All Relations between apoptosis and insulin

Publication Sentence Publish Date Extraction Date Species
Qing Chang, Yu Li, Morris F White, Jonathan A Fletcher, Sheng Xia. Constitutive activation of insulin receptor substrate 1 is a frequent event in human tumors: therapeutic implications. Cancer research. vol 62. issue 21. 2002-12-10. PMID:12414625. insulin receptor substrate 1 (irs-1) is a major substrate of insulin, insulin-like growth factors, and cytokine signaling and plays an important role in mediating apoptosis, cell differentiation, and cell transformation. 2002-12-10 2023-08-12 human
Loredana Farilla, Hongxiang Hui, Cristina Bertolotto, Elizabeth Kang, Angela Bulotta, Umberto Di Mario, Riccardo Perfett. Glucagon-like peptide-1 promotes islet cell growth and inhibits apoptosis in Zucker diabetic rats. Endocrinology. vol 143. issue 11. 2002-11-19. PMID:12399437. in this study, we investigated the effect of glucagon-like peptide-1 (glp-1) in zucker diabetic rats, an animal model in which the onset of diabetes occurs when the proliferative potential and the rate of beta-cell apoptosis no longer compensate for the increased demand for insulin. 2002-11-19 2023-08-12 rat
Francesca Galbiati, Luca Polastri, Silvia Gregori, Massimo Freschi, Mara Casorati, Ugo Cavallaro, Paolo Fiorina, Federico Bertuzzi, Alessandro Zerbi, Guido Pozza, Luciano Adorini, Franco Folli, Gerhard Christofori, Alberto M Davall. Antitumorigenic and antiinsulinogenic effects of calcitriol on insulinoma cells and solid beta-cell tumors. Endocrinology. vol 143. issue 10. 2002-10-21. PMID:12239113. in betatc(3), calcitriol induced growth inhibition; apoptosis; down-regulation of insulin gene expression; and nongenomic activation of the mapk pathway. 2002-10-21 2023-08-12 mouse
Yu-Hua Tseng, Kohjiro Ueki, Kristina M Kriauciunas, C Ronald Kah. Differential roles of insulin receptor substrates in the anti-apoptotic function of insulin-like growth factor-1 and insulin. The Journal of biological chemistry. vol 277. issue 35. 2002-10-17. PMID:12082100. insulin-like growth factor-1 (igf-1) and insulin are known to prevent apoptosis. 2002-10-17 2023-08-12 Not clear
France Bianchini, Rudolf Kaaks, Harri Vaini. Overweight, obesity, and cancer risk. The Lancet. Oncology. vol 3. issue 9. 2002-09-27. PMID:12217794. in part, these associations with cancer risk may be explained by alterations in the metabolism of endogenous hormones-including sex steroids, insulin, and insulin-like growth factors-which can lead to distortion of the normal balance between cell proliferation, differentiation, and apoptosis. 2002-09-27 2023-08-12 Not clear
Shin ichi Gorogawa, Yoshitaka Kajimoto, Yutaka Umayahara, Hideaki Kaneto, Hirotaka Watada, Akio Kuroda, Dan Kawamori, Tetsuyuki Yasuda, Munehide Matsuhisa, Yoshimitsu Yamasaki, Masatsugu Hor. Probucol preserves pancreatic beta-cell function through reduction of oxidative stress in type 2 diabetes. Diabetes research and clinical practice. vol 57. issue 1. 2002-09-04. PMID:12007724. oxidative stress is known to enhance apoptosis of beta-cells and to suppress insulin biosynthesis, but probucol treatment led to preservation of beta-cell mass and the insulin content. 2002-09-04 2023-08-12 mouse
Ivan Quesada, Juan M Rovira, Franz Martin, Enrique Roche, Angel Nadal, Bernat Sori. Nuclear KATP channels trigger nuclear Ca(2+) transients that modulate nuclear function. Proceedings of the National Academy of Sciences of the United States of America. vol 99. issue 14. 2002-08-08. PMID:12089327. glucose, the principal regulator of endocrine pancreas, has several effects on pancreatic beta cells, including the regulation of insulin release, cell proliferation, apoptosis, differentiation, and gene expression. 2002-08-08 2023-08-12 Not clear
Eva Tomás, Yen-Shou Lin, Zeina Dagher, Asish Saha, Zhijun Luo, Yasuo Ido, Neil B Ruderma. Hyperglycemia and insulin resistance: possible mechanisms. Annals of the New York Academy of Sciences. vol 967. 2002-08-02. PMID:12079834. here, it was associated with an increased propensity to apoptosis and, as in muscle, with an impaired ability of insulin to activate akt. 2002-08-02 2023-08-12 human
F J T Staal, R B van der Luijt, M R M Baert, J van Drunen, H van Bakel, E Peters, I de Valk, H K P van Amstel, M J B Taphoorn, G H Jansen, C W M van Veelen, B Burgering, G E J Staa. A novel germline mutation of PTEN associated with brain tumours of multiple lineages. British journal of cancer. vol 86. issue 10. 2002-08-02. PMID:12085208. in contrast to the wild-type molecule, the mutant pten protein is not capable of inducing apoptosis, induces increased cell proliferation and leads to high constitutive pkb/akt activation, which cannot be increased anymore by stimulation with insulin. 2002-08-02 2023-08-12 Not clear
A Toke. Phosphoinositides and signal transduction. Cellular and molecular life sciences : CMLS. vol 59. issue 5. 2002-07-29. PMID:12088277. signaling through various phosphoinositides has been shown to mediate cell growth and proliferation, apoptosis, cytoskeletal changes, insulin action and vesicle trafficking. 2002-07-29 2023-08-12 Not clear
S M de la Monte, J R Wand. Chronic gestational exposure to ethanol impairs insulin-stimulated survival and mitochondrial function in cerebellar neurons. Cellular and molecular life sciences : CMLS. vol 59. issue 5. 2002-07-29. PMID:12088287. in this regard, studies using in vitro models of ethanol exposure demonstrated impaired insulin signaling mechanisms associated with increased apoptosis and reduced mitochondrial function in neuronal cells. 2002-07-29 2023-08-12 rat
Keiju Hiromura, Toshiaki Monkawa, Arndt T Petermann, Raghu V Durvasula, Stuart J Shanklan. Insulin is a potent survival factor in mesangial cells: role of the PI3-kinase/Akt pathway. Kidney international. vol 61. issue 4. 2002-06-24. PMID:11918738. however, little is known about the anti-apoptotic effect of insulin and the role of the pi3-kinase/akt pathway in mesangial cells (mc) apoptosis. 2002-06-24 2023-08-12 Not clear
D Ross Laybutt, Gordon C Weir, Hideaki Kaneto, Judith Lebet, Richard D Palmiter, Arun Sharma, Susan Bonner-Wei. Overexpression of c-Myc in beta-cells of transgenic mice causes proliferation and apoptosis, downregulation of insulin gene expression, and diabetes. Diabetes. vol 51. issue 6. 2002-06-24. PMID:12031967. overexpression of c-myc in beta-cells of transgenic mice causes proliferation and apoptosis, downregulation of insulin gene expression, and diabetes. 2002-06-24 2023-08-12 mouse
D Ross Laybutt, Gordon C Weir, Hideaki Kaneto, Judith Lebet, Richard D Palmiter, Arun Sharma, Susan Bonner-Wei. Overexpression of c-Myc in beta-cells of transgenic mice causes proliferation and apoptosis, downregulation of insulin gene expression, and diabetes. Diabetes. vol 51. issue 6. 2002-06-24. PMID:12031967. in conclusion, these studies demonstrate that activation of c-myc in beta-cells leads to 1) increased proliferation and apoptosis, 2) initial hyperplasia with amorphous islet organization, and 3) selective downregulation of insulin gene expression and the development of overt diabetes. 2002-06-24 2023-08-12 mouse
Lu Cai, Wei Li, Guangwu Wang, Luping Guo, Youchun Jiang, Y James Kan. Hyperglycemia-induced apoptosis in mouse myocardium: mitochondrial cytochrome C-mediated caspase-3 activation pathway. Diabetes. vol 51. issue 6. 2002-06-24. PMID:12031984. supplementation of insulin inhibited diabetes-induced myocardial apoptosis as well as suppressed hyperglycemia. 2002-06-24 2023-08-12 mouse
E Shafri. Albert Renold memorial lecture: molecular background of nutritionally induced insulin resistance leading to type 2 diabetes--from animal models to humans. International journal of experimental diabetes research. vol 2. issue 4. 2002-06-14. PMID:11795838. some with labile beta cells exhibit apoptosis and lose their capacity of coping with insulin resistance after a relatively short period. 2002-06-14 2023-08-12 mouse
T Yamaok. Gene therapy for diabetes mellitus. Current molecular medicine. vol 1. issue 3. 2002-05-06. PMID:11899081. suppression of beta-cell apoptosis, recovery from insulin deficiency, and relief of diabetic complications are common therapeutic approaches to both types of diabetes. 2002-05-06 2023-08-12 Not clear
B Duvillié, C Currie, T Chrones, D Bucchini, J Jami, R L Joshi, D J Hil. Increased islet cell proliferation, decreased apoptosis, and greater vascularization leading to beta-cell hyperplasia in mutant mice lacking insulin. Endocrinology. vol 143. issue 4. 2002-04-29. PMID:11897712. increased islet cell proliferation, decreased apoptosis, and greater vascularization leading to beta-cell hyperplasia in mutant mice lacking insulin. 2002-04-29 2023-08-12 mouse
Francisco B Barbosa, Kirsten Capito, Hans Kofod, Peter Tham. Pancreatic islet insulin secretion and metabolism in adult rats malnourished during neonatal life. The British journal of nutrition. vol 87. issue 2. 2002-04-22. PMID:11895167. it is concluded that impairment of glucose-induced insulin secretion in rats fed a low-protein diet may be caused by attenuation of islet phosphatidylinositol hydrolysis, and it is tentatively suggested that the increased activity of ca-independent phospholipase a2 in islets of rats fed a low-protein diet may participate in the stimulation of apoptosis. 2002-04-22 2023-08-12 rat
E Glowacka, M Banasik, P Lewkowicz, H Tchorzewsk. The effect of LPS on neutrophils from patients with high risk of type 1 diabetes mellitus in relation to IL-8, IL-10 and IL-12 production and apoptosis in vitro. Scandinavian journal of immunology. vol 55. issue 2. 2002-04-11. PMID:11896938. the early stage of neutrophils apoptosis was assessed morphologically, and the later stage by dna-binding dye propidium iodide, both after treatment with lipopolysaccharide (lps), insulin or anti-cd95 antibody (ab) as stimulators. 2002-04-11 2023-08-12 Not clear