China
Africa
Explore chapters and articles related to this topic
Beta Cells and Diabetes
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nutraceuticals and Dietary Supplements, 2020
Shivani Srivastava, Durgavati Yadav, Kumar Sandeep, Harsh Pandey, Surya Kumar Singh, Yamini Bhusan Tripathi
Nuclear accumulation of Foxo1 is induced by AGEs, which leads to the downregulation of Pdx-1 expression at post-translational level via reducing its protein stability, ultimately leads to decreased synthesis of insulin in pancreatic β-cell (Shu et al., 2011).
Islet Transplantation in Type 1 Diabetes: Stem Cell Research and Therapy
Published in Debarshi Kar Mahapatra, Sanjay Kumar Bharti, Medicinal Chemistry with Pharmaceutical Product Development, 2019
DE then forms a primitive gut tube (GT) along which various endoderm organ domains are specified and directed [32]. Pancreas develops from the posterior foregut, emerging as buds from dorsal and ventral sides of the gut tube. At this early stage pancreatic development depends on retinoid signaling and inhibition of hedgehog signaling [33, 34]. The developing pancreas at this stage consists of epithelial progenitors that express Pdx1 (IPF1) and give rise to endocrine, exocrine and ductal cells of the pancreas. Moreover, this epithelium also expresses transcription factor genes such as Hlxb9, Hnf6, Ptf1a, and Nkx6-1. These transcription factors together with Pdx1 encode proteins that contribute to pancreatic development [35]. After initial bud formation, the epithelium grows, proliferates and differentiates in response to signals emanating from adjacent mesenchyme such as mesenchymal Fgf10 [36]. In addition to transcription factors, several growth factors regulate the process of gastrulation. For example, in mice Nodal, a member of transforming growth factor (TGF)-β super family, which, in turn, regulates the Wnt, fibroblast growth factor (FGF) and bone morphogenetic protein-4 (BMP-4) pathways that is important for development of anterior and posterior axes during gastrulation [31, 37].
Congenital Anomalies of the Pancreas
Published in John F. Pohl, Christopher Jolley, Daniel Gelfond, Pediatric Gastroenterology, 2014
Kathy D. Chen, Sohail Z. Husain
Both pancreatic agenesis and hypoplasia (OMIM #260370) are rare findings which are described in case reports and have been described alone or in association with other congenital abnormalities. The syndrome results from a more global defect in pancreatic development. Some cases are linked to homozygous or compound heterozygous mutations in the pancreatic and duodenal homeobox (PDX1) gene, also known as insulin promoter factor-1. Patients have both exocrine and endocrine deficiencies. Infants present with neonatal insulin-dependent diabetes mellitus, intrauterine growth retardation, subsequent failure to thrive from pancreatic insufficiency, and they require pancreatic enzyme replacement therapy. Imaging with ultrasound or CT scan can reveal absence of pancreatic tissue.
Jiedutongluotiaogan formula restores pancreatic function by suppressing excessive autophagy and endoplasmic reticulum stress
Published in Pharmaceutical Biology, 2022
Jinli Luo, Wenqi Jin, Meiying Jin, Weiwei Pan, Shengnan Gao, Xiaohua Zhao, Xingrong Lai, Liwei Sun, Chunli Piao
Then, we investigated the effects of JTTF on insulin secretion by injured INS-1 cells by using an ELISA kit. LPS exposure reduced INS-1 cell insulin content, while JTTF treatment exerted a potent insulinotropic effect on INS-1 cells (Figure 6(a)). The level of insulin secretion by INS-1 cells after treatment with JTTF at all tested concentrations was increased as compared to that of the LPS-only group, with the greatest effect observed for 200 µg/mL JTTF (Figure 6(b)). PDX1, a homeodomain transcription factor, is required for early embryonic development of the pancreas (Stoffers et al. 1997). In mature beta-cells, depletion and reduction of PDX1 induces glucose intolerance as evidence for a critical role of PDX1 for maintaining beta-cell function (Holland et al. 2002). Our preliminary results showed that JTTF treatment could restore PDX1 expression levels (Figure 6(c)). The expression of mRNA of PDX1, MafA, INS1 and INS2 were upregulated in all four groups (Figure 6(d–g)).
Effects of platelet-rich plasma on the pancreatic islet survival and function, islet transplantation outcome and pancreatic pdx1 and insulin gene expression in streptozotocin-induced diabetic rats
Published in Growth Factors, 2020
Marzieh Nemati, Narges Karbalaei, Pooneh Mokarram, Farzaneh Dehghani
RT-PCR analysis indicated that PRP could have a positive effect on the gene expression of the pancreatic islet pdx1 and insulin that lead to an increase in β-cell insulin content and secretion and amelioration of hyperglycemia in diabetic rats. A possible cause for positive effect of PRP on the gene expression of pdx1 and insulin can be related to various factors released from platelet of PRP specially growth factors. Effects of some growth factors on pdx1 and insulin gene expression were examined. It has been shown that treatment of INS-1 cell line with TGF- and pancreatic beta cell with PDGF-AA stimulates the pdx1 and insulin mRNA expression (Sayo et al. 2000; Chang et al. 2016). The combined administration of EGF and gastrin significantly also enhanced the mRNA levels of insulin and pdx1 in experimental Type 1 Diabetic Rats (Yu et al. 2011). Pdx1 plays an essential role in the development of the pancreas, islet differentiation, maintenance of β-cell function, and activation of insulin gene transcription and regulation of adult islet beta cells function and insulin secretion and regulate the islet cell proliferation and apoptosis and regulate the islet cell proliferation and apoptosis (Huang and Tsai 2000; Laybutt et al. 2007; Wu et al. 2017).
Dietary Garcinol Arrests Pancreatic Cancer in p53 and K-ras Conditional Mutant Mouse Model
Published in Nutrition and Cancer, 2018
Nadia Saadat, Sarah Akhtar, Arvind Goja, Nurul H. Razalli, Andreea Geamanu, Doina David, Yimin Shen, Smiti Vaid Gupta
K-ras is constantly turned on in 90% of the cases in PDA while P53 is turned off in 75% of the cases and SMAD 4 or DPC4 (turned off) is mutated in 55% of the cases (18). According to Hruban et al. more advanced PanIN accumulate more mutations and higher instability (21). Higher nuclear cytoplasmic ratio, genomic instability, and abnormal mitosis are all hallmarks of carcinogenesis. KPC mice are K-ras, and p53 conditional mutant mice and with Pdx cre recombinase (k-rasLSL.G12D/+; p53R172H/+; PdxCretg/+). Pdx is a protein expressed during embryonic development of the pancreas. Association with Pdx makes these mutations to appear only in the pancreatic tissue sparing rest of the body. Higher genomic instability, abnormal mitosis, anaphase bridges, and more centrosomes were observed in this model. These mice develop ductal metaplasia, different stages of pancreatic intraepithelial neoplasia, ductal adenocarcinoma, and macro-metastasis (18). Median survival rate is 4.5 month (19). Therefore, PDA in KPC mice resembles human tumors both physiologically and at the molecular level (19). In our study with KPC mice, we observed similar findings with reference to histology and overall presentation of the disease.