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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
GLUT-2 is essential for GSIS. GLUT-2-dependent glucose-sensing controls pancreatic islet cell mass and function through the nervous system. GSIS and glucose uptake get suppressed by genetic inactivation of GLUT in beta cells of rodents (Thorens, 2015).
Animal Models of Genetic Obesity: Peripheral Tissue Changes
Published in Claude Bouchard, The Genetics of Obesity, 2020
Patricia R. Johnson, Francine Gregoire
The normal insulin secretory response to hyperglycemia is dependent on glucose uptake into P-cells, mediated through the action of the glucose transporter GLUT2.105,106 In db/db mice, as well as in the Zucker substrain ZDF/drt, which is diabetic as well as obese, impaired glucose-stimulated insulin secretion is associated with down-regulation of the normal p-cell glucose transporter, GLUT2. GLUT2 protein and/or GLUT2 mRNA levels were lower than the levels detected in lean controls.105–108 Unger suggests that this down-regulation in GLUT2 expression may be the cause of diabetic hyperglycemia.106,108 However, since the decrease in GLUT2 expression appears to be reversible when islets are placed in nondiabetic conditions,105 this hypothesis may not be substantiated. In addition, this laboratory has obtained results in the WDF strain showing no decrease in GLUT2 mRNA in pancreas of frankly diabetic obese male rats.109 The reasons for these discrepancies between species and strains remain to be established, but at this point it appears unlikely that impaired regulation of insulin secretion associated with obesity and NIDDM can be explained solely by differences in GLUT2 expression.
Genetics of Endocrine Disorders and Diabetes Mellitus
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Bess Adkins Marshall, Abby Solomon Hollander
There is some evidence for a minor role of Glut2 in the etiology of diabetes. A missense mutation (Val197 to Ile) that destroys the transport activity of Glut291 has been identified in 1 of 48 patients with gestational diabetes.92 Studies have shown a possible association between a restriction length polymorphism of Glut2 and NIDDM in a British and a Caucasian population.88,93 But, polymorphism analyses in NIDDM patients from populations of Pima Indians,94 African Americans,90 British Caucasians,95 and MODY patients from French,96 Danish,97 and British97 families show no association of the Glut2 gene with diabetes. Based on all the available data, it appears that Glut2 has a minor role, if any, in the susceptibility to NIDDM or MODY
Streptozotocin mechanisms and its role in rodent models for Alzheimer’s disease
Published in Toxin Reviews, 2023
Mazzura Wan Chik, Nur Adiilah Ramli, Nurul Aqmar Mohamad Nor Hazalin, Gurmeet Kaur Surindar Singh
Along with the pancreas, kidneys, and liver (Grieb 2016), GLUT 2 is also present in the limbic system and plays an important function in the regulation of memory (Spinelli et al. 2019). This causes STZ to exert the same effect on the brain by dysregulation of insulin signaling and affect the neuronal glucose metabolism, which is crucial for energy consumption of the brain (Arluison et al. 2004). However, the mechanisms of STZ on GLUT 2 in the brain is not well understood, and it was not present in the brain of a murine single-cell study (Yuliani et al. 2021). Others proposed that GLUT 2 is poorly expressed in the brain (Shah et al. 2012, Koepsell, 2020). It is more likely that STZ in the brain enter the cells via GLUT 1 and GLUT 3 transporters (Yuliani et al. 2021). It was proposed that in the STZ-treated rat brain, both GLUT 1 and GLUT 3 expression was decreased, leading to a low glucose metabolism. This has resulted in a decreased level of uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) (the microtubule associated protein tau) (Shah et al. 2012). Decreased UDP-GlcNAc affects O-GlcNAcylation and tau O-GlcNAcylation, thereby facilitating hyperphosphorylation of tau, forming toxic tau oligomers and causing cognitive impairment (Deng et al. 2009). The effects of STZ on glucose transporters is summarized in Figure 1.
Cross talk between exosomes and pancreatic β-cells in diabetes
Published in Archives of Physiology and Biochemistry, 2022
One of the major developments in lncRNAs over the past several years is that lncRNAs exist in various body fluids, such as serum (Shen et al.2017), plasma (Tan et al.2016), and urine (Terracciano et al.2017). Circulating lncRNAs could target distant cells or organs and perform a regulatory function in a new location through exosomes. β-cell-derived lncRNAs in the circulation can restore insulin synthesis and increase the number of pancreatic β-cells. PDX-1 and MafA are key proteins for insulin secretion regulation (Guo et al.2012). GLUT2 is a glucose transporter essential for activating glucose-sensitive genes (Thorens 2015). Microarray technology indicated that the circulating level of lncRNA-p3134 in T2D patients was higher than in non-diabetic controls. Further research in MIN6 cells and isolated mouse islet cells shows β cell-derived lncRNA-p3134 regulating the expression of PDX-1, MafA, and transcription factor 7-like 2, thereby enhancing GSIS (Figure 3⑤). Furthermore, when the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signals were blocked by specific inhibitor, lncRNA-p3134-mediated insulin secretion decreased (Ruan et al.2018) (Figure 3⑤). Simulation of the PI3K/AKT pathway phosphorylates the mammalian target of rapamycin (mTOR), governing promoting cell proliferation (Ruan et al.2018). In summary, circulating lncRNA-p3134 maintains insulin levels through regulating both insulin section and β-cell mass.
Anti-diabetogenic and in vivo antioxidant activity of ethanol extract of Dryopteris dilatata in alloxan-induced male Wistar rats
Published in Biomarkers, 2021
Akpotu E. Ajirioghene, Samuel I. Ghasi, Lawrence O. Ewhre, Olusegun G. Adebayo, Jerome N. Asiwe
Glucose uptake occurs in the cell through the glycoproteins family mainly known as glucose transporters (GLUTs) (Simmons 2017). The liver’s glucose transporter is regulated by GLUT-2 which fuels glucose metabolism and also provide metabolites that stimulate the transcription of glucose sensitive genes (Leturque et al. 2005, Chunudom et al.2020). Moreover, insulin is responsible for the regulation of glucose metabolism and inhibiting the insulin secretion resulted in elevated hepatic glucose release and decrease uptake of glucose in the muscle cells (Al-Goblan et al. 2014, Chunudom et al. 2020). Studies on type 1 diabetes have been done in laboratory animals models with the used of chemically active diabetogenic agents like alloxan. This agent selectively impairs pancreatic beta-cells and are transported through the plasma membrane of the beta-cells by the GLUT-2 glucose uniporter (Gorus et al. 1982, Elsner et al. 2002, Haddad et al. 2020). Alteration of the glucose uptake led to various diabetic disorders like hyperglycaemia, hyperlipidaemia, hypertension, nephropathy, neuropathy, polyuria, polyphagia, stroke, ketosis and many more (Malfa et al. 2020).