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Mannogalactoglucan from mushrooms protects pancreatic islets via restoring UPR and promotes insulin secretion in TIDM mice

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Food Science and Human Wellness 2024年第3期13卷 1390-1401页

作者： Ting Liu Si Chen Yunhe Qu Lujuan Zheng Xiaoxuan Yang Shuhan Men Yuanning Wang Hanrui Ma Yifa Zhou Yuying Fan Engineering Research Center of Glycoconjugates Ministry of EducationJilin Provincial Key Laboratory of Chemistry and Biology of Changbai Mountain Natural DrugsSchool of Life SciencesNortheast Normal UniversityChangchun 130024China

Type 1 diabetes mellitus(T1DM) lacks insulin secretion due to autoimmune deficiency of pancreaticβ-cells.Protecting pancreatic islets and enhancing insulin secretion has been therapeutic approaches.Mannogalactoglucan is the main type of polysaccharide from natural mushroom,which has potential medicinal prospects.Nevertheless,the antidiabetic property of mannogalactoglucan in T1DM has not been fully elucidated.In this study,we obtained the neutral fraction of alkali-soluble Armillaria mellea polysaccharide(AAMP-N) with the structure of mannogalactoglucan from the fruiting body of A.mellea and investigated the potential therapeutic value of AAMP-N in T1DM.We demonstrated that AAMP-N lowered blood glucose and improved diabetes symptoms in T1DM mice.AAMP-N activated unfolded protein response(UPR) signaling pathway to maintain ER protein folding homeostasis and promote insulin secretion in vivo.Besides that,AAMP-N promoted insulin synthesis via upregulating the expression of transcription factors,increased Ca^(2+) signals to stimulate intracellular insulin secretory vesicle transport via activating calcium/calmodulin-dependent kinase Ⅱ(CamkⅡ) and cAMP/PKA signals,and enhanced insulin secretory vesicle fusion with the plasma membrane via vesicle-associated membrane protein 2(VAMP2).Collectively,these studies demonstrated that the therapeutic potential of AAMP-N on pancreatic islets function,indicating that mannogalactoglucan could be natural nutraceutical used for the treatment of T1DM.

关键词： Mannogalactoglucan Mushroom Pancreatic islets insulin secretion insulin synthesis Unfolded protein response(UPR) Type 1 diabetes mellitus(T1DM)

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Neurotransmitters regulateβcells insulin secretion:A neglected factor

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世界临床病例杂志 2023年第28期11卷 6670-6679页

作者： Chu-Chu Kong Ji-Dong Cheng Wei Wang Department of Endocrinology Xiang’an Hospital of Xiamen UniversitySchool of MedicineXiamen UniversityXiamen 361100Fujian ProvinceChina

βcells are the main cells responsible for the hypoglycemic function of pancreatic islets,and the insulin secreted by these cells is the only hormone that lowers blood glucose levels in the human body.βcells are regulated by various factors,among which neurotransmitters make an important contribution.This paper discusses the effects of neurotransmitters secreted by various sympathetic and parasympathetic nerves onβcells and summarizes the mechanisms by which various neurotransmitters regulate insulin secretion.Many neurotransmitters do not have a single source and are not only released from nerve terminals but also synthesized byβcells themselves,allowing them to synergistically regulate insulin secretion.Almost all of these neurotransmitters depend on the presence of glucose to function,and their actions are mostly related to the Ca^(2+)and cAMP concentrations.Although neurotransmitters have been extensively studied,many of their mechanisms remain unclear and require further exploration by researchers.

关键词： βcells insulin secretion Neurology Type 2 diabetes Islet

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Effects of supraphysiologic concentration glucose on pancreatic duodenal homeobox-1 expression and insulin secretion in rats

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Chinese Medical Journal 2007年第11期120卷 1020-1023页

作者： XIAO Chang-qing DENG Hong-ming HUANG Yun Diabetic Centre First Affiliated Hospital Guangxi Medical University Nanning 530021 China

The islet transcription factor pancreatic duodenal homeobox-1 （PDX-1, also known as insulin promoter factor-1 or IPF-1） is an orphan homeodomain protein that plays an important role in the development, proliferation, differentiation and maturation of pancreatic cells. It is initially detected in the part of the dorsal and ventral primitive gut epithelium that later develops into the pancreas in embryonic period. In adults, its expression is found predominantly in the differentiated islet beta-cells. A recent study shows that PDX-1 is a major islet transcription factor which activates insulin gene transcription.1 Glucose-induced insulin biosynthesis is concerned with some motifs in insulin gene promoter, and PDX-1 activates insulin gene transcription and biosynthesis through binding to these motifs. Targeted inactivation of PDX-1 gene in the mice as well as its mutation in humans2 results in agenesis of the pancreas.

关键词： pancreatic duodenal homeobox-1 insulin secretion islet cells glucose

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Roles of sulfonylurea receptor 1 and multidrug resistance protein 1 in modulating insulin secretion in human insulinoma

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Hepatobiliary & Pancreatic Diseases International 2011年第1期10卷 88-94页

作者： Cheng-Jiang Li,Hua-Li Zhou,Jun Li,Hong-Tian Yao,Rong Su and Wen-Peng Li Department of Endocrinology(Li CJ,Zhou HL and Li WP),Department of Pathology,and Key Laboratory of Multi-organ Transplantation of Ministry of Public Health,First Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310003,China Department of Endocrinology First Affiliated Hospital Zhejiang University School of Medicine Hangzhou 310003 China Department of Pathology First Affiliated Hospital Zhejiang University School of Medicine Hangzhou 310003 China Key Laboratory of Multi-organ Transplantation of Ministry of Public Health First Affiliated Hospital Zhejiang University School of Medicine Hangzhou 310003 China

BACKGROUND:Sulfonylurea receptor 1(SUR1)and multidrug resistance protein 1(MRP1)are two prominent members of multidrug resistance proteins associated with insulin secretion. The aims of this study were to investigate their expression in insulinomas and their sole and synergistic effects in modulating abnormal insulin secretion. METHODS:Fasting glucose,insulin and C-peptide were measured in 11 insulinoma patients and 11 healthy controls. Prolonged oral glucose tolerance tests were performed in 6 insulinoma patients.insulin content,SUR1 and MRP1 were detected in 11 insulinoma patients by immunohistochemistry. SUR1 and MRP1 were also detected in 6 insulinoma patients by immunofluorescence. RESULTS:insulinoma patients presented the typical demons-trations of Whipple’s triad.Fasting glucose of each insulinoma patient was lower than 2.8 mmol/L,and simultaneous insulin and C-peptide were increased in insulinoma patients. Prolonged oral glucose tolerance tests showed that insulin secretion in insulinoma patients were also stimulated by high glucose.Immunohistochemistry and immunofluorescence staining showed that SUR1 increased,but MRP1 decreased in insulinoma compared with the adjacent islets. CONCLUSIONS:The hypersecretion of insulin in insulinomas might be,at least partially,due to the enrichment of SUR1. In contrast,MRP1,which is down-regulated in insulinomas, might reflect a negative feedback in insulin secretion.

关键词： sulfonylurea receptor 1 multidrug resistance protein 1 ATP-binding cassette transporters insulinoma insulin secretion

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Vascular endothelial growth factor B inhibits insulin secretion in MIN6 cells and reduces Ca2+ and cyclic adenosine monophosphate levels through PI3K/AKT pathway

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World Journal of Diabetes 2021年第4期12卷 480-498页

作者： Jing-Dan Jia Wen-Guo Jiang Xu Luo Rong-Rong Li Yu-Chi Zhao Geng Tian Ya-Na Li Department of Pathophysiology School of Basic MedicineBinzhou Medical UniversityYantai 264003Shandong ProvinceChina Department of Pharmacy Binzhou Medical UniversityYantai 264003Shandong ProvinceChina Department of Surgery Yantaishan HospitalYantai 264001Shandong ProvinceChina

BACKGROUND Type 2 diabetes(T2 D) is characterized by insufficient insulin secretion caused by defective pancreatic β-cell function or insulin resistance,resulting in an increase in blood glucose.However,the mechanism involved in this lack of insulin secretion is unclear.The level of vascular endothelial growth factor B(VEGF-B) is significantly increased in T2 D patients.The inactivation of VEGF-B could restore insulin sensitivity in db/db mice by reducing fatty acid accumulation.It is speculated that VEGF-B is related to pancreatic β-cell dysfunction and is an important factor affecting β-cell secretion of insulin.As an in vitro model of normal pancreatic β-cells,the MIN6 cell line can be used to analyze the mechanism of insulin secretion and related biological effects.AIM To study the role of VEGF-B in the insulin secretion signaling pathway in MIN6 cells and explore the effect of VEGF-B on blood glucose regulation.METHODS The MIN6 mouse pancreatic islet β-cell line was used as the model system.By administering exogenous VEGF-B protein or knocking down VEGF-B expression in MIN6 cells,we examined the effects of VEGF-B on insulin secretion,Ca2+ and cyclic adenosine monophosphate(cAMP) levels,and the insulin secretion signaling pathway.RESULTS Exogenous VEGF-B inhibited the secretion of insulin and simultaneously reduced the levels of Ca2+ and cAMP in MIN6 cells.Exogenous VEGF-B also reduced the expression of phospholipase C gamma 1(PLCγ1),phosphatidylinositol 3-kinase(PI3 K),serine/threonine kinase(AKT),and other proteins in the insulin secretion pathway.Upon knockdown of VEGF-B,MIN6 cells exhibited increased insulin secretion and Ca2+ and cAMP levels and upregulated expression of PLCγ1,PI3 K,AKT,and other proteins.CONCLUSION VEGF-B can regulate insulin secretion by modulating the levels of Ca2+ and cAMP.VEGF-B involvement in insulin secretion is related to the expression of PLCγ1,PI3 K,AKT,and other signaling proteins.These results provide theoretical support and an experimental basis for the study of VEGF-B in t

关键词： Type 2 diabetes insulin secretion MIN6 cells Vascular endothelial growth factor B Blood glucose regulation

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Regulation of insulin secretion and Expression of SUR1 Gene by Chronic Exposure to Free Fatty Acids in Rat Pancreatic β Cells

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2004年第4期24卷 358-360,364页

作者：袁莉邓秀玲陈璐璐周愍 Department of Endocrinology Union Hospital Tongji Medical College Huazhong University of Science and Technology

To study the effects of free fatty acids on insulin secretion and expression of SUR1 gene in rat pancreatic B cells in vitro, and to explore the molecular mechanisms in lipotoxicity inducing insulin secretion dysfunction, pancreatic islet cells were isolated and digested from male SD rats. Purified islets were incubated with either 0.25 mmol/L palmitate or 0.125 mmol/L oleate for 48 h in vitro. Then islets were stimulated with either 5.6 mmol/L or 16.7 mmol/L glucose for 1 h. insulin release was measured by using radioimmunoassay, and the expression of SUR1 gene mRNA was quantified by reserve transcription-polymerase chain reaction (RT-PCR). The islets exposed to both palmitate and oleate for 48 h showed an increased basal and a decreased glucose-indused insulin release as compared with control islets. Palmitate increased basal insulin secretion by 110 % (Pinsulin secretion by 43 % (Pinsulin secretion by 80 % (Pinsulin secretion by 32 % (P0.05) of SUR1 gene expression. Our results suggested that chronic exposure to free fatty acids of pancreatic β cells inhibited glucose stimulated insulin secretion. Regulation of SUR1 gene expression may be involved in such effects, which may also be one of the molecular mechanisms in lipotoxocity inducing β cells secretion dysfunction.

关键词： fatty acids insulin secretion sulfonylurea receptor

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GENERATION OF TRANSGENIC MICE FOR IN VIVO DETECTION OF insulin-CONTAINING GRANULE EXOCYTOSIS AND QUANTIFICATION OF insulin secretion

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Journal of Innovative Optical Health Sciences 2009年第4期2卷 397-405页

作者： JINLING LU NATALIA GUSTAVSSON QIMING LI GEORGE KRADDA THOMAS C.SUUDHOF WEIPING HAN Laboratory of Metabolic Medicine Singapore Bioimaging Consortium A*STAR Singapore 138667 Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute Stanford University School of Medicine Palo Alto CA 94304USA Department of Biochemistry Yong Loo Lin School of Medicine National University of Singapore Singapore 117597

insulin secretion is a complex and highly regulated process.Although much progress has been made in understanding the cellular mechanisms of insulin secretion and regulation,it remains unclear how conclusions from these studies apply to living animals.That few studies have been done to address these issues is largely due to the lack of suitable tools in detecting secretory events at high spatial and temporal resolution in vivo.When combined with genetically encoded biosensor,optical imaging is a powerful tool for visualization of molecular events in vivo.In this study,we generated a DNA construct encoding a secretory granule resident protein that is linked with two spectrally separate fluorescent proteins,a highly pH-sensitive green pHluorin on the intra-granular side and a red mCherry in the cytosol.Upon exocytosis of secretory granules,the dim pHluorin inside the acidic secretory granules became highly fluorescent outside the cells at neutral pH,while mCherry fluorescence remained constant in the process,thus allowing ratiometric quantification of insulin secretory events.Furthermore,mCherry fluorescence enabled tracking the movement of secretory granules in living cells.We validated this approach in insulin-secreting cells,and generated a transgenic mouse line expressing the optical sensor specifically in pancreaticβ-cells.The transgenic mice will be a useful tool for future investigations of molecular mechanism of insulin secretion in vitro and in vivo.

关键词： insulin secretion diabetes optical imaging secretory granule exocytosis.

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Muscadine or amla extracts standardized to ellagic acid content ameliorate glucolipotoxicity associatedβ-cell dysfunction via inhibition of IL-1βand improved insulin secretion

食物生产加工与营养(英文)

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食物生产加工与营养(英文) 2020年第1期2卷 91-101页

作者： Srikanth Earpina Karen McDonough Millicent Yeboah-Awudzi Kristina J.Cook Sita Aggarwal Jack N.Losso Chronic Degenerative Disease Prevention Laboratory School of Nutrition and Food ScienceLouisiana State University AgCenterLouisiana State University SystemBaton RougeLA 70803USA School of Animal Science Louisiana State University AgCenterLouisiana State University SystemBaton RougeLA 70803USA William Hansel Cancer Prevention Pennington Biomedical Research CenterLouisiana State University SystemBaton RougeLA 70808USA Louisiana State University System Baton RougeLA 70803USA

Glucolipotocixity induces IL-1βsecretion which impairs pancreaticβ-cell insulin secretion.Ellagic acid and urolithin A have strong anti-inflammatory effect on cells.Muscadine and amla are very good sources of ellagic acid.The present study examined the effect of ellagic acid,ellagic acid-rich muscadine or amla extract,or urolothin A on inflammation inβcells under glucolipotoxic conditions.Rat NIT-1βcells were incubated in glucolipotoxic conditions(33.3 mM glucose,250μM palmitic acid or 33.3 mM glucose+250μM palmitic acid with or without ellagic acid,ellagic acid-rich muscadine or amla extracts standardized to its ellagic acid content,or urolithin A).Inflammatory status was evidenced by ELISA analysis of insulin and IL-1βsecretion.Ellagic acid-rich muscadine or amla extracts dose-dependently stimulated insulin secretion and down-regulated IL-1βbetter than pure ellagic acid,or urolithin A.Urolithin A did not statistically stimulate insulin secretion and did not inhibit IL-1β.

关键词： Muscadine Amla Ellagic acid NIT-1 pancreaticβ-cells glucose,Palmitic acid Glucolipotoxicity IL-1β Inflammation Inflammasome insulin secretion

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Short-Term Effects of Liraglutide versus Vildagliptin on insulin secretion and Sensitivity in Type 2 Diabetes: A Single Blinded Randomized Controlled Trial (LIRAVIS Study)

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Journal of Diabetes Mellitus 2023年第1期13卷 45-57页

作者： Martine Claude Etoa Etoga Estelle Amandine Well Simeon Pierre Choukem Mesmin Dehayem Francine Mendane Mekobe Anne Boli Ongmeb Astasselbe Hadja Inna Jean Claude Mbanya Eugene Sobngwi National Obesity Center Yaoundé Central Hospital Yaoundé Cameroon Department of Internal Medicine and Specialties Faculty of Medicine and Biomedical Sciences University of Yaoundé 1 Yaoundé Cameroon Department of Internal Medicine Faculty of Medicine and Pharmaceutical Sciences University of Dschang Dschang Cameroon Health and Human Development (2HD) Research Network Douala Cameroon Internal Medicine Essos Hospital Centre Yaoundé Cameroon Faculty of Health Sciences University of Bamenda Bamenda Cameroon Department of Internal Medicine Faculty of Medicine and Biomedical Sciences University of Garoua Garoua Cameroon Laboratory of Molecular Medicine and Metabolism Biotechnology Center University of Yaoundé 1 Yaoundé Cameroon

Background: We aimed to evaluate the short-term metabolic effects of a GLP-1a, (liraglutide) versus a DPP-4i, (vildagliptin) in a group of sub-Saharan type 2 diabetes patients. Methods: We conducted a randomized controlled single blinded clinical trial in 14 uncontrolled type 2 diabetes patients (HbA1c ≥ 53 mmol/mol) with mean duration of diabetes of 8 [1 - 12] years and median age of 57 [49 - 61] years. Baseline treatment consisted of metformin in monotherapy or metformin plus sulfonylureas. Participants were randomly allocated to 2 groups of add-on 1.2 mg/day subcutaneous liraglutide in group 1 or 100 mg/day of oral vildagliptin in group 2 for 2 weeks. In all participants, insulin secretion in response to mixed meal tolerance test, insulin sensitivity by 80 mU/m2/min hyperinsulinemic-euglycemic clamp, body composition, and lipid profile were measured before and after intervention. Results: At the end of intervention, insulin sensitivity remained unchanged both with liraglutide from 6.6 [4.2 - 7.9] to 6.9 [4.3 - 10.8] mg/kg/min;p = 0.61 and vildagliptin from 7.1 [5.3 - 9.0] to 6.5 [5.6 - 9.4] mg/kg/min (p = 0.86). The area under the C-peptide curve varied from 5.5 [1.0 - 10.9] to 14.9 [10.8 - 17.2] nmol/L/120min, p = 0.09 in group 1 and from 1.1 [0.5 - 14.1] to 13.0 [9.6 - 16.9] nmol/L/120min (p = 0.17) in group 2. LDL Cholesterol levels decreased significantly with liraglutide from 0.85 g/L [0.51 - 1.02] to 0.54 g/L [0.50 - 0.73] (p = 0.04) but not with Vildagliptin. Body weight tended to decrease in group 1 (−0.6 kg) versus modest increase in group 2 (+1.1 kg). Conclusion: Short-term metabolic effects of Liraglutide and Vildagliptin add-on therapy are comparable in sub-Saharan type 2 diabetes patients with a more favorable trend for Liraglutide on body weight, lipid profile, and insulin secretion.

关键词： insulin Sensitivity insulin secretion Liraglutide Vildagliptin Incretinomimetics

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Leptin Regulated insulin secretion via Stimulating IRS2-associated Phosphoinositide 3-kinase Activity in the isolated Rat Pancreatic Islets

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2003年第1期23卷 13-15,31页

作者：袁莉安汉祥李卓娅邓秀玲 Department of Endocrinology Xiehe Hospital Tongji Medical College Huazhong University of Science and Technology Cancer Research Center in Germany 69120 Heidelberg Department of Immunology School of Basic Medical Sciences Tongji Medical College Huazhong University of Science and Technology

To investigate the molecular mechanism of leptin regulating insulin secretion through determining the regulation of insulin secretion and the insulin receptor substrate (IRS)-2-associated phosphoinositide 3-kinase (PI3K) activity by leptin in the isolated rat pancreatic islets, pancreatic islets were isolated from male SD rats by the collagenase method. The purified islets were incubated with leptin 2 nmol/L for 1 h in the presence of 5.6 mmol/L or 11.1 mmol/L glucose. insulin release was measured using radioimmunoassay. IRS-2-associated activity of PI3K was determined by immunoprecipitate assay and Western blot. The results showed that in the presence of 5.6 mmol/L glucose, leptin had no significant effect on both insulin secretion and IRS-2-associated PI3K activity, but in the presence of 11.1 mmol/L glucose, insulin release was significantly inhibited after the islets were exposed to leptin for 1 h (Pinsulin release (Pinsulin secretion in the presence of 11.1 mmol/L glucose by stimulating IRS-2-associated activity of PI3K, which might be the molecular mechanism of leptin regulating insulin secretion.

关键词： leptin insulin secretion phosphoinositide 3-kinase signal transduction

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