Pancreas In Diabetes Mellitus Research Articles

Butterfly pea flower (Clitoria ternatea L.) extract displayed antidiabetic effect through antioxidant, anti-inflammatory, lower hepatic GSK-3β, and pancreatic glycogen on Diabetes Mellitus and dyslipidemia rat

Diabetes Mellitus (DM) is hyperglycemic or elevated blood glucose level and deficiency of insulin level. DM treatment using synthetic drugs has several complexities, side effects. Reducing the side effects of synthetic drugs, the utilization of herbal medicines is increasingly in demand. Butterfly pea flower (Clitoria ternatea L.) extract (CTE) has pharmacological activities such as hepatoprotective, diuretic, antioxidant, antidiabetic, and anti-inflammatory activities. Objective: This research was conducted to evaluate antidiabetic potent of CTE in DM and dyslipidemia rats model. Methods: LC-MS/MS was used to analyze the CTE compounds. Rats were given high fat diet for 28 days followed by nicotinamide and streptozotocin for inducing DM rats model. DM and dyslipidemia rats model were given CTE at 200, 400, 800 mg/kg of BW, glibenclamide, and simvastatin for 28 days. The glucose and insulin levels on day 28 were measured after treatment of CTE. The CAT, SOD, MDA, IL-18 and protein of pancreas were measured. The glycogen gene expression in pancreas was measured using q-RTPCR method. The GSK-3β expression of liver, IL-6 expression of pancreas were analyzed using IHC method. The data were analyzed using ANOVA and then continued to be analyzed using Tukey’s HSD post-hoc test. Results: CTE increased level of pancreatic CAT, SOD and protein, reduced pancreatic MDA, IL-18 levels, glycogen gene expression of pancreas, GSK-3β protein expression of liver, and IL-6 protein expression of pancreas in DM and dyslipidemia rats. CTE improved liver histopathology, reduced serum glucose, and enhanced insulin levels. Conclusion: CTE has the potency for DM treatment, through antioxidant, and anti-inflammatory in DM and dyslipidemia rats.

Цукровий діабет й екзокринна недостатність підшлункової залози (огляд літератури)

На сьогодні все більше значення надається дослідженню проблеми екзокринної панкреатичної недостатності, що спостерігається в значної кількості хворих на цукровий діабет (ЦД) 1-го і 2-го типу і може потенційно впливати на компенсацію ЦД. Механізм зниження зовнішньої секреції підшлункової залози при ЦД пов’язаний із дисбалансом інгібуючих і стимулю­ючих панкреатичну секрецію гормонів, із фіброзом залози в результаті діабетичної ангіопатії. При ЦД 2-го типу в патогенезі зовнішньосекреторної панкреатичної недостатності беруть участь механізми, що є наслідком метаболічного синдрому. Замісну ферментну терапію слід розглядати як один із перспективних методів лікування хворих на ЦД.

Shared Blood Transcriptomic Signatures between Alzheimer's Disease and Diabetes Mellitus.

Alzheimer’s disease (AD) and diabetes mellitus (DM) are known to have a shared molecular mechanism. We aimed to identify shared blood transcriptomic signatures between AD and DM. Blood expression datasets for each disease were combined and a co-expression network was used to construct modules consisting of genes with similar expression patterns. For each module, a gene regulatory network based on gene expression and protein-protein interactions was established to identify hub genes. We selected one module, where COPS4, PSMA6, GTF2B, GTF2F2, and SSB were identified as dysregulated transcription factors that were common between AD and DM. These five genes were also differentially co-expressed in disease-related tissues, such as the brain in AD and the pancreas in DM. Our study identified gene modules that were dysregulated in both AD and DM blood samples, which may contribute to reveal common pathophysiology between two diseases.

Comparative Decellularization and Recellularization of Normal Versus Streptozotocin-Induced Diabetes Mellitus Rat Pancreas.

Decellularized (DC) organs/tissues offer a promising scaffold for regenerative bioengineering. However, it is not clear whether the diabetic mellitus (DM) pancreas can be used in decellularized and recellularized bioengineering. For assessment of these questions, murine pancreatic scaffolds of normal, type 1DM (T1DM) and type 2 DM (T2DM) pancreas were generated using a perfusion decellularization technique and assessed by histology, scanning electron microscopy, immunohistochemistry, and enzyme-linked immunosorbent assay (ELISA). The capacity of DC pancreatic scaffolds to support attachment and proliferation ofhuman umbilical vein endothelial cells (HUVECs) and MIN-6 β cells was also assessed. Our results showed that DC pancreatic scaffolds were successfully produced from T1DM and T2DM pancreas and maintained their extracellular matrix (ECM) composition, 3D ultrastructure, and various cytokines. All of the pancreatic scaffolds were sufficiently cytocompatible and were able to support proliferation and adhesion of HUVECs and MIN-6 β cells. The preliminary results support the biological utility of diabetes mellitus pancreatic scaffolds and pave the way for further investigations to assess the potential ability of using diabetes mellitus pancreas as scaffolds for recellularization and eventual medical applications.

Apoptosis in the effector phase of autoimmune diabetes, multiple sclerosis and thyroiditis.

The immune system is unusual in two respects. It produces billions of new cells daily that traffic throughout the body and cells within the system proliferate rapidly following exposure to an infectious agent. Both of these attributes require that cell production be regulated by cell death. Human diseases characterized by accelerated cell death leading to immunodeficiency disorders or by reduced cell death leading to systemic autoimmune diseases have been identified. In certain autoimmune diseases, the immune system directs its powerful cytotoxic effector mechanisms against specialized cells such as oligodendrocytes in multiple sclerosis, the beta cells of the pancreas in diabetes mellitus and thyrocytes in Hashimoto's thyroiditis. In this review, we examine the cytotoxic effector pathways implicated in cell death in organ specific autoimmune disorders.

The effect of L-tryptophan load on endocrine system of pancreas in diabetes mellitus.

Tryptophan inhibits hepatic glyconeogenesis in vivo. There are two main explanations: 1/ tryptophan administration stimulates the secretion of gastric inhibitory polypeptide (GIP), whose possible role in mediating enteric insulin release is known (Thomas et al., 1976); 2/ the inhibition of gluconeogenesis can occur secondarily to the formation of quinolinate, which blocks the reaction catalysed by phosphoenolpyruvate carboxykinase (Ray and Foster, 1966). It is known that liver cells from diabetic rats synthesize less quinolinate from tryptophan because of increased flux through the glutarate pathway (Smith and Pogson, 1980). Therefore, gluconeogenesis in such cells are less sensitive to tryptophan.

Эндокринная функция поджелудочной железы при экспериментальном сахарном диабете у крыс и ее особенности при адаптации к гипоксии

The present research was aimed at examination of the endocrinal system of the pancreas in diabetes mellitus, adaptation to hypoxia, and their combination in rats in order to elucidate the relationships between A, B, and D cells under various conditions. The status of Langerhans islet cells was assessed by radioimmunoassay, measurements of blood hormones, and by immunologic method for their quantitative detection in cells. Development of the early stages of diabetes mellitus was found to be associated with a marked restructuring of the total endocrinal system of the gland. Reduction of insulin level was parallelled by a compensatory activation of glucagon- and somatostatin-producing systems. Islet cell changes under such conditions were characterized by sexspecific features. Adaptation to hypoxia was found to have a favorable effect on the course of diabetes mellitus in rats, this manifesting by an increase of blood and В cell insulin levels, by inhibition of islet destruction process, and by reduced production of glucagon and somatostatin.

Endocrinal function of the pancreas in rats with diabetes mellitus and specific features of this function adaptation to hypoxia

The present research was aimed at examination of the endocrinal system of the pancreas in diabetes mellitus, adaptation to hypoxia, and their combination in rats in order to elucidate the relationships between A, B, and D cells under various conditions. The status of Langerhans islet cells was assessed by radioimmunoassay, measurements of blood hormones, and by immunologic method for their quantitative detection in cells. Development of the early stages of diabetes mellitus was found to be associated with a marked restructuring of the total endocrinal system of the gland. Reduction of insulin level was parallelled by a compensatory activation of glucagon- and somatostatin-producing systems. Islet cell changes under such conditions were characterized by sexspecific features. Adaptation to hypoxia was found to have a favorable effect on the course of diabetes mellitus in rats, this manifesting by an increase of blood and В cell insulin levels, by inhibition of islet destruction process, and by reduced production of glucagon and somatostatin.

The Size of the Pancreas in Diabetes Mellitus

To determine whether there was an association between the size of the pancreas and the type of diabetes, ultrasonography of the pancreas was performed on 57 diabetic patients: 14 with Type 1 (insulin-dependent) diabetes, 10 insulin-treated and 33 tablet-treated patients with Type 2 (non-insulin-dependent) diabetes, and 19 non-diabetic subjects. The pancreas of patients with Type 1 diabetes was markedly smaller (p < 0.0001) than the pancreas in non-diabetic subjects. The pancreas of patients with Type 2 diabetes was more moderate in size: larger (p < 0.001) than that of Type 1 diabetic patients but smaller (p < 0.5) than the pancreas of the control group. Pancreatic size of patients with Type 2 diabetes was also related to basal insulin secretion with insulin-deficient patients (low or undetectable C-peptide) having smaller (p < 0.05) pancreases than those with normal insulin secretion. There was no difference in the size of the pancreas in the different treatment groups of Type 2 diabetic patients. Pancreatic size did not correlate with age, body mass index or the duration of diabetes. We conclude that the pancreas is a smaller organ in patients with diabetes mellitus and that the decrement in size is maximal in insulin-dependent/insulin-deficient subjects. Ultrasonography, therefore, can potentially serve to discriminate between the different types of diabetes.

Measurement of Body Area of Pancreas in Diabetes Mellitus by Real-time Ultrasonography

Measurement of Body Area of Pancreas in Diabetes Mellitus by Real-time Ultrasonography

Size of pancreas in diabetes mellitus: a study based on ultrasound.

Size of pancreas in diabetes mellitus: a study based on ultrasound.

Testing of exocrine function of pancreas in diabetes mellitus by use of 75Se-methionine and of secretin.

Acta Medica ScandinavicaVolume 182, Issue 3 p. 345-351 Testing of Exocrine Function of Pancreas in Diabetes Mellitus by Use of 75Se-methionine and of Secretin Juhani Lähdevirta, Juhani Lähdevirta Medical Department (Head: H. Honkapohja, M. D.), Central Hospital, Savon-linna, FinlandSearch for more papers by this author Juhani Lähdevirta, Juhani Lähdevirta Medical Department (Head: H. Honkapohja, M. D.), Central Hospital, Savon-linna, FinlandSearch for more papers by this author First published: January/December 1967 https://doi.org/10.1111/j.0954-6820.1967.tb11534.xCitations: 14AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume182, Issue3January/December 1967Pages 345-351 RelatedInformation

A HISTO- AND IMMUNOPATHOLOGIC STUDY OF THE VESSELS AND ISLETS OF LANGERHANS OF THE PANCREAS IN DIABETES MELLITUS.

A HISTO- AND IMMUNOPATHOLOGIC STUDY OF THE VESSELS AND ISLETS OF LANGERHANS OF THE PANCREAS IN DIABETES MELLITUS.

Endocrine Function of the Pancreas in Diabetes Mellitus

Clinical studies on the endocrine function of the pancreas in diabetes mellitus were performed before and after treatment. Mean serum insulin activity expressed as glucose uptake of the diaphragm was 0.97 mg. per unit weight of the diaphragm in type I diabetics before treatment, while in type II it was -0.33. Type I diabetics did not show an increase in serum insulin activity after the dietary treatment, however type II did show an increase. A significant correlation between serum insulin activity and fasting blood sugar was observed before treatment. Serum insulin activity after the administration of glucose increases in seven out of twelve cases of type I diabetics and five out of ten cases of type II diabetics. The increase in serum insulin activity, however, was not observed in five out of twelve cases of type I diabetics and five out of ten cases of type II. The mean levels of plasma glucagon-like activity before treatment were 5.5, 46.8 and 54.0μg. per dl. in normal subjects, type I diabetics and type II diabetics, respectively. Glucagon-like activity decreased after treatment in both types of diabetics. In several diabetics, whose diabetic state was not improved, it did not decrease. There was observed a significant correlation between glucagon-like activity in plasma and fasting blood sugar. The mean ratios of α to β cells in islets of the pancreas were 1:5.59, 1:5.04 and 1:4.03 for non-diabetics, type I diabetics and type II diabetics, respectively.

Alterations in Liver Function and in the External Secretory Activity of the Pancreas in Diabetes Mellitus: A Preliminary Report

Alterations in Liver Function and in the External Secretory Activity of the Pancreas in Diabetes Mellitus: A Preliminary Report