During diabetes, structural and functional changes in the alimentary tract are known to take place resulting in an increased absorption of intestinal glucose and alterations in the activities of brush-border disaccharidases. To elucidate the effect of administrating polysaccharide from Gynura divaricata (PGD) on disaccharidase activities, the specific activities of intestinal disaccharidases, namely sucrase, maltase and lactase, were measured in streptozotocin-induced diabetic rats. Normal control and diabetic rats were treated by oral administration with PGD. Specific activities of intestinal disaccharidases were increased significantly during diabetes, and amelioration of the activities of sucrase and maltase during diabetes was clearly visible by the treatment with PGD. However, the increased activity of lactase during diabetes mellitus was remarkably alleviated by the administration of PGD only in the duodenum. Meanwhile, oral sucrose tolerance tests demonstrated that PGD alleviated the hyperglycaemia during diabetes mellitus, resulting from the amelioration in the activities of intestinal disaccharidases. The present investigation suggests that PGD exerted an anti-diabetic effect partly via inhibiting the increased intestinal disaccharidase activities of diabetic rats. This beneficial influence of administration of PGD on intestinal disaccharidases clearly indicates their helpful role in the management of diabetes.

The dietary lectin phytohaemagglutinin (PHA) induces gut growth and precocious maturation in suckling rats after mucosal binding. The present study investigated the dose range in which PHA provokes gut maturation and if it coincided with immune activation. Suckling rats, aged 14 d, were orogastrically fed a single increasing dose of PHA: 0 (control), 2, 10, 50 or 250 μg/g body weight (BW) in saline. The effect on gut, lymphoid organs and appearance of CD3+ (T-lymphocyte) and CD19+ (B-lymphocyte) cells in the small-intestinal mucosa was studied at 12 h (acute) and 3 d (late phase) after treatment. The low PHA doses (2 and 10 μg/g BW) induced intestinal hyperplasia without mucosal disarrangement but did not provoke gut maturation. Only the high PHA doses (50 and 250 μg/g BW) temporarily disturbed the intestinal mucosa with villi shortening and decrease in disaccharidase activities, and later after 3 d provoked precocious maturation, resulting in an increase in maltase and sucrase activities and decrease in lactase activity and disappearance of the fetal vacuolated enterocytes in the distal small intestine. Exposure to the high, but not to the low, PHA doses increased the number of mucosal CD19+ and CD3+ cells in the small intestine after 12 h, a finding also observed in untreated weaned rats aged 21–28 d. In conclusion, there was a dose-related effect of PHA on gastrointestinal growth and precocious maturation that coincided with a rapid expansion of mucosal B- and T-lymphocytes, indicating a possible involvement of the immune system in this process.

The objective of this study was to investigate the effect of orally administered spermine at various doses on intestinal maturation in sucking piglets. Thirty-six 11-day-old sucking piglets were assigned randomly to one of six treatments to receive via a stomach tube 0, 0·1, 0·2, 0·3, 0·4, or 0·5 mmol spermine per kg live weight (LW) per day for 3 days. At day 14 of age, duodenum, jejunum and ileum were obtained for biochemical and morphological analysis. Increasing the dose of orally administered spermine increased intestinal weight (linear effect, P<0·01), mucosal weight (linear effect, P<0·05), and mucosal protein, DNA and RNA contents of the duodenum (linear effect, P≤0·01) and jejunum (linear effect, P<0·01). Elevating spermine doses also enhanced (linear effect, P≤0·02) the specific activities of maltase and sucrase but decreased (linear effect, P<0·01) lactase specific activity in the jejunum and duodenum. Furthermore, augmenting oral doses of spermine increased crypt depth and villus width but reduced villus height in the jejunum (linear effect, P<0·05) and duodenum (linear effect, P<0·01). For most measurements, the effects were observed at the oral spermine doses of 0·3 to 0·5 mmol/kg LW per day. Collectively, the results show that oral administration of optimal doses of spermine to 11-day-old sucking piglets induces precocious intestinal maturation and promotes intestinal growth.

A purified pancreatic α-amylase inhibitor (α-AI) from white beans (Phaseolus vulgaris) was administered orally (100m/g body weight dissolved in 9g NaC/) for 22d to non-diabetic (ND) and type 2 diabetic (neonatal diabetes models n0-STZ and n5-STZ) male Wistar rats. Mean glycaemia (mmo/) declined from day 4 of the α-AI administration in ND rats (5·48 (sem 0·08) v. 4·39 (sem 0·13); P<0·05), n0-STZ diabetic rats (7·94 (sem 0·42) v. 5·56 (sem 0·32); P<0·01) and n5-STZ diabetic rats (17·34 (sem 2·58) v. 11·93 (sem 1·96)), until the end of treatment: ND (5·22 (sem 0·21) v. 3·97 (sem 0·06); P<0·01); n0-STZ (8·10 (sem 0·19) v. 5·21 (sem 0·30); P<0·01); and n5-STZ (16·36 (sem 2·14) v. 7·69 (sem 1·34); P<0·01). There was a decrease in water intake (m/) in the α-AI-treated diabetic rats: n0-STZ (30 (sem 0·10) v. 22 (sem 1·50); P<0·01) and n5-STZ (76 (sem 5·04) v. 57 (sem 4·85); P<0·01). Food intake (/) decreased in all three groups: ND (23 (sem 0·31) v. 20 (sem 0·03); P<0·05); n0-STZ (22 (sem 0·55) v. 16 (sem 0·98); P<0·01); and n5-STZ (31 (sem 0·58) v. 23 (sem 1·20); P<0·01). The enterocyte sucrase and maltase activities (/ proteins) were high (P<0·01) in the untreated diabetic rats, n0-STZ (45 (sem 4) and 152 (sem 10), respectively) and n5-STZ (67 (sem 12) and 151 (sem 10), respectively) with respect to the ND rats (24 (sem 2) and 74 (sem 10), respectively). After α-AI treatment, enzyme activities declined in both diabetic rats, n0-STZ (21 (sem 2) and 85 (sem 11); P<0·01) and n5-STZ (28 (sem 7) and 75 (sem 19); P<0·05), to values close to those in the ND rats. In conclusion, α-AI significantly reduced glycaemia in both the ND and diabetic animals and reduced the intake of food and water, and normalized the elevated disaccharidase levels of the diabetic rats.

Enteral exposure of suckling rats to phytohaemagglutinin (PHA) has been shown to induce growth and precocious functional maturation of the gastrointestinal tract. The aim of the present study was to explore the mechanism of this action. Suckling rats, 14d old, were fed a single dose of PHA (0·05mg/g body weight) or saline. The binding of PHA to the gut epithelium and its effect on the morphology and functional properties of the gut and pancreas were studied up to 3d after treatment. Initially, at 1–24h, the PHA bound along the gut mucosal lining, resulting in disturbed gut morphology with villi shortening and rapid decreases in disaccharidase activities and macromolecular absorption capacity. During a later phase, between 1 and 3d, the PHA binding had declined, and an uptake by enterocytes was observed. An increase in crypt cell proliferation and gut growth became evident during this period, together with a functional maturation, as indicated by increases in disaccharidase (maltase and sucrase) activities and the low macromolecular absorption capacity. Pancreas growth also increased, as did its content of digestive enzymes. We conclude that enteral exposure to PHA in suckling rats temporarily causes mucosal disarrangement and functional impediment of the gut, which may be explained by binding to and disruption of the gut mucosa and a two-fold increase in the plasma corticosterone concentration. These findings may lead to a better understanding of the role of diet in gastrointestinal maturation and may constitute a basis for the treatment of mammals having an immature gut.

An inhibitor of α-amylase was isolated and purified from an extract of white kidney beans (Phaseolus vulgaris). The acute oral administration of the inhibitor (50 mg/kg body weight) to adult Wistar rats together with a starch load (2 g/kg body weight suspended in NaCl (9 g/l)) reduced the increase in glycaemia over the basal value (NaCl, 222 (SEM 49); inhibitor, 145 (SEM 16) mmol/l×180 min; P<0.05) without modifying the insulin response. On administering the inhibitor orally (50 mg/kg body weight dissolved in NaCl (9 g/l)) for 21 d to rats fed on a standard diet, a decline was observed in the glycaemia values on day 0 (NaCl, 5.53 (SEM 0.12); inhibitor, 5.25 (SEM 0.16) mmol/l) relative to those obtained on days 10 (NaCl, 5.00 (SEM 0.14); inhibitor, 4.60 (SEM 0.08) mmol/l; P<0.05) and 21 (NaCl, 5.22 (SEM 0.22); inhibitor, 4.50 (SEM 0.12) mmol/l; P<0.01) of treatment, without modifying the plasma concentration of insulin. There was found to be a significant anorexigenic action of the inhibitor; there was reduced food intake (NaCl, 23.07 (SEM 0.31); inhibitor, 19.50 (SEM 0.49) g/d; P<0.01), a reduced weight gain (NaCl, 52 (SEM 3); inhibitor, −1.33 (SEM 8.9) g/21 d; P<0.01), as well as changes in the activity of some intestinal enzymes such as maltase (NaCl, 87 (SEM 7); inhibitor, 127 (SEM 11) U/g proteins; P<0.05). The present study has shown, for the first time, that the prolonged administration of an α-amylase inhibitor reduces blood glucose levels and body-weight gain in Wistar rats.

Diabetes-prone BioBreeding (BBdp) rats often present an enteropathy that may precede the onset of autoimmune insulitis. The aim of the present study was to assess the influence of sex, the time course, the strain specificity, the distribution along the intestinal tract and the effect of diet for the changes in the activity of gut invertase, maltase and lactase found in BBdp rats, as compared with both Wistar–Furth (WF) and diabetes-resistant BioBreeding (BBc) rats. These hydrolases were measured, therefore, at day 10, 30, 45, 70, 95 and 120 in three intestinal segments of WF, BBc and BBdp rats fed, after weaning, either a protective high-casein diet, which decreases the incidence of diabetes in the BBdp rats, or one of two diabetogenic diets (National Toxicology Program; NTP or wheat-gluten-based; WG). Except for a somewhat lower lactase activity in the BBdp rats, no obvious difference in hydrolyase activity between the three strains of rats was observed at day 10. Between days 30 and 120, however, the activity of the hydrolases, especially that of invertase and lactase, was lower in the BBdp rats than in either the WF or BBc rats, at least when considering the animals fed either the NTP or WG diet. These findings support the view that BBdp rats exposed to a diabetogenic diet develop an enteropathy well before the onset of autoimmune insulitis, in a manner somehow comparable with the situation found in some type 1 diabetic patients, in whom coeliac disease may be diagnosed before diabetes onset.

The effects of oat saponins (a mixture of avenacosides A and B) and dietary fibre (cellulose and guar gum) on the disaccharidase activities in the proximal small intestine of the rat were investigated. The influence of avenacosides A and B on the activity of disaccharidases and α-amylase (EC 3·2·1·1) was also studied in vitro. In vivo, oat diets with three avenacoside contents (negligible, normal and twice normal) were used. No significant differences in sucrase (EC 3·2·1·48), maltase (EC 3·2·1·20), trehalase (EC 3·2·1·28) and lactase (EC 3·2·1·21) activities were found between the oat groups after 19 d feeding. The rats that were given cellulose tended to have higher disaccharidase activities compared with the other groups. The avenacosides inhibited the lactase activity significantly in vitro while no or small effects on the other disaccharidases were found. In contrast, the in vitro hydrolysis of starch by α-amylase was increased in the presence of saponins, probably due to their detergent effect. Thus, the in vitro studies showed that the avenacosides could influence the enzyme activities. In vivo, these effects are probably minor due to the low avenacoside concentrations found in oats.