scholarly journals SEL BETA PANKREAS SINTESIS DAN SEKRESI INSULIN

2013 ◽  
Vol 4 (3) ◽  
Author(s):  
Eka Banjarnahor ◽  
Sunny Wangko
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Plasma Membranes ◽  
Secretory Granules ◽  
Chromosome 11 ◽  
Insulin Synthesis ◽  
Glucose Levels ◽  
Blood Glucose Levels

Abstract: Insulin synthesis and secretion are done by pancreatic beta cells. Preceding the insulin synthesis, there is a gen translation in chromosome 11 that produces insulin, packed in secretory granules. Insulin secretion is induced by the alteration of blood glucose levels, resulting in the occurence of intracellular reactions preceded by changes of ATP/ADP ratios that trigger the depolarisation of plasma membranes. Furthermore, extracellular Ca2+ ions move inward to beta cells to activate exocytosis. There are still many unknown problems so far in either the synthesis or secretion of insulin that cause unfulfilled insulin needs in the body.Keywords: beta cells, insulin, synthesis, secretionAbstrak: Sintesis dan sekresi insulin dilakukan oleh sel beta pankreas. Sintesis insulin diawali oleh salinan gen pada kromosom 11, yang akan menghasilkan insulin, di kemas di dalam granul-granul sekretorik. Sekresi insulin diinduksi oleh perubahan kadar glukosa, yang berakibat terjadinya reaksi intrasel yang diikuti adanya perbedaan rasio ATP/ADP yang memicu reaksi depolarisasi membran plasma. Sebagai akibat lanjut Ca2+ ekstrasel akan masuk ke dalam sel beta yang berfungsi mengaktifkan eksositosis. Sampai saat ini masih banyak ditemui masalah baik dalam hal sintesis maupun sekresi insulin yang mengakibatkan kebutuhan insulin tubuh tidak terpenuhi.Kata kunci: sel beta, insulin, sintesis, sekresi

scholarly journals Inhibitory effect of somatostatin on insulin secretion is not mediated via the CNS

2015 ◽  
Vol 225 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Astrid C Hauge-Evans ◽  
James Bowe ◽  
Zara J Franklin ◽  
Zoheb Hassan ◽  
Peter M Jones
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Pancreatic Beta Cells ◽  
Plasma Insulin ◽  
Inhibitory Effect ◽  
Isolated Islets ◽  
Glucose Levels ◽  
Blood Glucose Levels

The inhibitory effect of somatostatin (SST) on insulin secretionin vivois attributed to a direct effect on pancreatic beta cells, but this is inconsistent with somein vitroresults in which exogenous SST is ineffective in inhibiting secretion from isolated islets. We therefore investigated whether insulin secretion from the pancreatic islets may partly be regulated by an indirect effect of SST mediated via the CNS. Islet hormone secretion was assessedin vitroby perifusion and static incubations of isolated islets andin vivoby i.v. or i.c.v. administration of the SST analogue BIM23014C with an i.v. glucose challenge to conscious, chronically catheterised rats. Hormone content of samples was assessed by ELISA or RIA and blood glucose levels using a glucose meter. Exogenous SST14/SST28 or BIM23014C did not inhibit the release of insulin from isolated rodent isletsin vitro, whereas peripheral i.v. administration of BIM23014C (7.5 μg) with glucose (1 g/kg) led to decreased plasma insulin content (2.3±0.5 ng insulin/ml versus 4.5±0.5 ng/ml att=5 min,P<0.001) and elevated blood glucose levels compared with those of the controls (29.19±1.3 mmol/l versus 23.5±1.7 mmol/l,P<0.05). In contrast, central i.c.v. injection of BIM23014C (0.75 μg) had no significant effect on either plasma insulin (3.3±0.4 ng/ml,P>0.05) or blood glucose levels (23.5±1.7 mmol/l,P>0.05) although i.v. administration of this dose increased blood glucose concentrations (32.3±0.7 mmol/l,P<0.01). BIM23014C did not measurably alter plasma glucagon, SST, GLP1 or catecholamine levels whether injected i.v. or i.c.v. These results indicate that SST does not suppress insulin secretion by a centrally mediated effect but acts peripherally on islet cells.

scholarly journals Effect of Pleurotus Ostreatus on Pancreatic Beta Cells of Diabetes Mellitus Mice Model

2017 ◽  
Vol 15 (2) ◽  
pp. 155 ◽  
Author(s):  
Ningrum Wahyuni ◽  
Syafrudin Ilyas ◽  
Alya Amila Fitrie
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Beta Cells ◽  
Pleurotus Ostreatus ◽  
Pancreatic Beta Cells ◽  
Low Dose ◽  
Ethanol Extract ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
One Way Anova

Over the last 30 years, the number of people suffering from diabetes mellitus has doubled globally. Adipose tissue dysfunction plays an important role in insulin resistance. Mushroom has been traditionally used to prevent diabetes. This research aims to study the anti-oxidative effect of Pleurotus ostreatus on pancreatic beta cells. This study is an experimental posttest only control group design. The subjects were 24 male wistar mice, divided into six groups. Group P0 was given distilled water and citrate buffer. Group P1 was given high fat diet (HFD) and low dose streptozotocin (STZ). Group P2 and 3 were given HFD and low dose STZ along with Pleurotus ostreatus ethanol extract. Group P4 and P5 were given HFD and low dose STZ, and then given Pleurotus ostreatus ethanol extract. Blood glucose levels and pancreatic beta cells area count were done after treatment. Data obtained was analyzed using one-way ANOVA test. One-way ANOVA test showed signifi cant difference in all the groups (p<0.05). Post Hoc test results showed difference in blood glucose levels and pancreatic beta cells area count. Pleurotus ostreatus ethanol extract can prevent cellular damage to murine pancreatic beta cells but unable to reverse the damage to the beta cells.

scholarly journals Vanadyl Sulfate Treatment Stimulates Proliferation and Regeneration of Beta Cells in Pancreatic Islets

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Samira Missaoui ◽  
Khémais Ben Rhouma ◽  
Mohamed-Tahar Yacoubi ◽  
Mohsen Sakly ◽  
Olfa Tebourbi
Keyword(s):  
Blood Glucose ◽  
Insulin Sensitivity ◽  
Pancreatic Islets ◽  
Beta Cells ◽  
Control Level ◽  
Diabetic Rats ◽  
Diabetic Group ◽  
Dependent Manner ◽  
Glucose Levels ◽  
Blood Glucose Levels

We examined the effects of vanadium sulfate (VOSO4) treatment at 5 and 10 mg/kg for 30 days on endocrine pancreas activity and histology in nondiabetic and STZ-induced diabetic rats. In diabetic group, blood glucose levels significantly increased while insulinemia level markedly decreased. At the end of treatment, VOSO4at a dose of 10 mg/Kg normalized blood glucose level in diabetic group, restored insulinemia, and significantly improved insulin sensitivity. VOSO4also increased in a dose-dependent manner the number of insulin immunopositive beta cells in pancreatic islets of nondiabetic rats. Furthermore, in the STZ-diabetic group, the decrease in the number of insulin immunopositive beta cells was corrected to reach the control level mainly with the higher dose of vanadium. Therefore, VOSO4treatment normalized plasma glucose and insulin levels and improved insulin sensitivity in STZ-experimental diabetes and induced beta cells proliferation and/or regeneration in normal or diabetic rats.

scholarly journals Altered Glucose and Insulin Responses to Brain Medullary Thyrotropin-Releasing Hormone (TRH)-Induced Autonomic Activation in Type 2 Diabetic Goto-Kakizaki Rats

Endocrinology ◽  
2005 ◽  
Vol 146 (12) ◽  
pp. 5425-5432 ◽  
Author(s):  
Yan Ao ◽  
Natalie Toy ◽  
Moon K. Song ◽  
Vay Liang W. Go ◽  
Hong Yang
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Wistar Rats ◽  
Mrna Levels ◽  
Gk Rats ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Autonomic Activation ◽  
Insulin Responses

Insulin secretion is impaired in type 2 diabetes (T2D). The insulin and glucose responses to central autonomic activation induced by excitation of brain medullary TRH receptors were studied in T2D Goto-Kakizaki (GK) rats. Blood glucose levels in normally fed, pentobarbital-anesthetized GK and nondiabetic Wistar rats were 193 and 119 mg/100 ml in males and 214 and 131 mg/100 ml in females. Intracisternal injection (ic) of the stable TRH analog RX 77368 (10 ng) induced significantly higher insulin response in both genders of overnight-fasted GK rats compared with Wistar rats and slightly increased blood glucose in female Wistar rats but significantly decreased it from 193 to 145 mg/100 ml in female GK rats. RX 77368 (50 ng) ic induced markedly greater glucose and relatively weaker insulin responses in male GK rats than Wistar rats. Bilateral vagotomy blocked ic RX 77368-induced insulin secretion, whereas adrenalectomy abolished its hyperglycemic effect. In adrenalectomized male GK but not Wistar rats, ic RX 77368 (50 ng) dramatically increased serum insulin levels by 6.5-fold and decreased blood glucose levels from 154 to 98 mg/100 ml; these changes were prevented by vagotomy. GK rats had higher basal pancreatic insulin II mRNA levels but a lower response to ic RX 77368 (50 ng) compared with Wistar rats. These results indicate that central-vagal activation-induced insulin secretion is susceptible in T2D GK rats. However, the dominant sympathetic-adrenal response to medullary TRH plays a suppressing role on vagal-mediated insulin secretion. This unbalanced vago-sympathetic activation by medullary TRH may contribute to the impaired insulin secretion in T2D.

scholarly journals Molecular Mechanism of Corticosteroid-Induced Hyperglycemia

10.51511/pr.1 ◽  
2021 ◽  
Author(s):  
Destika Ambar Sari ◽  
Galih Samodra ◽  
Ikhwan Yuda Kusuma
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Immunosuppressive Drugs ◽  
Hormone Sensitive Lipase ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Hormone Sensitive ◽  
Beta Cell Response

Corticosteroids are widely used as strong anti-inflammatory and immunosuppressive drugs to treat various diseases. However, the use of corticosteroids can cause several side effects, such as hyperglycemia. This review aims to examine the effect of corticosteroids on increasing glucose in molecular levels based on literature studies. A literature searching was carried out on the PubMed, Science Direct, and Google Scholar databases published in 2010-2020. Corticosteroids can cause an increase in blood glucose levels by several mechanisms. In the liver, glucocorticoids increase endogenous plasma glucose and stimulate gluconeogenesis. Glucocorticoids increase the production of non-esterified fatty acids which affect the signal transduction of insulin receptor substrate-1 in skeletal muscle. In adipose, glucocorticoids increase lipolysis and visceral adiposity through increased transcription and expression of protein adipose triglyceride lipase and hormone-sensitive lipase. In pancreatic beta cells, glucocorticoids directly inhibit the beta cell response to glucose through the role of protein kinase B and protein kinase C. At the molecular level, corticosteroids can cause hyperglycemia through mechanisms in the liver, skeletal muscle tissue, adipose tissue, and pancreatic beta cells.

scholarly journals HYPOGLYCEMIC ACTIVITY OF A NOVEL POLYHERBAL FORMULATION IN STREPTOZOTOCIN-INDUCED DIABETIC RATS: A THERAPEUTIC STUDY

2019 ◽  
pp. 218-223
Author(s):  
PULAK MAJUMDER ◽  
PARIDHAVI M
Keyword(s):  
Body Weight ◽  
Blood Glucose ◽  
Beta Cells ◽  
Density Lipoprotein ◽  
Diabetic Rats ◽  
Glucose Levels ◽  
Polyherbal Formulation ◽  
Blood Glucose Levels ◽  
Therapeutic Study ◽  
Glutamyl Transferase

Objective: The concept of the synergistic effect of poly-herbalism was as old as medicine history. Present novel polyherbal formulation (PHF) composed of five different herbs. The present investigation aimed to evaluate the synergistic therapeutic hypoglycemic potential of PHF against streptozotocin (STZ) (60 mg/kg b.w, ip)-induced diabetic rats. Methods: For this therapeutic study, the dose was framed orally once a day to the test objects after STZ dosing at 500 mg/kg/5 ml dosage levels for 21 days. The transformation of body weight and blood glucose level was examined, and the histopathological changes of beta cells of the pancreas, cellular architectures of liver and kidney were also perceived after scarification of the objects. Results: The outcomes were compared to that of glibenclamide (5 mg/kg) treated group. Declines of body weight and blood glucose levels were perceived in STZ-induced diabetic animals very significantly (p<0.01 or p<0.05). However, these diabetic changes were significantly (p<0.01 or p<0.05) decreased in PHF-dosing groups revealed more encouraging effects compared to that of glibenclamide. In the other hand, various liver function and enzymes test (creatinine, urea, total bilirubin, total albumin, alkaline phosphatase, gamma-glutamyl transferase, aspartate transaminases, and alanine transaminases) and lipid profile (total cholesterol, triglycerides, high-density lipoprotein cholesterol, total protein, low-density lipoprotein [LDL], and very LDL) studies strongly indicate the potential action of this novel formulation. Conclusions: It is deliberated that PHF has the favorable effect to normalize the blood glucose levels, and also rejuvenation and reproduction of beta cells lead a better futuristic ant diabetic therapy for diabetic management.

scholarly journals Clinical and Functional Characteristics of a Novel KLF11 Cys354Phe Variant Involved in Maturity-Onset Diabetes of the Young

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yujing Sun ◽  
Jingru Qu ◽  
Jing Wang ◽  
Ruxing Zhao ◽  
Chuan Wang ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Luciferase Reporter ◽  
Maturity Onset Diabetes ◽  
Insulin Expression ◽  
Insulin Promoter ◽  
Impaired Insulin ◽  
Reporter Assays

Background. Mutations in human KLF11 may lead to the development of maturity-onset diabetes of the young 7 (MODY7). This occurs due to impaired insulin synthesis in the pancreas. To date, the clinical and functional characteristics of the novel KLF11 mutation c.1061G > T have not yet been reported. Methods. Whole-exon sequencing was used to screen the proband and family members with clinical suspicion of the KLF11 variant. Luciferase reporter assays were used to investigate whether the KLF11 variant binds to the insulin promoter. Real-time PCR, western blotting, and glucose-stimulated insulin secretion (GSIS) analysis were used to analyze the KLF11 variant that regulates insulin expression and insulin secretion activity in beta cell lines. The Freestyle Libre H (Abbott Diabetes Care Ltd) was used to dynamically monitor the proband daily blood glucose levels. Results. Mutation screening for the whole exon genes identified a heterozygous KLF11 (c.1061G > T) variant in the proband, her mother, and her maternal grandfather. Cell-based luciferase reporter assays using wild-type and mutant transgenes revealed that the KLF11 (c.1061G > T) variant had impaired insulin promoter regulation activity. Moreover, this variant was found to impair insulin expression and insulin secretion in pancreatic beta cells. The proband had better blood glucose control without staple food intake ( p < 0.05 ). Conclusions. Herein, for the first time, we report a novel KLF11 (c.1061G > T) monogenic mutation associated with MODY7. This variant has impaired insulin promoter regulation activity and impairs insulin expression and secretion in pancreatic beta cells. Therefore, administering oral antidiabetic drugs along with dietary intervention may benefit the proband.

scholarly journals Activity of Water Soluble Polysaccharide White Bentul (Colocasia Esculenta Schott [L]) As a Candidate for Antidiabetic Agent

2018 ◽  
Vol 2 (1) ◽  
pp. 1
Author(s):  
Sentot Joko Raharjo
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Pancreatic Beta Cells ◽  
Water Soluble ◽  
Antidiabetic Activity ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Pancreatic Cells ◽  
Soluble Polysaccharide

White bentul tuber is one of tuber plant species which have bioactive compound of Water Soluble Polysaccharide (WSP) and potentially healthy nutrition in the therapy of metabolic syndrome disease. The purpose of this research is to prove the ability of WSP isolate to reduce blood glucose level in white mice.  Research method include the yield of WSP isolates white bentul tuber using enzymatic method, WSP identification using HPLC with Aminex HPX-87C BIORAD5 columns, and antidiabetic activity test using white mices. Test activity was performed in six treatment groups (Normal, Induction STZ 20 mg/ kgBW, Induction STZ 20 mg / kgBW + metformin 195mg / KgBW, three treatment with STZ induction 20 mg/ kgBW and WSP isolate with concentration 200, 400, and 600mg / kgBW). Determination of blood glucose levels using glucometer and supported by observation of histologic improvement of beta pancreatic cells in white mice that have necrosis. The result research are WSP yield of 4.81% and WSP level of 94.45%. Results of blood glucose levels of mice induced STZ 20mg/kgBW decreased optimal blood glucose with a dose of WSP 400mg/kgBW in the first week and histologic improvement of beta pancreatic cells that experienced the most optimal necrosis at WSP dose of 200 mg/kgBW. The conclusion of this research is the provision WSP isolate of white bentul tubers at doses of 200, 400, 600 mg/kgBW can decrease the blood glucose level induced STZ 20mg/kg BW and histological improvement in pancreatic beta cells at the most optimal dose of 200 mg / kgKeywords: White bentul tuber, water soluble polysaccharides, diabetes mellitus, beta pancratic cells   

scholarly journals The KCNJ11-E23K Gene Variant Hastens Diabetes Progression by Impairing Glucose-Induced Insulin Secretion

2021 ◽  
Author(s):  
Gregor Sachse ◽  
Elizabeth Haythorne ◽  
Thomas Hill ◽  
Peter Proks ◽  
Russell Joynson ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Beta Cell ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Diabetes Risk ◽  
Standard Diet ◽  
Glucose Levels ◽  
Genetically Engineered Mouse Model ◽  
Increased Risk ◽  
Diabetes Progression

The ATP-sensitive potassium (K<sub>ATP</sub>) channel controls blood glucose levels by coupling glucose metabolism to insulin secretion in pancreatic beta cells. E23K, a common polymorphism in the pore-forming K<sub>ATP</sub> channel subunit (<i>KCNJ11)</i> gene, has been linked to increased risk of type 2 diabetes. Understanding the risk-allele-specific pathogenesis has the potential to improve personalized diabetes treatment, but the underlying mechanism has remained elusive. Using a genetically engineered mouse model, we now show that the K23 variant impairs glucose-induced insulin secretion and increases diabetes risk when combined with a high fat diet (HFD) and obesity. K<sub>ATP</sub>-channels in beta cells with two K23 risk alleles (KK) showed decreased ATP inhibition and the threshold for glucose-stimulated insulin secretion from KK islets was increased. Consequently, the insulin response to glucose and glycaemic control were impaired in KK mice on a standard diet. On a HFD, the effects of the KK genotype were exacerbated, accelerating diet-induced diabetes progression and causing beta cell failure. We conclude that the K23 variant increases diabetes risk by impairing insulin secretion at threshold glucose levels, thus accelerating loss of beta cell function in the early stages of diabetes progression.

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