scholarly journals The Angiotensin-(1–7)/Mas Axis Improves Pancreatic β-Cell Function in Vitro and in Vivo

Endocrinology ◽  
2016 ◽  
Vol 157 (12) ◽  
pp. 4677-4690 ◽  
Author(s):  
Anika Sahr ◽  
Carmen Wolke ◽  
Jonas Maczewsky ◽  
Peter Krippeit-Drews ◽  
Anja Tetzner ◽  
...  
Keyword(s):  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Β Cell Function

Lipid-induced pancreatic β-cell dysfunction: focus on in vivo studies

2011 ◽  
Vol 300 (2) ◽  
pp. E255-E262 ◽  
Author(s):  
Adria Giacca ◽  
Changting Xiao ◽  
Andrei I. Oprescu ◽  
Andre C. Carpentier ◽  
Gary F. Lewis
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Secretion ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Β Cell Function

The phenomenon of lipid-induced pancreatic β-cell dysfunction (“lipotoxicity”) has been very well documented in numerous in vitro experimental systems and has become widely accepted. In vivo demonstration of β-cell lipotoxicity, on the other hand, has not been consistently demonstrated, and there remains a lack of consensus regarding the in vivo effects of chronically elevated free fatty acids (FFA) on β-cell function. Much of the disagreement relates to how insulin secretion is quantified in vivo and in particular whether insulin secretion is assessed in relation to whole body insulin sensitivity, which is clearly reduced by elevated FFA. By correcting for changes in in vivo insulin sensitivity, we and others have shown that prolonged elevation of FFA impairs β-cell secretory function. Prediabetic animal models and humans with a positive family history of type 2 diabetes are more susceptible to this impairment, whereas those with severe impairment of β-cell function (such as individuals with type 2 diabetes) demonstrate no additional impairment of β-cell function when FFA are experimentally raised. Glucolipotoxicity (i.e., the combined β-cell toxicity of elevated glucose and FFA) has been amply demonstrated in vitro and in some animal studies but not in humans, perhaps because there are limitations in experimentally raising plasma glucose to sufficiently high levels for prolonged periods of time. We and others have shown that therapies directed toward diminishing oxidative stress and ER stress have the potential to reduce lipid-induced β-cell dysfunction in animals and humans. In conclusion, lipid-induced pancreatic β-cell dysfunction is likely to be one contributor to the complex array of genetic and metabolic insults that result in the relentless decline in pancreatic β-cell function in those destined to develop type 2 diabetes, and mechanisms involved in this lipotoxicity are promising therapeutic targets.

scholarly journals Islet-on-a-chip for the study of pancreatic β-cell function

2021 ◽  
Author(s):  
Júlia Rodríguez-Comas ◽  
Javier Ramón-Azcón
Keyword(s):  
Cell Biology ◽  
Cell Function ◽  
Public Health Problem ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Technological Advances ◽  
Significant Public Health ◽  
Β Cell Function

AbstractDiabetes mellitus is a significant public health problem worldwide. It encompasses a group of chronic disorders characterized by hyperglycemia, resulting from pancreatic islet dysfunction or as a consequence of insulin-producing β-cell death. Organ-on-a-chip platforms have emerged as technological systems combining cell biology, engineering, and biomaterial technological advances with microfluidics to recapitulate a specific organ’s physiological or pathophysiological environment. These devices offer a novel model for the screening of pharmaceutical agents and to study a particular disease. In the field of diabetes, a variety of microfluidic devices have been introduced to recreate native islet microenvironments and to understand pancreatic β-cell kinetics in vitro. This kind of platforms has been shown fundamental for the study of the islet function and to assess the quality of these islets for subsequent in vivo transplantation. However, islet physiological systems are still limited compared to other organs and tissues, evidencing the difficulty to study this “organ” and the need for further technological advances. In this review, we summarize the current state of islet-on-a-chip platforms that have been developed so far. We recapitulate the most relevant studies involving pancreatic islets and microfluidics, focusing on the molecular and cellular-scale activities that underlie pancreatic β-cell function.

Tributyltin exposure at noncytotoxic doses dysregulates pancreatic β-cell function in vitro and in vivo

2017 ◽  
Vol 91 (9) ◽  
pp. 3135-3144 ◽  
Author(s):  
Ya-Wen Chen ◽  
Kuo-Cheng Lan ◽  
Jing-Ren Tsai ◽  
Te-I Weng ◽  
Ching-Yao Yang ◽  
...  
Keyword(s):  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Β Cell Function

scholarly journals Impact of in vitro heavy metal exposure on pancreatic β-cell function

2018 ◽  
Vol 299 ◽  
pp. 137-144 ◽  
Author(s):  
E. Nicole Dover ◽  
Naishal Y. Patel ◽  
Miroslav Stýblo
Keyword(s):  
Heavy Metal ◽  
Cell Function ◽  
Metal Exposure ◽  
Pancreatic Β Cell ◽  
Heavy Metal Exposure ◽  
Β Cell ◽  
Β Cell Function

scholarly journals The Estrogenic Effect of Bisphenol A Disrupts Pancreatic β-Cell Function In Vivo and Induces Insulin Resistance

2006 ◽  
Vol 114 (1) ◽  
pp. 106-112 ◽  
Author(s):  
Paloma Alonso-Magdalena ◽  
Sumiko Morimoto ◽  
Cristina Ripoll ◽  
Esther Fuentes ◽  
Angel Nadal
Keyword(s):  
Insulin Resistance ◽  
Bisphenol A ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Estrogenic Effect ◽  
Β Cell Function

Vitamin D supplementation induces CatG-mediated CD4+ T cell inactivation and restores pancreatic beta-cell function in mice with type 1 diabetes

2021 ◽  
Author(s):  
Xiaoyang Lai ◽  
Xuyang Liu ◽  
Xia Cai ◽  
Fang Zou
Keyword(s):  
Vitamin D ◽  
Type 1 Diabetes ◽  
Beta Cell ◽  
Cell Function ◽  
Pancreatic Beta Cell ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Β Cell Function

Type 1 diabetes (T1D) is a chronic autoimmune disease accompanied by the immune-mediated destruction of pancreatic β-cells. In this study, we aimed to explore the regulatory effects of Vitamin D (VD) supplementation on pancreatic β-cell function by altering the expression of bioinformatically identified cathepsin G (CatG) in T1D model mice. A T1D mouse model was established in non-obese diabetic (NOD) mice, and their islets were isolated and purified. Pancreatic mononuclear cells (MNCs) were collected, from which CD4+ T cells were isolated. The levels of interleukin (IL)-2, IL-10, tumor necrosis factor-α (TNF-α) and interferon-gamma (IFN-γ) in the supernatant of mouse pancreatic tissue homogenate were assessed using ELISA. Immunohistochemistry and TUNEL staining were conducted to evaluate the effects of VD supplementation on pancreatic tissues of T1D mice. The pancreatic beta-cell line MIN6 was used for in vitro substantiation of findings in vivo. VD supplementation reduced glucose levels and improved glucose tolerance in T1D mice. Further, VD supplementation improved pancreatic β-cell function and suppressed immunological and inflammatory reactions in the T1D mice. We documented overexpression of CatG in diabetes tissue samples, and then showed that VD supplementation normalized the islet immune microenvironment through down-regulating CatG expression in T1D mice. Experiments in vitro subsequently demonstrated that VD supplementation impeded CD4+ T activation by down-regulating CatG expression, and thereby enhanced pancreatic β-cell function. Results of the present study elucidated that VD supplementation can down-regulate the expression of CatG and inhibit CD4+ T cell activation, thereby improving β-cell function in T1D.

scholarly journals Integrated In Vivo Quantitative Proteomics and Nutrient Tracing Reveals Age-Related Metabolic Rewiring of Pancreatic β Cell Function

Cell Reports ◽  
2018 ◽  
Vol 25 (10) ◽  
pp. 2904-2918.e8 ◽  
Author(s):  
Matthew Wortham ◽  
Jacqueline R. Benthuysen ◽  
Martina Wallace ◽  
Jeffrey N. Savas ◽  
Francesca Mulas ◽  
...  
Keyword(s):  
Quantitative Proteomics ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Age Related ◽  
Β Cell Function
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