Oral Sucrose Load Research Articles

An in-vivo study on postprandial hyperglycemia to assess antidiabetic activity of alcoholic extract of Cinnamomum verum bark

Background and objective Cinnamomum verum bark is locally known as ‘Daruchini’ and is traditionally reputed as an Ayurvedic medicine, which is used in the treatment of flatulence, toothache, heart diseases, fever, cough, cold, headache, and many others. In this study, we intended to explore the effectiveness of its activity on hyperglycemia.Materials and methods To evaluate its antihyperglycemic activity, we used various experimental designs, including the effect of plant extract on gastrointestinal (GI) motility in the Swiss albino mice model and intestinal disaccharidase enzyme activity and carbohydrate digestion and absorption in the gut of the Long Evans rats.Results and discussion The plant extract significantly (P<0.001) increased the GI motility rate by ∼16% than the control (distilled water, 10 ml/kg body weight) and indicated that it interfered with the rate of glucose absorption in the gut. Furthermore, treatment with C. verum caused a significant (P<0.05) dose-dependent reduction of intestinal disaccharidase enzyme activity from 1.63 to 1.21 µmol/mg protein/h in fasting Long Evans rats. Besides, the extract produced a similar effect in the acute oral sucrose (2.5 g/kg body weight) load assay, in which a substantial amount of unabsorbed sucrose was found in six different parts of the GI tract after sucrose administration. This indicates that C. verum can liberate GI content and reduce or delay glucose absorption.Conclusion All the findings of the present study point to the conclusion that C. verum has the potential to exert postprandial antihyperglycemic activity within type 2 diabetic animal models through reducing or delaying carbohydrate digestion and absorption in the gut.

Reduced Body Fat and Epididymal Adipose Apelin Expression Associated With Raspberry Ketone [4-(4-Hydroxyphenyl)-2-Butanone] Weight Gain Prevention in High-Fat-Diet Fed Mice.

Raspberry ketone [4-(4-hydroxyphenyl)-2-butanone] is a natural aromatic compound found in raspberries and other fruits. Raspberry ketone (RK) is synthetically produced for use as a commercial flavoring agent. In the United States and other markets, it is sold as a dietary supplement for weight control. The potential of RK to reduce or prevent excessive weight gain is unclear and could be a convergence of several different actions. This study sought to determine whether acute RK can immediately delay carbohydrate hyperglycemia and reduce gastrointestinal emptying. In addition, we explored the metabolic signature of chronic RK to prevent or remedy the metabolic effects of diet-induced weight gain. In high-fat diet (HFD; 45% fat)-fed male mice, acute oral gavage of RK (200 mg/kg) reduced hyperglycemia from oral sucrose load (4 g/kg) at 15 min. In HFD-fed female mice, acute oral RK resulted in an increase in blood glucose at 30 min. Chronic daily oral gavage of RK (200 mg/kg) commencing with HFD access (HFD_RK) for 11 weeks resulted in less body weight gain and reduced fat mass compared with vehicle treated (HFD_Veh) and chronic RK starting 4 weeks after HFD access (HFD_RKw4) groups. Compared with a control group fed a low-fat diet (LFD; 10% fat) and dosed with vehicle (LFD_Veh), glucose AUC of an oral glucose tolerance test was increased with HFD_Veh, but not in HFD_RK or HFD_RKw4. Apelin (Apln) gene expression in epididymal white adipose tissue was increased in HFD_Veh, but reduced to LFD_Veh levels in the HFD_RK group. Peroxisome proliferator activated receptor alpha (Ppara) gene expression was increased in the hepatic tissue of HFD_RK and HFD_RKw4 groups. Overall, our findings suggest that long term daily use of RK prevents diet-induced weight gain, normalizes high-fat diet-induced adipose Apln, and increases hepatic Ppara expression.

Effects of D-allulose on glucose tolerance and insulin response to a standard oral sucrose load: results of a prospective, randomized, crossover study

IntroductionCurrent dietary guidelines recommend limiting sugar intake for the prevention of diabetes mellitus (DM). Reduction in sugar intake may require sugar substitutes. Among these, D-allulose is a non-calorie rare monosaccharide...

Effects of Spirulina platensis on insulin secretion, dipeptidyl peptidase IV activity and both carbohydrate digestion and absorption indicate potential as an adjunctive therapy for diabetes.

Spirulina platensis has been found to be useful in the treatment of type 2 diabetes. The present study aims to elucidate the effects of ethanol extract and butanol fraction of S. platensis on insulin release and glucose homoeostasis in type 2 diabetic rats, together with their mechanism of actions. In vitro and in vivo methods were used including cellular studies to determine potential role of ion channels and cAMP in the insulinotropic actions of the extracts. The ethanol extract and butanol fraction stimulated insulin release from mouse islets and pancreatic β-cells in a concentration-dependent manner. The butanol fraction also similarly stimulated insulin release from perfused rat pancreas. The insulin-releasing action was augmented by glucose, isobutylmethylxanthine, tolbutamide and a depolarising concentration of KCl. The insulin secretory effect was attenuated with diazoxide and verapamil and by omission of extracellular Ca2+. Butanol fraction was found to significantly inhibit dipeptidyl peptidase IV enzyme activity. Moreover, butanol fraction improved glucose tolerance following oral glucose administration (2·5 g/kg body weight (b.w.)). The butanol fraction was tested on 24 h starved rats given an oral sucrose load (2·5 g/kg b.w.) to examine possible effects on carbohydrate digestion and absorption. S. platensis substantially decreased postprandial hyperglycaemia after oral sucrose load and increased unabsorbed sucrose content throughout the gut. During in situ intestinal perfusion with glucose, the butanol fraction reduced glucose absorption and promoted gut motility. Finally, chronic oral administration of butanol fraction for 28 d significantly decreased blood glucose, increased plasma insulin, pancreatic insulin stores, liver glycogen and improved lipid profile. The characterisation of active compounds from butanol fraction revealed the presence of p-coumaric acid, β-carotene, catechin and other antioxidant polyphenols. In conclusion, S. platensis could be an adjunctive therapy for the management of type 2 diabetes.

Nigella sativa stimulates insulin secretion from isolated rat islets and inhibits the digestion and absorption of (CH2O)n in the gut.

Nigella sativa seeds are traditionally reputed as possessing anti-diabetic properties. As a result, we aim to explore the mechanism of its anti-hyperglycemic activity. The present study uses various experimental designs including gastrointestinal (GI) motility, intestinal disaccharidase activity and inhibition of carbohydrate digestion and absorption in the gut. The animals used as type 2 diabetic models were induced with streptozotocin to make them as such. Oral glucose tolerance test was performed to confirm that the animals were indeed diabetic. The extract reduced postprandial glucose, suggesting it interfered with glucose absorption in the gut. It also improved glucose (2.5g/kg, b/w) tolerance in rats. Furthermore, treatment with N. sativa produced a significant improvement in GI motility, while reduced disaccharidase enzyme activity in fasted rats. The extract produced a similar effect within an acute oral sucrose (2.5g/kg, b/w) load assay. Following sucrose administration, a substantial amount of unabsorbed sucrose was found in six different parts of the GI tract. This indicates that N. sativa has the potentiality to liberate GI content and reduce or delay glucose absorption. A potential hypoglycemic activity of the extract found in insulin release assay, where the extract significantly improved insulin secretion from isolated rat islets. These concluded present findings give rise to the implication that N. sativa seeds are generating postprandial anti-hyperglycemic activity within type 2 diabetic animal models via reducing or delaying carbohydrate digestion and absorption in the gut as well as improving insulin secretion in response to the plasma glucose.

Salacia Extract Improves Post‐Prandial Glucose and Insulin Response: A Randomized Double Blind, Placebo‐Controlled, Cross‐over Study in Healthy Volunteers

Extracts of Salacia species from roots, stems, and leaves have been used for the treatment of diabetes and other associated risk factors in Asia. Studies indicate that Salacia extracts modulate multiple targets that influence carbohydrate and lipid metabolism. This study is to examine the effect of differing doses of a novel form of Salacia extract (SE) on glucose and insulin response to an oral sucrose load in healthy individuals (South Asian Population). Thirty five (N=35, 18 to 55 years of age; BMI ≥24.50 to 29.50 Kg/m2) adult healthy individuals (male and female)were randomly assigned to ingest SE at dosages of 200 mg SE, 300 mg SE and 500 mg (OmniLeanTM) or placebo (PLA) in a single center, double‐blind, randomized, placebo controlled parallel design. Plasma glucose and plasma insulin responses were measured after 0, 30, 60, 90, 120, 180 min of ingesting oral sucrose standard solution and Area under curve for glucose (AUCglucose) and insulin response (AUCinsulin) was calculated. ANOVA and paired t‐tests were used to examine differences between treatments and over baseline. Compared with PLA, SE 500 mg significantly lowered blood sugars and insulin from 60 minutes, 90 minutes and 120 minutes, SE 300 mg significantly lower at 90 min and 180 min and 200 mg at 90 min and 120 minutes. AUCglucose was not significant. Plasma insulin levels and AUCinsulin were significantly lowered after ingestion of SE. No significant adverse events were observed at any dose. Thus, in reducing the early rise in blood glucose and insulin after sucrose ingestion, Salacia extract (SE) prevents the occurrence of reactive hypoglycemia; the present study confirm that this nutritional ingredient may be of value in reducing post prandial insulin and glucose.Support or Funding InformationOmniActive Health Technologies Ltd., Mumbai, India

Comparison of the effects of slowly and rapidly absorbed carbohydrates on postprandial glucose metabolism in type 2 diabetes mellitus patients: a randomized trial

Isomaltulose attenuates postprandial glucose and insulin concentrations compared with sucrose in patients with type 2 diabetes mellitus (T2DM). However, the mechanism by which isomaltulose limits postprandial hyperglycemia has not been clarified. The objective was therefore to assess the effects of bolus administration of isomaltulose on glucose metabolism compared with sucrose in T2DM. In a randomized, double-blind, crossover design, 11 participants with T2DM initially underwent a 3-h euglycemic-hyperinsulinemic (0.8 mU · kg(-1) · min(-1)) clamp that was subsequently combined with 1 g/kg body wt of an oral (13)C-enriched isomaltulose or sucrose load. Hormonal responses and glucose kinetics were analyzed during a 4-h postprandial period. Compared with sucrose, absorption of isomaltulose was prolonged by ∼50 min (P = 0.004). Mean plasma concentrations of insulin, C-peptide, glucagon, and glucose-dependent insulinotropic peptide were ∼10-23% lower (P < 0.05). In contrast, glucagon-like peptide 1 (GLP-1) was ∼64% higher (P < 0.001) after isomaltulose ingestion, which results in an increased insulin-to-glucagon ratio (P < 0.001) compared with sucrose. The cumulative amount of systemic glucose appearance was ∼35% lower after isomaltulose than after sucrose (P = 0.003) because of the reduction in orally derived and endogenously produced glucose and a higher first-pass splanchnic glucose uptake (SGU). Insulin action was enhanced after isomaltulose compared with sucrose (P = 0.013). Ingestion of slowly absorbed isomaltulose attenuates postprandial hyperglycemia by reducing oral glucose appearance, inhibiting endogenous glucose production (EGP), and increasing SGU compared with ingestion of rapidly absorbed sucrose in patients with T2DM. In addition, GLP-1 secretion contributes to a beneficial shift in the insulin-to-glucagon ratio, suppression of EGP, and enhancement of SGU after isomaltulose consumption. This trial was registered at clinicaltrials.gov as NCT01070238.

Inhibitory effect of leaf extract of &lt;i&gt;Newbouldia laevis&lt;/i&gt; on the metabolic activities of alpha-glucosidase and alpha-amylase

In this study, the effect of ethanol extract of the leaves of Newbouldia laevis on the activity of α-amylase and α-glucosidase was investigated. Inhibitory effect of N. laevis extract on α-glucosidase was tested in vitro using baker's yeast α-glucosidase and rat intestinal α-glucosidase while α-amylase inhibitory effect was assayed using rat pancreatic α-amylase. α-Glucosidase inhibitory effect of the extract was also tested in vivo in diabetic and non-diabetic rats. N. laevis extract exhibited good α-glucosidase inhibitory activity in vitro with IC50 values of 2.2 µg/mL and 43.5 µg/mL for baker's yeast and rat intestinal α-glucosidase respectively. The extract also inhibited rat pancreatic α-amylase activity with IC50 value of 58.7 µg/mL. In both diabetic and non-diabetic rats, N. laevis extract caused a significant reduction in postprandial blood glucose level after oral sucrose load. The results of this study indicate that N. laevis extract exerts its glucose-lowering effect through inhibition of α-glucosidase and α-amylase.

Mexican antidiabetic herbs: A valuable source of alpha-glucosidase inhibitors

In Mexico, there are more than 300 hundred plants species employed for the treatment of type-2 diabetes mellitus (T2 DM), the commonest endocrine disorder affecting more than 100 million people worldwide. A few Asteraceae of the genus Brickellia, Ligusticum porteri (Apiaceae), and some Rubiaceae [Hintonia standleyana, Hintonia latiflora and Exostema caribaeum] are among the most highly prized species. The chemistry of the latter group of plants has been investigated by our research group since 1987 and the results published in the Journal of Natural Products. More recently, we have shown that the extracts and some of the hypoglycemic active principles of H. latiflora, L. porteri, and Brickellia cavanillesii inhibited the activity of the α-glucosidases. These findings revealed some of the molecular mechanisms underlying the antidiabetic action of these plants as well as a few novel templates for the development α-glucosidases of new drugs useful for controlling fasting and postprandial blood glucose levels. Thus, some phthalides of L. porteri, in particular, 3-Z-butylidenephthalide (1, 56.2mg/kg), decreased blood glucose levels in STZ-diabetic mice after an oral sucrose load, suggesting that its antihyperglycemic effect is due to inhibition of α-glucosidases at the intestinal level. Furthermore, 1 inhibited yeast α-glucosidase activity (IC50 2.35 mM) in a non-competitive fashion with a Ki of 4.86 mM. Docking analysis predicted that 1 binds to the enzyme in a pocket close to the catalytic site but different to that for acarbose. Bioassay-guided fractionation of the active extract of B. cavanillesii using the same α-glucosidase inhibitory assay yielded several active compounds including 6-hydroxyacetyl-5-hydroxy-2,2-dimethyl-2H-chromene (2, IC50 0.42 mM vs. 1.7 mM for acarbose), a new chemical entity. Kinetic analysis revealed that 2 is a non-competititive inhibitor with a Ki of 0.13 mM. From the Rubiaceae, the most active inhibitor was 5,7,3′,4′-tetrahydroxy-4-phenylcoumarin (3, IC50 3µM).

Antihyperglycaemic activity ofAsparagus racemosusroots is partly mediated by inhibition of carbohydrate digestion and absorption, and enhancement of cellular insulin action

Asparagus racemosus roots have been shown to enhance insulin secretion in perfused pancreas and isolated islets. The present study investigated the effects of ethanol extracts of A. racemosus roots on glucose homeostasis in diabetic rats, together with the effects on insulin action in 3T3 adipocytes. When administered orally together with glucose, A. racemosus extract improved glucose tolerance in normal as well as in two types of diabetic rats. To investigate the possible effects on carbohydrate absorption, the sucrose content of the gastrointestinal tract was examined in 12 h fasted rats after an oral sucrose load (2.5 g/kg body weight). The extract significantly suppressed postprandial hyperglycaemia after sucrose ingestion and reversibly increased unabsorbed sucrose content throughout the gut. The extract also significantly inhibited the absorption of glucose during in situ gut perfusion with glucose. Furthermore, the extract enhanced glucose transport and insulin action in 3T3-L1 adipocytes. Daily administration of A. racemosus to type 2 diabetic rats for 28 d decreased serum glucose, increased pancreatic insulin, plasma insulin, liver glycogen and total oxidant status. These findings indicate that antihyperglycaemic activity of A. racemosus is partly mediated by inhibition of carbohydrate digestion and absorption, together with enhancement of insulin secretion and action in the peripheral tissue. Asparagus racemosus may be useful as a source of novel antidiabetic compounds or a dietary adjunct for the management of diabetes.

(Z)-3-Butylidenephthalide from Ligusticum porteri, an α-Glucosidase Inhibitor

An extract from the roots of Ligusticum porteri, orally administered to groups of normal and diabetic mice, showed significant hypoglycemic and antihyperglycemic effects. Experimental type-II DM was achieved by treating mice with streptozotocin 15 min after an injection of β-nicotinamide adenine dinucleotide. (Z)-6,6',7,3'α-diligustilide (1), (Z)-ligustilide (2), 3-(Z)-butylidenephthalide (3), myristicin (4), and ferulic acid (5) were isolated from the active extract. When tested In Vivo, compounds 1-3 showed antihyperglycemic activity, with 3 being the most active. Compound 3 (56.2 mg/kg) decreased blood glucose levels in NAD-STZ-diabetic mice after an oral sucrose load, suggesting that its antihyperglycemic effect is due to inhibition of α-glucosidase at the intestinal level. Furthermore, 3 inhibited the activity of yeast-α-glucosidase (IC(50) 2.35 mM) in a noncompetitive fashion with a K(i) of 4.86 mM. Docking analysis predicted that 3 binds to the enzyme in a pocket close to the catalytic site, but different from that for acarbose, with a K(i) of 11.48 mM. Compounds 1 and 2 did not affect α-glucosidase In Vivo, but altered glucose absorption by a mechanism yet to be determined. The stimulatory effect of 5 on insulin secretion, present in high amounts in the extract, has been demonstrated in previous investigations. The present study provides scientific support of the use of L. porteri in Mexican folk medicine for the treatment of diabetes.

Atrophic Gastritis Is Associated with Increased Sucrose Permeability Related to Chronic Inflammation

Background: Different theories have been presented to explain how atrophic gastritis may lead to gastric cancer development. One contributing factor could be impaired function of the gastric mucosal barrier. The aim of this study was to investigate if there are changes in gastric mucosal permeability to sucrose in atrophic gastritis.Methods: The study comprised 22 patients with atrophic gastritis and 21 normal controls. Gastritis was classified according to the Sydney system from endoscopic biopsies of the gastric corpus and antrum. All subjects were exposed to oral sucrose load (100 g), and the fraction of sucrose excreted in urine was measured by gas chromatography-mass spectrometry. Results: The fraction of sucrose excreted in urine after oral load was significantly increased in atrophic gastritis compared with controls (median 0.08 vs. 0.04%; p = 0.003). Sucrose excretion was positively related to the degree of chronic inflammation (median fraction excreted: mild inflammation 0.06%, moderate inflammation 0.08%, severe inflammation 0.18%; p = 0.04) rather than to the degree of atrophy in the gastric mucosa. Occurrence of intestinal metaplasia was also associated with significantly higher sucrose excretion. However, in multivariate analysis, including intestinal metaplasia, only the degree of inflammation was positively related to sucrose excretion. Conclusion: Atrophic gastritis is associated with increased sucrose permeability, suggesting paracellular leakage of the gastric mucosa. This leakage seems to be related to the degree of inflammation rather than the degree of atrophy. The findings may have implications for the diseases and complications associated with atrophic gastritis.

Delayed gastric emptying occurs following acarbose administration and is a further mechanism for its anti-hyperglycaemic effect

The therapeutic effect of acarbose is generally attributed to inhibition of amylase and brush border glucosidases and consequent impaired digestion and absorption of carbohydrates. We have investigated the possibility that acarbose may also influence the rate of gastric emptying by comparing plasma glucose and gastrointestinal hormone responses to an oral sucrose load with and without acarbose in 11 healthy subjects. Gastric emptying was assessed indirectly by measuring circulating paracetamol concentrations following administration of paracetamol along with the sucrose load. Peak plasma glucose, insulin, and glucose-dependent insulinotropic polypeptide (GIP) responses were reduced when sucrose was given with acarbose. There was a significant reduction in post-sucrose paracetamol levels with acarbose suggestive of a significant delay in gastric emptying. The failure of acarbose to induce change in circulating paracetamol concentrations until after 60 min is indicative of a delay in gastric emptying rather than an osmotic malabsorption. The exaggerated and sustained release of glucagon-like peptide-1 (7-36)amide (GLP-1) seen when sucrose was given with acarbose may play a part in the inhibition of gastric emptying. This study indicates that a significant delay in gastric emptying may be an added mechanism contributing to the therapeutic effect of acarbose.

Effect of guar gum on glucose metabolism in cecectomized rats

We hypothesized that short chain fatty acid (SCFA) fermented in the cecum of rats fed a guar gum diet is responsible for the hypoglycemic effect. Thus, to evaluate the role of SCFA in glucose metabolim, rats with or without cecum were fed a guar gum-containing diet for 4 weeks, and parameters including blood glucose and SCFA in portal blood were determined. The level of insulin-responsive glucose transporter (GLUT4) was also measured to evaluate the effect of SCFA on glucose metabolism at the cellular level. Blood glucose levels in both cecectomized and normal rats that were fed a cellulose-based diet significantly, decreased after their diet was changed to one containing guar gum at the level of 5% ( w w ). However, no subsequent difference was found between the two groups. When an oral sucrose load was performed after 3 weeks, untreated and cecectomized rats responded similarly. After feeding a guar gum diet for 4 weeks, the rats were killed, and blood from the portal vein and aorta was taken to measure SCFA and plasma biochemical parameters. Cecectomy did not have any influence on glucose, lipids, and insulin levels in the blood. Portal plasma acetic and propionic acids in ceoectomized rats dramatically decreased by one-half and one-tenth those of the control rats, respectively. There was no difference in the amount and translocation rate of GLUT4 isolated from adipose tissues between the two groups when the animals were killed after 4 weeks. From these results, it is suggested that, at least in normal rats, SCFA fermented in the digestive tract, if any, is not a primary cause of glucose-lowering action by guar gum. Physicochemical characteristics of guar gum in the upper intestine (e.g., gel-forming capacity) may be important in determining blood glucose level.

Resting energy expenditure and food-induced thermogenesis in obese children.

Nineteen overweight girls 14.54 +/- 0.38 years of age were studied. Results were compared with those obtained in eight age-matched (14.07 +/- 0.51 years) and sex-matched normal weight controls. Energy expenditure (EE) was determined using open-circuit indirect calorimetry at rest, both after a 12-h fast and after an oral sucrose load of 3 g/kg ideal body weight. Food-induced thermogenesis (FIT) was evaluated by computing the area under the curve of the EE response above resting energy expenditure (REE) during the first 3 h after the sucrose load, REE (kcal/day) was higher in the overweight patients (1,818 +/- 46 vs. 1,527 +/- 67; p = 0.002); REE standardized by fat-free mass (FFM) (kcal/kg FFM/day) was lower in obese children than in controls (35.2 +/- 1.0 vs. 44.9 +/- 1.9; p = 0.0001). A linear correlation between REE and FFM was evidenced in both controls and overweight subjects (r = 0.78 and 0.68, respectively; p = 0.05 and p < 0.001, respectively). Actual REE in the obese children was significantly lower than the value predicted by applying the regression equation of REE on FFM in controls to the actual FFM in obese children (paired t test; p = 0.003). FIT was identical in overweight and normal weight subjects, regardless of whether it was expressed in absolute value, as the percentage calorie intake, or standardized by FFM.(ABSTRACT TRUNCATED AT 250 WORDS)

Resting Energy Expenditure and Food‐Induced Thermogenesis in Obese Children

SummaryNineteen overweight girls 14.54 ± 0.38 years of age were studied. Results were compared with those obtained in eight age‐matched (14.07 ± 0.51 years) and sex‐matched normal weight controls. Energy expenditure (EE) was determined using open‐circuit indirect calorimetry at rest, both after a 12‐h fast and after an oral sucrose load of 3 g/kg ideal body weight. Food‐induced thermogenesis (FIT) was evaluated by computing the area under the curve of the EE response above resting energy expenditure (REE) during the first 3 h after the sucrose load, REE (kcal/day) was higher in the overweight patients (1,818 ± 46 vs. 1,527 ± 67; p = 0.002); REE standardized by fat‐free mass (FFM) (kcal/kg FFM/day) was lower in obese children than in controls (35.2 ± 1.0 vs. 44.9 ± 1.9; p = 0.0001). A linear correlation between REE and FFM was evidenced in both controls and overweight subjects (r = 0.78 and 0.68, respectively; p = 0.05 and p &lt; 0.001, respectively). Actual REE in the obese children was significantly lower than the value predicted by applying the regression equation of REE on FFM in controls to the actual FFM in obese children (paired t test; p = 0.003). FIT was identical in overweight and normal weight subjects, regardless of whether it was expressed in absolute value, as the percentage calorie intake, or standardized by FFM. However, obese children were assigned to two groups according to whether FIT was lower than the value in controls (group 1, &lt;mean −1 SD; n = 9) or at least equal to the value in controls (group 2, mean ‐ 1 SD, n = 10); the only feature that discriminated between these two groups was the presence or absence of a family history for obesity (FHO): FIT was significantly higher in obese children with a negative FHO than in obese children with a positive FHO. Our results support the presence of an energy metabolism disorder in some obese children and suggest that its cause may be constitutional in obese children with a positive FHO.

The effects of indigestible dextrin on sugar tolerance: III. Improvement in sugar tolerance by indigestible dextrin on the impaired glucose tolerance model

Recently developed, Indigestible Dextrin (PF-C) is a low viscosity, water-soluble dietary fiber obtained by heating and enzyme-treatment of potato starch. It has an average molecular weight of 1600. Results from methylation analysis via gas chromatography show the indigestible portion to be a dextrin composed of alpha-1.4, alpha-1.6, beta-1.2, beta-1.3, and beta-1.6 glucosidic bonds and 1.6-anhydro-beta-D-glucose (levoglucosan) as part of the reducing terminal. Physiological attributes such as an improvement in sucrose tolerance and a reduction in blood lipid levels have since been demonstrated. In this study to establish a dose response for PF-C on blood glucose and insulin levels following a sucrose load, administration studies were conducted on normal rats and rats with impaired glucose tolerance. The results are summarized as follows: 1) To estimate an effective dose of PF-C on the reduction in blood glucose and insulin levels following an oral sucrose load, an oral sucrose (1.5g/kg body weight) tolerance test was conducted on rats. The increase in both plasma glucose and insulin levels following a sucrose+PF-C (0.075, 0.15, 0.60, and 1.5g/kg body weight) load was significantly lower compared to the sucrose load. The results show that the most effective dose of PF-C was found to be 0.15g/kg body weight. 2) Another sucrose tolerance test was conducted on three different rat model groups with drug or diet induced impaired glucose tolerance. Impaired glucose tolerance was achieved by injecting one group with streptozotocin at 1.5 days (60mg/kg body weight); a second group was injected at seven weeks (30mg/kg body weight), and a third group was fed on a high (65%) sucrose diet. For this sucrose tolerance test, the adult (7-week) streptozotocin induced diabetic rats and the high-sucrose diet rats on concurrent administrations of PF-C (0.15g/kg body weight) showed decreases in both plasma glucose and insulin levels following a sucrose (1.5g/kg body weight) load. For the neonatal (1.5-day) streptozotocin induced diabetic rat group, reduced increases in plasma glucose were observed with no change in insulin levels as a result of concurrent administration of PF-C following a sucrose load.(ABSTRACT TRUNCATED AT 400 WORDS)

Utilization of oral sucrose load during exercise in humans. Effect of the alpha-glucosidase inhibitor acarbose

Utilization of oral sucrose load during exercise in humans. Effect of the alpha-glucosidase inhibitor acarbose

The effects of an alpha-glucoside hydrolase inhibitor on glycemia and the absorption of sucrose in man determined using a tracer method.

Acarbose, an alpha-glucosidase inhibitor, lowers the glycemic excursion following the ingestion of carbohydrates, in particular, sucrose. This was confirmed with increasing doses of acarbose (0, 50, and 100 mg) and the causes investigated. The absorption of the glucose moiety of sucrose was determined from plasma tracer concentrations when overnight-fasted normal subjects received a 100-g oral sucrose load labeled with sucrose [(1-14C]glucose and a simultaneous intravenous infusion of [3-3H]glucose. As the dose of acarbose given with the sucrose load was increased from 0 to 100 mg, the percentage of the load appearing in the peripheral circulation decreased from 90% to 62%. Malabsorption was confirmed by the appearance of breath hydrogen. Simultaneously, absorption time increased from 243 to 411 min. Maximal glycemic excursions were therefore lowered from 64 to 31 mg/dl. The plasma concentrations of gastric inhibitory polypeptide and insulin decreased with the acarbose dose so that the fractional disappearance rate of glucose also decreased. However, the concentrations of glucagon-like immunoreactivity (GLI) rose, confirming the ileal appearance of malabsorbed sucrose.