scholarly journals Therapy of experimental type 1 diabetes by isolated Sertoli cell xenografts alone

2009 ◽  
Vol 206 (11) ◽  
pp. 2511-2526 ◽  
Author(s):  
Francesca Fallarino ◽  
Giovanni Luca ◽  
Mario Calvitti ◽  
Francesca Mancuso ◽  
Claudio Nastruzzi ◽  
...  
Keyword(s):  
Immune Tolerance ◽  
Cell Function ◽  
Type I Diabetes ◽  
Nod Mice ◽  
Surrounding Tissue ◽  
Main Task ◽  
Type I ◽  
Β Cell ◽  
Β Cell Function ◽  
Experimental Type

Type I diabetes mellitus is caused by autoimmune destruction of pancreatic β cells, and effective treatment of the disease might require rescuing β cell function in a context of reinstalled immune tolerance. Sertoli cells (SCs) are found in the testes, where their main task is to provide local immunological protection and nourishment to developing germ cells. SCs engraft, self-protect, and coprotect allogeneic and xenogeneic grafts from immune destruction in different experimental settings. SCs have also been successfully implanted into the central nervous system to create a regulatory environment to the surrounding tissue which is trophic and counter-inflammatory. We report that isolated neonatal porcine SC, administered alone in highly biocompatible microcapsules, led to diabetes prevention and reversion in the respective 88 and 81% of overtly diabetic (nonobese diabetic [NOD]) mice, with no need for additional β cell or insulin therapy. The effect was associated with restoration of systemic immune tolerance and detection of functional pancreatic islets that consisted of glucose-responsive and insulin-secreting cells. Curative effects by SC were strictly dependent on efficient tryptophan metabolism in the xenografts, leading to TGF-β–dependent emergence of autoantigen-specific regulatory T cells and recovery of β cell function in the diabetic recipients.

Effects of insulin administration on β-cell function in subjects at high risk for type I diabetes mellitus

Metabolism ◽  
1996 ◽  
Vol 45 (7) ◽  
pp. 873-875 ◽  
Author(s):  
C. Rodríguez-Villar ◽  
I. Conget ◽  
J.M. González-Clemente ◽  
J. Vidal ◽  
P. Navarro ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
High Risk ◽  
Cell Function ◽  
Type I Diabetes ◽  
Type I Diabetes Mellitus ◽  
Type I ◽  
Insulin Administration ◽  
Β Cell ◽  
Β Cell Function

scholarly journals Association of Insulin Resistance and β-cell Function With Bone Turnover Biomarkers in Dysglycemia Patients

2021 ◽  
Vol 12 ◽  
Author(s):  
Hui Guo ◽  
Chiyu Wang ◽  
Boren Jiang ◽  
Shaohong Ge ◽  
Jian Cai ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Bone Turnover ◽  
Type I Collagen ◽  
Cell Function ◽  
Cross Sectional Study ◽  
Type I ◽  
Model Assessment ◽  
Β Cell ◽  
Cross Sectional ◽  
Β Cell Function

BackgroundThe interrelation between glucose and bone metabolism is complex and has not been fully revealed. This study aimed to investigate the association between insulin resistance, β-cell function and bone turnover biomarker levels among participants with abnormal glycometabolism.MethodsA total of 5277 subjects were involved through a cross-sectional study (METAL study, http://www.chictr.org.cn, ChiCTR1800017573) in Shanghai, China. Homeostasis model assessment of insulin resistance (HOMA-IR) and β-cell dysfunction (HOMA-%β) were applied to elucidate the nexus between β-C-terminal telopeptide (β-CTX), intact N-terminal propeptide of type I collagen (P1NP) and osteocalcin (OC). β-CTX, OC and P1NP were detected by chemiluminescence.ResultsHOMA-IR was negatively associated with β-CTX, P1NP and OC (regression coefficient (β) -0.044 (-0.053, -0.035), Q4vsQ1; β -7.340 (-9.130, -5.550), Q4vsQ1 and β -2.885 (-3.357, -2.412), Q4vsQ1, respectively, all P for trend <0.001). HOMA-%β was positively associated with β-CTX, P1NP and OC (β 0.022 (0.014, 0.031), Q4vsQ1; β 6.951 (5.300, 8.602), Q4vsQ1 and β 1.361 (0.921, 1.800), Q4vsQ1, respectively, all P for trend <0.001).ConclusionsOur results support that lower bone turnover biomarker (β-CTX, P1NP and OC) levels were associated with a combination of higher prevalence of insulin resistance and worse β-cell function among dysglycemia patients. It is feasible to detect bone turnover in diabetes or hyperglycemia patients to predict the risk of osteoporosis and fracture, relieve patients’ pain and reduce the expenses of long-term cure.

Effect of porcine gastric inhibitory polypeptide on β-cell function in type I and type II diabetes mellitus

Metabolism ◽  
1987 ◽  
Vol 36 (7) ◽  
pp. 677-682 ◽  
Author(s):  
Thure Krarup ◽  
Nina Saurbrey ◽  
Alister J. Moody ◽  
Claus Kühl ◽  
Sten Madsbad
Keyword(s):  
Diabetes Mellitus ◽  
Type Ii Diabetes ◽  
Cell Function ◽  
Gastric Inhibitory Polypeptide ◽  
Type Ii Diabetes Mellitus ◽  
Type I ◽  
Type Ii ◽  
Β Cell ◽  
Β Cell Function

scholarly journals Metabolic Endotoxemia-Activated Macrophages Promote Pancreatic β Cell Death via IFNβ-Xaf1 Pathway

2017 ◽  
Vol 50 (02) ◽  
pp. 160-167 ◽  
Author(s):  
Mitsudai Tsuruta ◽  
Misaki Iwashita ◽  
Takanori Shinjo ◽  
Hiroaki Matsunaga ◽  
Akiko Yamashita ◽  
...  
Keyword(s):  
Cell Line ◽  
Cell Apoptosis ◽  
Cell Function ◽  
Type I ◽  
Β Cells ◽  
Β Cell ◽  
Genes Expression ◽  
Exogenous Addition ◽  
Β Cell Function ◽  
Metabolic Endotoxemia

AbstractMetabolic endotoxemia has been implicated in the pathogenesis of type 2 diabetes. In addition to adipose tissue inflammation, inflammatory cell infiltration is also observed in islets, although its effect on islets is largely unknown. We hypothesized that macrophage infiltration into islets leads to impairment of α or β cell function, which ultimately act to exacerbate the pathophysiology of diabetes. Gene expression in a murine α cell line, αTC1, and β cell line, βTC6, was investigated by DNA microarray after co-culturing the cells with a murine macrophage cell line, RAW 264.7, in the presence or absence of bacterial endotoxin. Among the genes showing highly upregulated expression, genes specifically upregulated only in β cells were evaluated to determine the roles of the gene products on the cellular function of β cells. In both α and β cells, expression of type I interferon-responsive genes was highly upregulated upon endotoxin stimulation. Among these genes, expression of the X-linked inhibitor of apoptosis (Xiap)-associated factor 1 (Xaf1) gene, which is associated with the induction of apoptosis, was specifically enhanced in β cells by endotoxin stimulation. This upregulation appeared to be mediated by macrophage-derived interferon β (IFNβ), as endotoxin-stimulated macrophages produced higher amounts of IFNβ, and exogenous addition of IFNβ into βTC6 cultures resulted in increased Xaf1 protein production and cleaved caspase 3, which accelerated β-cell apoptosis. Macrophages activated by metabolic endotoxemia infiltrated into islets and produced IFNβ, which induced β-cell apoptosis by increasing the expression of Xaf1.

scholarly journals Glucose and Inflammation Control Islet Vascular Density and β-Cell Function in NOD Mice

Diabetes ◽  
2011 ◽  
Vol 60 (3) ◽  
pp. 876-883 ◽  
Author(s):  
Eitan M. Akirav ◽  
Maria-Teresa Baquero ◽  
Lynn W. Opare-Addo ◽  
Michael Akirav ◽  
Eva Galvan ◽  
...  
Keyword(s):  
Cell Function ◽  
Nod Mice ◽  
Vascular Density ◽  
Β Cell ◽  
Β Cell Function

Adipokines as key players in β cell function and failure

2019 ◽  
Vol 133 (22) ◽  
pp. 2317-2327 ◽  
Author(s):  
Nicolás Gómez-Banoy ◽  
James C. Lo
Keyword(s):  
Metabolic Diseases ◽  
Cell Function ◽  
Whole Body ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Axis ◽  
Β Cell Function ◽  
Prevalence Of Obesity ◽  
Specific Factors ◽  
Whole Body Metabolism

Abstract The growing prevalence of obesity and its related metabolic diseases, mainly Type 2 diabetes (T2D), has increased the interest in adipose tissue (AT) and its role as a principal metabolic orchestrator. Two decades of research have now shown that ATs act as an endocrine organ, secreting soluble factors termed adipocytokines or adipokines. These adipokines play crucial roles in whole-body metabolism with different mechanisms of action largely dependent on the tissue or cell type they are acting on. The pancreatic β cell, a key regulator of glucose metabolism due to its ability to produce and secrete insulin, has been identified as a target for several adipokines. This review will focus on how adipokines affect pancreatic β cell function and their impact on pancreatic β cell survival in disease contexts such as diabetes. Initially, the “classic” adipokines will be discussed, followed by novel secreted adipocyte-specific factors that show therapeutic promise in regulating the adipose–pancreatic β cell axis.

Effects of Ovariectomy on Insulin Resistance and β-Cell Function and Mass

2004 ◽  
Vol 9 (4) ◽  
pp. 367-373
Author(s):  
Soo-Bong Choi ◽  
Chun-Hee Park ◽  
Dong-Wha Jun ◽  
Jin-Sun Jang ◽  
Sun-Min Park
Keyword(s):  
Insulin Resistance ◽  
Cell Function ◽  
Β Cell ◽  
Β Cell Function
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