± 0.065 vs. 0.038 ± 0.013 � mol/g; *P<0.05) were reduced in the group microinjected with BMI into PVN. We conclude that PVN disinhibition changes the absorption and peripheral glucose metabolism.

Evidence for tryptaminergic and noradrenergic involvement in the antisecretory action of morphine in the rat jejunum.

Experiments have been performed to determine whether the antisecretory (antidiarrhoeal) effect of morphine in the intestine is mediated by a direct action of morphine on enteric nerves. Rats were pretreated with 6-hydroxydopamine (6-OHDA) or p-chlorophenylalanine (PCPA) to deplete intestinal stores of noradrenaline and 5-hydroxytryptamine (5-HT). Intraperitoneal injection of 6-OHDA (3 doses at 50 mg kg-1) caused a selective reduction in the level of noradrenaline in the jejunum to 7.3% of control. Intraperitoneal injection of PCPA (200 mg kg-1) selectively reduced the jejunal level of 5-HT to 30.5% of control. Groups of rats that had been treated as described above were anaesthetized and then injected intravenously with saline or with blocking doses of either atropine (0.25 mg kg-1), hexamethonium (20 mg kg-1), ketanserin (30 micrograms kg-1), methysergide (30 micrograms kg-1), phentolamine (2 mg kg-1) or propranolol (1 mg kg-1). Following perfusion of the lumen of the jejunum, the rate of glucose absorption was measured to assess the integrity of the mucosa. Glucose absorption was unaltered in animals pretreated with hexamethonium and propranolol but there was a small enhancement in animals pretreated with atropine, PCPA, methysergide, 6-OHDA and phentolamine. The rate of net water absorption from the lumen of the jejunum and the rate of fluid secretion into the lumen following intra-arterial infusion of vasoactive intestinal peptide (VIP, 0.8 microgram min-1) were unaltered by any of the drug treatments. Intravenous injection of morphine (10 mg kg-1) did not alter the levels of noradrenaline or 5-HT in the whole jejunum. However, this dose of morphine did cause a 63.5% decrease in the VIP-induced change in water transport. This antisecretory effect of morphine was unaltered in animals pretreated with atropine, hexamethonium and propranolol. In contrast, methysergide, ketanserin and 6-OHDA abolished the antisecretory effect of morphine. PCPA and phentolamine produced a partial inhibition of morphine's antisecretory effect. It is concluded that morphine produces its antisecretory effect in the jejunum by activation of noradrenergic and tryptaminergic systems.

Tetrodotoxin inhibits directly acting stimulants of intestinal fluid secretion.

Intravenous injection of tetrodotoxin (20 micrograms kg-1) to anaesthetized rats blocks PGE1- and inhibits VIP-induced fluid secretion from the mucosa of the jejunum without affecting the physiological rates of net water and glucose absorption. It is suggested that the toxin might release an endogenous inhibitor of secretion or that it might possess direct antisecretory activity on the epithelial cells of the jejunum. It is further suggested that results where tetrodotoxin has been used to investigate secretagogue action should be treated with caution.

Intestinal transit of a glucose bolus and incretin kinetics: a mathematical model with application to the oral glucose tolerance test

The rate of appearance (R(a)) of exogenous glucose in plasma after glucose ingestion is presently measured by tracer techniques that cannot be used in standard clinical testing such as the oral glucose tolerance test (OGTT). We propose a mathematical model that represents in a simple way the gastric emptying, the transport of glucose along the intestinal tract, and its absorption from gut lumen into portal blood. The model gives the R(a) time course in terms of parameters with a physiological counterpart and provides an expression for the release of incretin hormones as related to glucose transit into gut lumen. Glucose absorption was represented by assuming two components related to a proximal and a distal transporter. Model performance was evaluated by numerical simulations. The model was then validated by fitting OGTT glucose and GLP-1 data in healthy controls and type 2 diabetic patients, and useful information was obtained for the rate of gastric emptying, the rate of glucose absorption, the R(a) profile, the insulin sensitivity, and the glucose effectiveness. Model-derived estimates of insulin sensitivity were well correlated (r = 0.929 in controls and 0.886 in diabetic patients) to data obtained from the euglycemic hyperinsulinemic clamp. Although the proposed OGTT analysis requires the measurement of an additional hormone concentration (GLP-1), it appears to be a reasonable choice since it avoids complex and expensive techniques, such as isotopes for glucose R(a) measurement and direct assessment of gastric emptying and intestinal transit, and gives additional correlated information, thus largely compensating for the extra expense.

In vitro hypoglycemic effects of Gymnema sylvestre, Tinospora cordifolia, Eugenia jambolana and Aegle marmelos

Medicinal plants can exert their hypoglycemic effect by several mechanisms such as modulation of glucose diffusion, inhibition of carbohydrate hydrolyzing enzymes, manipulation of glucose transporters etc. Therefore, the present study was planned to evaluate the in vitro hypoglycemic effects of some common medicines used in the management of type 2 diabetes in India. The present study evaluated the effect Gymnema sylvestre (GS), Tinospora cordifolia (TC), Eugenia jambolana (JB) and Aegle Marmelos (AM) on the movement of glucose in the intestinal lumen using suitable in vitro techniques. All the samples effectively adsorbed glucose and retarded its diffusion across the dialysis membrane. The glucose adsorption capacities of all the samples were higher than that of wheat bran (WB) and acarbose (ACB). WB exhibited significantly higher (P ≤ 0.01) glucose diffusion rate at all time compared to other samples. The maximal glucose diffusion retardation index (GDRI) was exhibited by AM followed by JB and TC. All of these mechanisms might create a concerted function in lowering the rate of glucose absorption and as a result decrease postprandial blood glucose concn. It is concluded that the mechanism of hypoglycemic action varies greatly from one medicinal plant to other and hence, there is a need for in-depth research to establish the mode of action of each medicinal plant for their effective utilization as therapeutic agents.

Mechanism and Effects of Glucose Absorption during an Oral Glucose Tolerance Test Among Females and Males

Several epidemiological studies revealed sex-specific differences during oral glucose tolerance tests (OGTTs), such as higher prevalence of glucose intolerance (i.e. increased glucose at the end of the OGTT) in females, which was not yet explained. Thus, we aimed to analyze sex-related distinctions on OGTT glucose metabolism, including gut absorption, in healthy humans. Females (n = 48) and males (n = 26) with comparable age (females, 45 ± 1 yr; males, 44 ± 2 yr) and body mass index (both, 25 ± 1 kg/m(2)) but different height (females, 166 ± 1 cm; males, 180 ± 2 cm; P < 0.000001), all normally glucose tolerant, as tested by frequently sampled, 3-h (75-g) OGTTs, underwent hyperinsulinemic [40 mU/(min · m(2))] isoglycemic clamp tests with simultaneous measurement of endogenous glucose (d-[6,6-(2)H(2)]glucose) production (EGP). EGP and glucose disappearance during OGTT were calculated from logarithmic relationships with clamp test insulin concentrations. After reliable model validation by double-tracer technique (r = 0.732; P < 0.007), we calculated and modeled gut glucose absorption (ABS). Females showed lower (P < 0.05) fasting EGP [1.4 ± 0.1 mg/(kg · min)] than males [1.7 ± 0.1 mg/(kg · min)] but comparable whole-body insulin sensitivity in clamp tests [females, 8.1 ± 0.4 mg/(kg · min); males, 8.3 ± 0.6 mg/(kg · min)]. Plasma glucose OGTT concentrations were higher (P < 0.04) from 30-40 min in males but from 120-180 min in females. Glucose absorption rates were 21-46% increased in the initial 40 min in males but in females by 27-40% in the third hour (P < 0.05). Gut glucose half-life was markedly higher in females (79 ± 2 min) than in males (65 ± 3 min, P < 0.0001) and negatively related to body height (r = -0.481; P < 0.0001). This study in healthy, glucose-tolerant humans shows for the first time different ABS rates during OGTT in women and men and a negative relationship between body height and gut glucose half-life. Prolonged ABS in females might therefore contribute to higher plasma glucose concentrations at the end of OGTT.

In vitro hypoglycemic effects of selected dietary fiber sources.

The physiological functions of dietary fiber and its role in health promotion and risk reduction of some chronic diseases has been well documented. In the present investigation, the effect of three dietary fiber sources, oats (OA), barley (BA) and psyllium husk (PH) on glucose adsorption, diffusion and starch hydrolysis were studied using in vitro techniques by simulating gastrointestinal conditions and compared with the commercial dietary fiber sources wheat bran (WB), acarbose (ACB) and guar gum (GG). The glucose binding capacity of all the samples was higher than WB and ACB at 5mM concentration. In all the samples, the diffusion of glucose was directly proportional to the time and diffusion rate was significantly lower (p ≤ 0.01) in the system containing various samples compared to control. Glucose dialysis retardation index (GDRI) was 100 for OA, BA and PH at 60min, at 120min the maximal GDRI was in PH. Whereas; WB and ACB exhibited maximal GDRI at 180 and 240min. All of these mechanisms might create a concerted function in lowering the rate of glucose absorption and as a result, decrease the postprandial hyperglycemia.

Intestinal Fluid and Glucose Transport in Wistar Rats following Chronic Consumption of Fresh or Oxidised Palm Oil Diet

Chronic ingestion of thermoxidized palm oil causes functional derangement of various tissues. This study was therefore carried out to determine the effect of chronic ingestion of thermoxidized and fresh palm oil diets on intestinal fluid and glucose absorption in rats using the everted sac technique. Thirty Wistar rats were divided into three groups of 10 rats per group. The first group was the control and was fed on normal rat chow while the second (FPO) and third groups (TPO) were fed diet containing either fresh or thermoxidized palm oil (15% wt/wt) for 14 weeks. Villus height and crypt depth were measured. The gut fluid uptake and gut glucose uptake were significantly (P < .001) lower in the TPO group than those in the FPO and control groups, respectively. The villus height in the TPO was significantly (P < .01) lower than that in FPO and control. The villus depth in TPO was significantly (P < .05) higher than that in FPO and control groups, respectively. These results suggest that ingestion of thermoxidized palm oil and not fresh palm oil may lead to distortion in villus morphology with a concomitant malabsorption of fluid and glucose in rats due to its harmful free radicals.

Dietary purified oat β-glucan reduces peak glucose absorption and portal insulin release in portal-vein catheterized grower pigs

Kinetics of glucose absorption may affect insulin secretion into the portal vein. The role of wet-fractionated oat β-glucan on these variables is unknown; thus, three 35-kg pigs were fitted with catheters in the portal vein and carotid artery and a portal vein flow probe. Pigs were fed 3 diets containing 0, 3, or 6% purified β-glucan for 7-d in a repeated 3 × 3 Latin square. On d 7, blood was sampled for 12 h postprandially. Net glucose absorption rate was calculated from plasma portal-arterial differences × flow. Blood flow increased ( P < 0.001) after feeding, without a diet effect. Postprandially, β-glucan reduced ( P < 0.05) net glucose absorption during the first h by 22 to 51%. At 30 and 90 min postprandially, β-glucan decreased ( P < 0.05) portal release of C-peptide but did not affect portal insulin at 30 min, indicating that β-glucan reduces peak insulin release while maintaining prehepatic insulin homeostasis. In conclusion, oat β-glucan as a soluble, viscous fibre decreases rate of glucose absorption and peak insulin release in portal vein.

Effects of Physiological Hyperglycemia on Duodenal Motility and Flow Events, Glucose Absorption, and Incretin Secretion in Healthy Humans

Acute hyperglycemia slows gastric emptying, but its effects on small intestinal motor activity and glucose absorption are unknown. In type 2 diabetes, the postprandial secretion of glucose-dependent insulinotropic polypeptide (GIP) is preserved, but that of glucagon-like peptide-1 (GLP-1) is possibly reduced; whether the latter is secondary to hyperglycemia or diabetes per se is unknown. The aim was to investigate the effects of acute hyperglycemia on duodenal motility and flow events, glucose absorption, and incretin hormone secretion. Nine healthy volunteers were studied on two occasions. A combined manometry/impedance catheter was positioned in the duodenum. Blood glucose was clamped at either 9 mmol/liter (hyperglycemia) or 5 mmol/liter (euglycemia) throughout the study. Manometry and impedance recordings continued between T=-10 min and T=180 min. Between T=0 and 60 min, an intraduodenal glucose infusion was given (approximately 3 kcal/min), together with 14C-labeled 3-O-methylglucose (3-OMG) to evaluate glucose absorption. Hyperglycemia had no effect on duodenal pressure waves or flow events during the 60 min of intraduodenal glucose infusion, when compared to euglycemia. During hyperglycemia, there was an increase in plasma GIP (P<0.05) and 14C-3-OMG (P<0.05) but no effect on GLP-1 concentrations in response to the intraduodenal infusion, compared to euglycemia. Acute hyperglycemia in the physiological range has no effect on duodenal pressure waves and flow events but is associated with increased GIP secretion and rate of glucose absorption in response to intraduodenal glucose.

Effects of exogenous glucagon-like peptide-1 on gastric emptying and glucose absorption in the critically ill: Relationship to glycemia*

To determine the acute effects of exogenous glucagon-like peptide-1 on gastric emptying, glucose absorption, glycemia, plasma insulin, and glucagon in critically ill patients. Randomized, double-blind, crossover study. Intensive care unit. Twenty-five mechanically ventilated patients, without known diabetes, studied on consecutive days. Intravenous glucagon-like peptide-1 (1.2 pmol/kg/min) or placebo was infused between -30 and 330 mins. At 0 min, 100 mL liquid nutrient (1 kcal/mL) including 100 microg of 13C-octanoic acid and 3 grams of 3-O-methyl-glucose was administered. Blood glucose, serum 3-O-methyl-glucose (as an index of glucose absorption), insulin and glucagon concentrations, as well as exhaled 13CO2 were measured. The gastric emptying coefficient was calculated to quantify gastric emptying. Data are presented as mean (sd). There was a nonsignificant trend for glucagon-like peptide-1 to slow gastric emptying (gastric emptying coefficient) (glucagon-like peptide-1, 2.45 [0.93] vs. placebo, 2.75 [0.83]; p = .09). In 11 of the 25 patients, gastric emptying was delayed during placebo infusion and glucagon-like peptide-1 had no detectable effect on gastric emptying in this group (1.92 [0.82] vs. 1.90 [0.68]; p = .96). In contrast, in patients who had normal gastric emptying during placebo, glucagon-like peptide-1 slowed gastric emptying substantially (2.86 [0.58] vs. 3.41 [0.37]; p = .006). Glucagon-like peptide-1 markedly reduced the rate of glucose absorption (3-O-methyl-glucose area under the curve(0-330), 37 [35] vs. 76 [51] mmol/L/min; p < .001), decreased preprandial glucagon (at 0 min change in glucagon, -15 [15] vs. -3 [14] pmol/L; p < .001), increased the insulin/glucose ratio throughout the infusion (area under the curve(-30-330), 1374 [814] vs. 1172 [649] mU/mmol/min; p = .041), and attenuated the glycemic response to the meal (glucose area under the curve(0-330), 2071 [353] vs. 2419 [594] mmol/L/min; p = .001). Exogenous glucagon-like peptide-1 lowers postprandial glycemia in the critically ill. This may occur, at least in part, by slowing gastric emptying when the latter is normal but not when it is delayed.

Effect of the artificial sweetener, sucralose, on small intestinal glucose absorption in healthy human subjects

It has been reported that the artificial sweetener, sucralose, stimulates glucose absorption in rodents by enhancing apical availability of the transporter GLUT2. We evaluated whether exposure of the proximal small intestine to sucralose affects glucose absorption and/or the glycaemic response to an intraduodenal (ID) glucose infusion in healthy human subjects. Ten healthy subjects were studied on two separate occasions in a single-blind, randomised order. Each subject received an ID infusion of sucralose (4 mM in 0.9% saline) or control (0.9% saline) at 4 ml/min for 150 min (T = - 30 to 120 min). After 30 min (T = 0), glucose (25 %) and its non-metabolised analogue, 3-O-methylglucose (3-OMG; 2.5 %), were co-infused intraduodenally (T = 0-120 min; 4.2 kJ/min (1 kcal/min)). Blood was sampled at frequent intervals. Blood glucose, plasma glucagon-like peptide-1 (GLP-1) and serum 3-OMG concentrations increased during ID glucose/3-OMG infusion (P < 0.005 for each). However, there were no differences in blood glucose, plasma GLP-1 or serum 3-OMG concentrations between sucralose and control infusions. In conclusion, sucralose does not appear to modify the rate of glucose absorption or the glycaemic or incretin response to ID glucose infusion when given acutely in healthy human subjects.