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Intestinal electrical stimulation attenuates hyperglycemia and prevents loss of pancreatic ? cells in type 2 diabetic Goto-Kakizaki rats.

ABSTRACT: BACKGROUND/OBJECTIVE:Recently, intestinal electrical stimulation (IES) has been reported to result in weight loss; however, it is unclear whether it has a therapeutic potential for diabetes. The aim of the present study was to explore the potential hypoglycemic effects of IES and its possible mechanisms involving ? cells in diabetic rats. SUBJECTS/METHODS:Diabetic Goto-Kakizaki (GK) rats were chronically implanted with one pair of electrodes in the duodenum. The oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) were performed with or without IES, and plasma glucagon-like peptide-1 (GLP-1) and insulin level were measured. In the other two OGTT sessions, rats were treated with either Exendin (9-39) (GLP-1 antagonist) or Exendin (9-39) plus IES to investigate the underlying mechanism involving GLP-1. Gastric emptying and small intestinal transit were also measured with or without IES. In a chronic study, GK rats were treated with IES or Sham-IES for 8 weeks. Blood glucose, plasma GLP-1 and insulin level, body weight, and food intake were measured. Pancreas weight, islet ?-cell apoptosis, and proliferation were also analyzed. RESULTS:Acute IES reduced blood glucose level from 60 to 120?min during OGTT by 16-20% (all p?

SUBMITTER: Ouyang X

PROVIDER: S-EPMC6365494 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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Intestinal electrical stimulation attenuates hyperglycemia and prevents loss of pancreatic β cells in type 2 diabetic Goto-Kakizaki rats.

Ouyang Xiaojun X Li Shiying S Tan Yan Y Lin Lin L Yin Jieyun J Chen Jiande D Z JDZ

Nutrition & diabetes 20190206 1

<h4>Background/objective</h4>Recently, intestinal electrical stimulation (IES) has been reported to result in weight loss; however, it is unclear whether it has a therapeutic potential for diabetes. The aim of the present study was to explore the potential hypoglycemic effects of IES and its possible mechanisms involving β cells in diabetic rats.<h4>Subjects/methods</h4>Diabetic Goto-Kakizaki (GK) rats were chronically implanted with one pair of electrodes in the duodenum. The oral glucose toler ...[more]

PMID: 30728346

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Project description:Type 2 diabetes (T2DM) is a heterogeneous group of diseases that is progressive and involves multiple tissues. Goto-Kakizaki (GK) rats are a polygenic model with elevated blood glucose, peripheral insulin resistance, a non-obese phenotype, and exhibit many degenerative changes observed in human T2DM. As part of a systems analysis of disease progression in this animal model, this study characterized the contribution of adipose tissue to pathophysiology of the disease. We sacrificed subgroups of GK rats and appropriate controls at 4, 8, 12, 16 and 20 weeks of age and carried out a gene array analysis of white adipose tissue. We expanded our physiological analysis of the animals that accompanied our initial gene array study on the livers from these animals. The expanded analysis included adipose tissue weights, HbA1c, additional hormonal profiles, lipid profiles, differential blood cell counts, and food consumption. HbA1c progressively increased in the GK animals. Altered corticosterone, leptin, and adiponectin profiles were also documented in GK animals. Gene array analysis identified 412 genes that were differentially expressed in adipose tissue of GKs relative to controls. The GK animals exhibited an age-specific failure to accumulate body fat despite their relatively higher calorie consumption which was well supported by the altered expression of genes involved in adipogenesis and lipogenesis in the white adipose tissue of these animals, including Fasn, Acly, Kklf9, and Stat3. Systemic inflammation was reflected by chronically elevated white blood cell counts. Furthermore, chronic inflammation in adipose tissue was evident from the differential expression of genes involved in inflammatory responses and activation of natural immunity, including two interferon regulated genes, Ifit and Iipg, as well as MHC class II genes. This study demonstrates an age specific failure to accumulate adipose tissue in the GK rat and the presence of chronic inflammation in adipose tissue from these animals.

Project description:Type 2 diabetes mellitus is a disease caused by hyperglycemia, an imbalance in the intestinal flora and disruption of the endocrine system. At present, it is primarily controlled through drug treatment and an improved diet. Mulberry leaf and fu brick tea were considered to have excellent hypoglycemic effects. This study used mulberry leaves and fu brick tea as raw materials to develop a dietary regulator that can assist in the prevention and alleviation of diabetes. The experiment used the Goto-Kakizaki (GK) rat model to investigate the hypoglycemic effect of mulberry leaf fu tea (MFT) and its influence on the intestinal flora of diabetic rats through methods including ELISA, tissue section observation and 16S RNA microbial sequencing. The results showed that, compared with the GK group, the intervention of mulberry leaf fu tea significantly reduced the activities of α-glucosidase (p < 0.05) and α-amylase (p < 0.05) in the duodenum of GK diabetic rats. The height of the duodenal villi was significantly reduced (p < 0.001), leading to decreased intestinal sugar absorption. At the same time, MFT alleviates the imbalance of intestinal flora caused by high blood sugar, promotes the growth of beneficial bacteria (Lactobacillus, Bifidobacterium, etc.), and inhibits the reproduction of harmful bacteria (Blautia, Klebsiella, Helicobacter, Alistipes, etc.). MFT helps reduce the secretion of toxic substances (lipopolysaccharide, p < 0.001), decreases oxidative stress and inflammation, mitigates organ damage, and improves symptoms of diabetes. Finally, the random blood glucose value of GK rats dropped from 22.79 mmol/L to 14.06 mmol/L. In summary, mulberry leaf fu tea can lower sugar absorption in diabetic rats, reduce the body's oxidative stress and inflammatory response, regulate intestinal flora, and reduce blood sugar levels in GK rats. It is hinted that mulberry leaf fu tea could be used as a functional drink to help prevent the occurrence of diabetes.

Project description:BackgroundThere is a spectacular rise in the global prevalence of type 2 diabetes mellitus (T2DM) due to the worldwide obesity epidemic. However, a significant proportion of T2DM patients are non-obese and they also have an increased risk of cardiovascular diseases. As the Goto-Kakizaki (GK) rat is a well-known model of non-obese T2DM, the goal of this study was to investigate the effect of non-obese T2DM on cardiac alterations of the transcriptome in GK rats.MethodsFasting blood glucose, serum insulin and cholesterol levels were measured at 7, 11, and 15 weeks of age in male GK and control rats. Oral glucose tolerance test and pancreatic insulin level measurements were performed at 11 weeks of age. At week 15, total RNA was isolated from the myocardium and assayed by rat oligonucleotide microarray for 41,012 genes, and then expression of selected genes was confirmed by qRT-PCR. Gene ontology and protein-protein network analyses were performed to demonstrate potentially characteristic gene alterations and key genes in non-obese T2DM.ResultsFasting blood glucose, serum insulin and cholesterol levels were significantly increased, glucose tolerance and insulin sensitivity were significantly impaired in GK rats as compared to controls. In hearts of GK rats, 204 genes showed significant up-regulation and 303 genes showed down-regulation as compared to controls according to microarray analysis. Genes with significantly altered expression in the heart due to non-obese T2DM includes functional clusters of metabolism (e.g. Cyp2e1, Akr1b10), signal transduction (e.g. Dpp4, Stat3), receptors and ion channels (e.g. Sln, Chrng), membrane and structural proteins (e.g. Tnni1, Mylk2, Col8a1, Adam33), cell growth and differentiation (e.g. Gpc3, Jund), immune response (e.g. C3, C4a), and others (e.g. Lrp8, Msln, Klkc1, Epn3). Gene ontology analysis revealed several significantly enriched functional inter-relationships between genes influenced by non-obese T2DM. Protein-protein interaction analysis demonstrated that Stat is a potential key gene influenced by non-obese T2DM.ConclusionsNon-obese T2DM alters cardiac gene expression profile. The altered genes may be involved in the development of cardiac pathologies and could be potential therapeutic targets in non-obese T2DM.

Dataset Information

Intestinal electrical stimulation attenuates hyperglycemia and prevents loss of pancreatic ? cells in type 2 diabetic Goto-Kakizaki rats.

Publications

Intestinal electrical stimulation attenuates hyperglycemia and prevents loss of pancreatic β cells in type 2 diabetic Goto-Kakizaki rats.

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