Iron status in diabetes mellitus

2019 ◽  
pp. 7-12
Keyword(s):  
Diabetes Mellitus ◽  
Beta Cells ◽  
Defense Mechanism ◽  
Acute Stress ◽  
Islet Cells ◽  
Iron Status ◽  
Acute Phase Reactant ◽  
Iron Deposition ◽  
Muscle Tissues ◽  
High Production

Diabetes mellitus can be defined as chronic metabolic disease which results from either relative or complete absence of insulin by the pancreatic beta islet cells. This in-turn may lead to hyperglycemia due to disturbances in the metabolism of glucose. In the human body, iron is con- sidered to be an effective pro-oxidant and participates in the generation of reactive oxygen species (ROS) such as hydroxyl radical. Because of the poor antioxidant defense mechanism of beta cells (low production of antioxidant enzymes such as catalase, glutathione peroxidase and dismutase), so they are highly prone to iron-induced oxidative stress and iron deposition in it and this will lead to apoptosis, and subsequently insulin deficiency. This iron deposition in beta cells will also lead to insulin resistance by reducing insulin extracting ability of the liver and inhibiting glucose uptake in muscle tissues and fats, this in turn will result in high production of hepatic glucose. Ferritin which is an acute phase reactant protein, that responds to acute stress like trauma, infections, tissue necrosis and surgery, it can produce diabetes mellitus either through inflammation or by increasing iron stores.

scholarly journals Involvement of C4 allotypes in the pathogenesis of human diseases

2004 ◽  
Vol 59 (3) ◽  
pp. 138-144 ◽  
Author(s):  
Eliana Sueco Tibana Samano ◽  
Lia de Melo Ribeiro ◽  
Rosa G. Gorescu ◽  
Katya Cristina Rocha ◽  
Anete S. Grumach
Keyword(s):  
Diabetes Mellitus ◽  
Systemic Sclerosis ◽  
Lupus Erythematosus ◽  
Topoisomerase I ◽  
Defense Mechanism ◽  
Islet Cells ◽  
Case Reports ◽  
Initial Step ◽  
Isolated Populations ◽  
C4 Deficiency

The complement system is an important humoral defense mechanism that plays a relevant role against microbial agents, inflammatory response control, and immunocomplex clearance. Classical complement pathway activation is antibody-dependent. The C4 component participates in the initial step of activation, and C4 expression is determined by 2 pairs of allotypes: C4A and C4B. Deficiencies in C4 allotypes have been associated with several diseases. The aim of the present review is evaluate the reported data in the literature regarding specific C4A and C4B deficiencies and characterize their clinical relevance. We searched the MEDLINE and LILACS databases. Papers referring to total C4 deficiency without allotype evaluation and case reports of primary C4 deficiency were not included. Deficiencies in C4 allotypes have been associated with Mycobacterium leprae infection, erythema nodosum, systemic sclerosis with anti-topoisomerase I antibodies, intermediate congenital adrenal hyperplasia with DR5 genotype, diabetes mellitus type 1 with DR3,4 genotype, and diabetes mellitus with antibodies against islet cells. C4 allotype deficiency is also related to C4B deficiency and autoimmune-associated diseases, such as systemic lupus erythematosus, or diseases with an autoimmune component, such as autism. Some reports associate C4A with thyroiditis after delivery as well as limited and systemic sclerosis without anti-topoisomerase I antibodies. However, the studies with C4A and C4B have been concentrated in isolated populations, and some of the studies could not be reproduced by other authors.

scholarly journals CLERODENDRUM VOLUBILE ETHANOL LEAF EXTRACT: AN EFFECTIVE MITIGATOR AGAINST DOXORUBICIN-INDUCED HEPATORENAL TOXICITIES IN RATS

2021 ◽  
Vol 2 (1) ◽  
pp. 01-09
Author(s):  
O. B. Akinsanya ◽  
P. F. Ayodele ◽  
O. F. Onifade ◽  
M. O. Salimom
Keyword(s):  
Diabetes Mellitus ◽  
Beta Cells ◽  
Pancreatic Islet ◽  
Islet Cells ◽  
Diabetic Rats ◽  
Persea Americana ◽  
Control Group ◽  
Albino Rats ◽  
Pancreatic Islet Cells ◽  
Standard Drug

Diabetes mellitus develops either due to insufficient insulin secretion or lack of insulin resulting from damaged pancreas beta cells. Dyslipidaemia is an acute complication in diabetes mellitus. The aim of this study was to investigate the extenuating effects of T. cattapa leaves and P. americana seed aqueous extracts on streptozotocin-induced lipids profile perturbation and pancreatic damage in experimental rats. Thirty male albino rats were randomly divided into six groups (n = 5). Group 1: (negative control), group 2: 80 mg/kgbwt streptozotocin (positive control), group 3: (80 mg/kgbwt streptozotocin + 200 mg/kgbwt T. catappa leave extract), group 4: (80 mg/kgbwt streptozotocin + 200 mg/kgbwt Persea americana seed extract), group 5: (80 mg/kgbwt streptozotocin + 200 mg/kgbwt extracts-mixture), group 6: (80 mg/kgbwt streptozotocin + 5 mg/kgbwt glibenclamide (standard drug). A single dose of streptozotocin was administered to the rats intraperitoneally; the extracts and glibenclamide were administered orally for 21 days, after which their pancreas was excised for histology. Thereafter, extracts of T. catappa leaves and P. americana seed on serum lipid levels imbalance in streptozotocin-induced diabetic rats were investigated. Histological studies showed a degenerative effect of the pancreatic islet cells of strotozotocin-induced groups. Results showed improvement in the regulation of lipid metabolism as well as the regeneration of the beta cells of pancreas on treatment with T. catappa leaves and P. americana seed. The extracts both equally exert significant antidyslipidemic effects in diabetic rats, in view of the extenuating effects of the extracts on pancreatic islet cells.

Serum Ferritin Status of Patients with Type 2 DM Attending OPD of BIRDEM General Hospital

2020 ◽  
Vol 11 (1) ◽  
pp. 7-10
Author(s):  
Khadiza Begum ◽  
Fahmida Islam ◽  
Farjana Aktar ◽  
Murshida Aziz ◽  
Tohfa E Ayub Tahiya
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Serum Ferritin ◽  
Study Groups ◽  
Acute Phase Reactant ◽  
The Body ◽  
Iron Stores ◽  
Normal Healthy Individual ◽  
Diabetes Patients

Background: In recent times much is talked about of serum ferritin, an acute phase reactant a marker of iron stores in the body and its association with diabetes mellitus. Studies implicate that increased body iron stores and subclinical hemochromatosis has been associated with the development of glucose intolerance, type 2 diabetes and its micro as well as macrovascular complications. Material & Methods: This study was carried out to examine and to observe for any relationship between serum ferritin with Type 2 diabetes mellitus. Our study populations were included 163. Among them 81 type 2 diabetes patients as a case (M=49,F=32, mean 44.68 age in years)and 82 normal healthy individual as a control ( M=35, F=47 , mean 34.71 in years). Results: Majority were healthy outpatients who had come for regular checkup and were matched with controls. Serum ferritin and FBS were estimated and other investigations. Results showed that although Serum ferritin was in the normal range value it was increased in type 2 diabetes patients than in controls and was statistically significant, we did get a positive correlation with duration of diabetes. It can be concluded that there were positive associations between serum ferritin and FBG, age, sex among study groups. Conclusion: In conclusion our study shows that there is significant correlation between increased serum ferritin in diabetes compared to individuals with normal blood sugars in this part and hyper ferritinemia may be one of the causes for development of insulin resistance before overt diabetes. Anwer Khan Modern Medical College Journal Vol. 11, No. 1: Jan 2020, P 7-10

scholarly journals Patterns and Relevance of Langerhans Islet Invasion in Pancreatic Cancer

Cancers ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 249
Author(s):  
Ruediger Goess ◽  
Ayse Ceren Mutgan ◽  
Umut Çalışan ◽  
Yusuf Ceyhun Erdoğan ◽  
Lei Ren ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Islet Cells ◽  
Human Pancreatic Cancer ◽  
Type I ◽  
Type Iv ◽  
Pancreatic Cancer Cells

Background: Pancreatic cancer‐associated diabetes mellitus (PC‐DM) is present in most patients with pancreatic cancer, but its pathogenesis remains poorly understood. Therefore, we aimed to characterize tumor infiltration in Langerhans islets in pancreatic cancer and determine its clinical relevance. Methods: Langerhans islet invasion was systematically analyzed in 68 patientswith pancreatic ductal adenocarcinoma (PDAC) using histopathological examination and 3D in vitro migration assays were performed to assess chemoattraction of pancreatic cancer cells to isletcells. Results: Langerhans islet invasion was present in all patients. We found four different patterns of islet invasion: (Type I) peri‐insular invasion with tumor cells directly touching the boundary, but not penetrating the islet; (Type II) endo‐insular invasion with tumor cells inside the round islet; (Type III) distorted islet structure with complete loss of the round islet morphology; and (Type IV)adjacent cancer and islet cells with solitary islet cells encountered adjacent to cancer cells. Pancreatic cancer cells did not exhibit any chemoattraction to islet cells in 3D assays in vitro. Further, there was no clinical correlation of islet invasion using the novel Islet Invasion Severity Score (IISS), which includes all invasion patterns with the occurrence of diabetes mellitus. However, Type IV islet invasion was related to worsened overall survival in our cohort. Conclusions: We systematically analyzed, for the first time, islet invasion in human pancreatic cancer. Four different main patterns of islet invasion were identified. Diabetes mellitus was not related to islet invasion. However, moreresearch on this prevailing feature of pancreatic cancer is needed to better understand underlying principles.

Impaired migration and delayed differentiation of pancreatic islet cells in mice lacking EGF-receptors

Development ◽  
2000 ◽  
Vol 127 (12) ◽  
pp. 2617-2627 ◽  
Author(s):  
P.J. Miettinen ◽  
M. Huotari ◽  
T. Koivisto ◽  
J. Ustinov ◽  
J. Palgi ◽  
...  
Keyword(s):  
Beta Cells ◽  
Islet Cells ◽  
Branching Morphogenesis ◽  
Late Gestation ◽  
Pancreatic Ducts ◽  
Egf Receptors ◽  
Plasminogen Activator Inhibitor 1 ◽  
Pancreatic Acini ◽  
Delayed Differentiation ◽  
Pai 1

Pancreatic acini and islets are believed to differentiate from common ductal precursors through a process requiring various growth factors. Epidermal growth factor receptor (EGF-R) is expressed throughout the developing pancreas. We have analyzed here the pancreatic phenotype of EGF-R deficient (−/−) mice, which generally die from epithelial immaturity within the first postnatal week. The pancreata appeared macroscopically normal. The most striking feature of the EGF-R (−/−) islets was that instead of forming circular clusters, the islet cells were mainly located in streak-like structures directly associated with pancreatic ducts. Based on BrdU-labelling, proliferation of the neonatal EGF-R (−/−) beta-cells was significantly reduced (2.6+/−0.4 versus 5.8+/−0.9%, P<0.01) and the difference persisted even at 7–11 days of age. Analysis of embryonic pancreata revealed impaired branching morphogenesis and delayed islet cell differentiation in the EGF-R (−/−) mice. Islet development was analyzed further in organ cultures of E12.5 pancreata. The proportion of insulin-positive cells was significantly lower in the EGF-R (−/−) explants (27+/−6 versus 48+/−8%, P<0.01), indicating delayed differentiation of the beta cells. Branching of the epithelium into ducts was also impaired. Matrix metalloproteinase (MMP-2 and MMP-9) activity was reduced 20% in EGF-R (−/−) late-gestation pancreata, as measured by gelatinase assays. Furthermore, the levels of secreted plasminogen activator inhibitor-1 (PAI-1) were markedly higher, while no apparent differences were seen in the levels of active uPA and tPa between EGF-R (−/−) and wild-type pancreata. Our findings suggest that the perturbation of EGF-R-mediated signalling can lead to a generalized proliferation defect of the pancreatic epithelia associated with a delay in beta cell development and disturbed migration of the developing islet cells as they differentiate from their precursors. Upregulated PAI-1 production and decreased gelatinolytic activity correlated to this migration defect. An intact EGF-R pathway appears to be a prerequisite for normal pancreatic development.

scholarly journals The Potency of Senggani (Melastoma malabathricum L) Leaves in Repair of Pancreatic Beta Cells for Diabetes Mellitus Patients: A Narrative Review

2020 ◽  
Vol 7 (2) ◽  
pp. 61-70
Author(s):  
Galuh Rizal Prayoga ◽  
Aziz Syamsul Huda ◽  
Syndilona Br Sitepu
Keyword(s):  
Diabetes Mellitus ◽  
Binding Site ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Docking Simulation ◽  
The Body ◽  
Inhibition Mechanism ◽  
Active Compounds ◽  
Glucose Levels ◽  
Melastoma Malabathricum

Diabetes mellitus is often caused by damage to pancreatic beta cells which play a role in secreting insulin in the body. Damage to pancreatic beta cells causes the body to lack insulin. Dipeptidyl peptidase-4 (DPP-4) is a peptidase enzyme complex located on the surface of the cell membrane. Inhibition of the DPP4 enzyme will increase blood GLP-1 levels and induce regeneration of pancreatic beta cells. Senggani leaf (Melastoma malabathricum) boiled water is believed by the people of the Ciamis area to be used as a diabetes medicine. There have been many studies and reviews related to Senggani (Melastoma malabathricum) and its potential. This review focuses on the discussion of Senggani as an antidiabetic by analyzing the reduction in glucose levels and the repair ability of pancreatic beta cells. The results of the literature study that show that senggani leaves have the ability to reduce blood glucose levels and repair activity of pancreatic beta cells through the DPP-4 enzyme inhibition mechanism supported by molecular docking simulation data. There are 12 active compounds that have a binding site similarity above 50% with the comparison compound vildagliptin. Rutin is the best active compound which has a 100% similarity of the binding site. Based on in vivo research and toxicity analysis on the admetsar database, senggani leaf extract and active compounds of senggani leaves have low toxicity, making it safe to be used as antidiabetic herbal preparations.

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