Gut Permeability and Intestinal Mucins, Invertase, and Peroxidase in Control and Diabetes-Prone BB Rats Fed Either a Protective or a Diabetogenic Diet (original) (raw)
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Invertase, maltase, lactase, and peroxidase activities in duodenum of BB rats
Endocrine, 2002
The development of immune-mediated diabetes in BB rats may involve a defect of the gastrointestinal tract (GI), as suggested by increased gut permeability. This study aimed at measuring invertase, maltase, lactase, and peroxidase activities in the duodenum of diabetesprone BioBreeding (BBdp) rats and control BioBreeding rats (BBc) given free access to NIH-07 diet up to the time of killing at 60 66 d of age. After washing the entire small intestine, the duodenal mucosa was scraped off in the first 5-cm segment from the pylorus and frozen in distilled water. Invertase, maltase, and lactase activities were measured by monitoring the conversion of [U-(14)C]sucrose, [U-(14)C]maltose, and [D-[1-(14)C]glucose] lactose to radioactive hexoses, which were phosphorylated in the presence of adenosine triphosphatase and yeast hexokinase and then separated from their precursor by ion-exchange chromatography. Peroxidase activity was measured by a spectrophotometric procedure. In the BBdp rats, the...
Nutrients, 2022
The reactions of intestinal functional parameters to type 2 diabetes at a young age remain unclear. The study aimed to assess changes in the activity of intestinal enzymes, glucose absorption, transporter content (SGLT1, GLUT2) and intestinal structure in young Wistar rats with type 2 diabetes (T2D) and impaired glucose tolerance (IGT). To induce these conditions in the T2D (n = 4) and IGT (n = 6) rats, we used a high-fat diet and a low dose of streptozotocin. Rats fed a high-fat diet (HFD) (n = 6) or a standard diet (SCD) (n = 6) were used as controls. The results showed that in T2D rats, the ability of the small intestine to absorb glucose was higher in comparison to HFD rats (p < 0.05). This was accompanied by a tendency towards an increase in the number of enterocytes on the villi of the small intestine in the absence of changes in the content of SGLT1 and GLUT2 in the brush border membrane of the enterocytes. T2D rats also showed lower maltase and alkaline phosphatase (AP) a...
Abnormal intestinal permeability to sugars in diabetes mellitus
Diabetologia, 1986
A test of intestinal mucosal function which utilizes the differential permeability of L-rhamnose and lactulose has been reported to be helpful in the diagnosis of gluten-sensitive enteropathy. We have applied this test to 48 male subjects with diabetes mellitus to evaluate its usefulness as a screening test in diabetic patients and to further study sugar absorption in these individuals. Total urinary lactulose excretion in the 13 healthy control subjects was 54.5 + 8.5 rag/5 h, while excretion by diabetic patients was increased at 116.1 _+ 15.7 mg/5 h (p < 0.01). Similarly, total L-rhamnose excretion by diabetic patients was significantly higher (139.7_ 14.3 mg/5 h vs 84.3 +18.4 mg/5 h, p<0.05). The ratio of percent urinary excretion for lactulose/L-rhamnose (L/R ratio) for diabetic patients (0.197 + 0.024) was not different from the control subjects (0.151 + 0.2). Nine out of 48 diabetic patients studied had lactulose/L-rhamnose ratios higher than the mean plus two standard deviations of the control group, which might lead to the diagnosis of small bowel mucosal disease. Although we may have been detecting subclinical mucosal disease or gluten sensitive enteropathy in a subgroup, it appears that this test of intestinal mucosal function should be interpreted with caution in diabetic patients.
Diabetologia, 2006
Aims/hypothesis Accumulating data suggest that the gut immune system plays a role in the development of type 1 diabetes. The intestinal flora is essential for the development of the (gut) immune system and the establishment of tolerance. It has been reported that oral administration of food and bacterial antigens early in life suppresses later development of diabetes in the Bio-Breeding diabetesprone (BB-DP) rat. This study was designed to investigate the possible relationship between the development of diabetes and the composition of intestinal flora. Materials and methods The intestinal flora of BB-DP rats, a rat model for type 1 diabetes, was characterised long before the clinical onset of diabetes by fluorescent in situ hybridisation. In a separate experiment, BB-DP rats were treated with antibiotics and the effect on diabetes incidence and level of insulitis was analysed. Results We observed a difference in bacterial composition between rats that eventually did and those that did not develop diabetes. This difference was detectable long before clinical onset of the disease. Rats that did not develop diabetes at a later age displayed a lower amount of Bacteroides sp. Modulation of the intestinal flora through antibiotic treatment decreased the incidence and delayed the onset of diabetes. A combination of antibiotic treatment and a protective hydrolysed casein diet completely prevented diabetes in the BB-DP rat. Conclusions/interpretation Our data suggest that the intestinal flora is involved in the development of type 1 diabetes. Factors influencing composition of the intestinal flora could be a target for therapeutic intervention.
Intestinal transport of sugars and amino acids in diabetic rats
Journal of Clinical Investigation, 1970
specificity and mechanism of altered intestinal transport of diabetic rats was studied with an everted ring technique. Increased intracellular accumulation of amino acids, as well as galactose and 3-0methylglucose, was demonstrated in diabetes. The greater accumulation by diabetic intestine could not be attributed to a direct effect of the agent used to induce diabetes or to an alteration in food consumption. Although the changes were related to the severity of diabetes and could be reversed with treatment with insulin, they could not be modified by addition of insulin in vitro. The changes could not be induced in control intestine either with hyperglycemia from glucose infusion or preincubation with glucose in vitro. Although the higher concentration gradients of amino acids, galactose, and 3-0-methylglucose could result from increased energy utilization by diabetic intestine, an alteration of cell membrane function, as well, is suggested by the demonstration with kinetic studies of increased influx with an increase in Vmax.
Clinical Nutrition, 2016
Background: The hyperglycemia leads to increased oxidative stress, causing lipid peroxidation and imbalance in the immune system. Aims: To investigate the effect of Kefir e a probiotic containing different strains e on metabolic parameters, cytokines, nitric oxide (NO) production, phagocytic activity of peritoneal macrophages and intestinal modulation in diabetes. Methods: Wistar rats received injection of streptozotocin (45 mg/kg, intravenously) and diabetes was defined as glycemia !200 mg/dL. The animals were distributed in four groups: control (CTL); control Kefir (CTLK); diabetic (DM); diabetic Kefir (DMK). Kefir was given at 1.8 mL/day by gavage, started on the 5th day of diabetes, during 8 weeks. The animals were allocated in metabolic cages, pre and post treatment with Kefir, for measurement of the metabolic parameters, such as water intake, food intake, diuresis, glycemia, body mass, insulin and lipid profile, these last two were only measured at the end of Kefir protocol. After treatment, the animals were euthanized and the peritoneal cavity was prepared, resident macrophages were collected and cultured for analysis of the phagocytic activity, cytokines (IL-10, TNF-a, IL-17, IL-1b) and NO. The intestinal modulation was performed by the quantification of Peyer's patches (PP) in the small intestine. The data were presented as mean ± SEM, with significance of p < 0.05. Results: DM when compared to CTL showed increase in water intake (133 ± 7 vs. 28 ± 1 mL, p < 0.0001), food intake (40 ± 2 vs. 16 ± 1 g, p < 0.0001), diuresis (102 ± 5 vs. 13 ± 1 mL, p < 0.0001) and glycemia (567 ± 12 vs. 84 ± 3 mg/dL, p < 0.0001), while in DMK group all these metabolic parameters were decreased (96 ± 14; 36 ± 1; 86 ± 7 and 407 ± 19, respectively, p < 0.0001), presenting increase of body mass (42 ± 5 vs. 16 ± 4D, p < 0.0001) and insulin levels (0.3 ± 0.8 vs. 0.1 ± 0.04 ng/mL, p < 0.0001) compared to DM. The lipid profile of the diabetic groups showed tendency to increase compared to the respective controls. In relation to function of peritoneal macrophages, DMK group vs. DM showed improvement in phagocytic capacity (70 ± 5 vs. 51 ± 7%, p ¼ 0,0023) and increased concentration of all the cytokines analyzed (pg/mL), as IL-10 (926 ± 69 vs. 556 ± 92, p ¼ 0.0004), TNF-a (178 ± 20 vs. 109 ± 20, p ¼ 0.005), IL-17 (33 ± 1 vs. 9 ± 1, p ¼ 0.0001) and IL-1b (102 ± 14 vs. 70 ± 5, p ¼ 0.0129), after 24 h of LPS stimulation; including NO bioavailability after 24 h (102 ± 9 vs. 66 ± 5 mM/mL, p ¼ 0.0029) or 48 h (143 ± 8 vs. 119 ± 4 mM/mL, p ¼ 0.0102) of LPS stimulation. Moreover, the number of PP in the whole small intestine of DMK group was also increased as compared to DM (22 ± 1 vs. 18 ± 1, p ¼ 0.0292). Conclusion: These results show that Kefir has a potential to modulate the immune response and activate peritoneal macrophages in diabetic animals, which suggests that it could enhance the immunocompetence of patients affected by diabetes mellitus. The hypoglycemic effect of this probiotic could be used as a tool to control glycemia, reducing or delaying the onset of complications associated with this disease.
International Journal of Molecular Sciences
Evidence suggests that microbiota-derived metabolites, including short-chain fatty acids (SCFAs) and trimethylamine-oxide (TMAO), affect the course of diabetic multiorgan pathology. We hypothesized that diabetes activates the intestinal renin–angiotensin system (RAS), contributing to gut pathology. Twelve-week-old male rats were divided into three groups: controls, diabetic (streptozotocin-induced) and diabetic treated with enalapril. Histological examination and RT-qPCR were performed to evaluate morphology and RAS expression in the jejunum and the colon. SCFA and TMAO concentrations in stools, portal and systemic blood were evaluated. In comparison to the controls, the diabetic rats showed hyperplastic changes in jejunal and colonic mucosa, increased plasma SCFA, and slightly increased plasma TMAO. The size of the changes was smaller in enalapril-treated rats. Diabetic rats had a lower expression of Mas receptor (MasR) and angiotensinogen in the jejunum whereas, in the colon, the ...
Annals of Surgery, 1994
The authors investigated the role of mucin and secretory immunoglobulin A (sigA) in a model of nutritionally induced bacterial translocation. Background Parenteral and certain elemental diets have been shown to impair intestinal barrier function, whereas fiber has been shown to protect against nutritionally induced bacterial translocation. However, the factors responsible for these phenomenon have not been fully determined. Methods Intestinal mucin levels, mucosal protein content, sIgA, intestinal morphology, and permeability to horseradish peroxidase, bacterial translocation, and intestinal bacterial population levels were measured in rats 7 days after receiving total parenteral nutrition (TPN) solution (28% glucose, 4.25% amino acids; 307 kcal/kg/day) enterally (ORAL-TPN) or parenterally (IV-TPN) with or without enteral bulk fiber supplementation. Chow-fed rats served as control subjects. Results The incidence of bacterial translocation in the ORAL-TPN and IV-TPN groups was reduced significantly by the provision of fiber (p < 0.05). Mucosal protein, sIgA, and insoluble mucin levels were decreased in the jejunum of the ORAL-TPN and IV-TPN groups, with mucosal protein levels being decreased to a greater extent than sIgA or mucin. Although similar decreases in these parameters were observed in the fiber-fed groups, fiber appeared to improve intestinal barrier function as measured by horseradish peroxidase permeability. Conclusions The provision of bulk-forming fiber improves intestinal barrier function as measured by peroxidase permeability and bacterial translocation, but does not restore mucosal protein content, intestinal mucin, or sIgA levels to normal.