Islet β cell expression of constitutively active Akt1/PKBα induces striking hypertrophy, hyperplasia, and hyperinsulinemia

Journal of Clinical Investigation

Volumn 108, Issue 11, 2001, Pages 1631-1638

  Bernal Mizrachi, E ^a   Wen, W ^a   Stahlhut, S ^a   Welling, C M ^a   Permutt, M A ^a  

^a WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN SERINE THREONINE KINASE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL HYPERPLASIA; CONTROLLED STUDY; ENZYME ACTIVITY; GLUCOSE TOLERANCE; HYPERINSULINEMIA; HYPERTROPHY; IMMUNOHISTOCHEMISTRY; MITOGENESIS; MOUSE; NONHUMAN; PANCREAS ISLET CELL HYPERPLASIA; PRIORITY JOURNAL; PROTEIN EXPRESSION; TRANSGENIC MOUSE;

ANIMALS; BLOOD GLUCOSE; CELL DIVISION; HYPERINSULINISM; HYPERPLASIA; HYPERTROPHY; INSULIN; MICE; MICE, INBRED C57BL; MICE, INBRED CBA; MICE, TRANSGENIC; PANCREAS; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-AKT;

EID: 0035210374     PISSN: 00219738     EISSN: None     Source Type: Journal    
DOI: 10.1172/JCI200113785     Document Type: Article

References (34)

1. Differential signaling by insulin receptor substrate 1 (IRS-1) and IRS-2 in IRS-1-deficient cells
2. Adaptation of beta-cell mass to substrate over-supply: Enhanced function with normal gene expression
3. Dynamics of beta-cell mass in the growing rat pancreas. Estimation with a simple mathematical model
4. Hot topic - Using beta-cell growth factors to enhance human pancreatic islet transplantation
5. The role of glucose in the in vitro regulation of cell cycle kinetics and proliferation of fetal pancreatic B-cells
6. Insulin-like growth factor I (IGF-I)-stimulated pancreatic beta-cell growth is glucose-dependent. Synergistic activation of insulin receptor substrate-mediated signal transduction pathways by glucose and IGF-I in INS-1 cells
7. The regulation and activities of the multifunctional serine/threonine kinase Akt/PKB
8. Protein kinases as mediators of phosphoinositide 3-kinase signaling
9. Cellular survival: A play in three Akts
10. Differential activation of ptotein kinase B and p70(S6K) by glucose and insulin-like growth factor 1 in pancreatic beta-cells (INS-1)
11. Akt, a pleckstrin homology domain containing kinase, is activated primarily by phosphorylation
12. Tissue-specific expression of the rat insulin I gene in vivo requires both the enhancer and promoter regions
13. Regulatory regions of rat insulin I gene necessary for expression in transgenic mice
14. Method for the isolation of intact islets of Langerhans from the rat pancreas
15. Life and death of the pancreatic beta cells
16. Transgenic mice overexpressing insulin-like growth factor-II in beta cells develop type 2 diabetes
17. Progressive pancreatic islet hyperplasia in the islet-targeted, parathyroid hormone-related protein-overexpressing mouse
18. Hepatocyte growth factor overexpression in the islet of transgenic mice increases beta cell proliferation, enhances islet mass, and induces mild hypoglycemia
19. Targeted expression of placental lactogen in the beta cells of transgenic mice results in beta cell proliferation, islet mass augmentation, and hypoglycemia
20. Tissue-specific insulin resistance in mice with mutations in the insulin receptor, IRS-1, and IRS-2
21. Size control in animal development
22. Autonomous control of cell and organ size by CHICO, a Drosophila homolog of vertebrate IRS1-4
23. Cell-autonomous regulation of cell and organ growth in Drosophila by Akt/PKB
24. The conserved phosphoinositide 3-kinase pathway determines heart size in mice
25. Hypoinsulinaemia, glucose intolerance and diminished beta-cell size in S6K1-deficient mice
26. Drosophila S6 kinase: A regulator of cell size
27. GSK-3: New thoughts on an old enzyme
28. Forkhead transcription factors: New insights into protein kinase B (c-akt) signaling
29. Growth factor-dependent signaling and cell cycle progression
30. Loss of Cdk4 expression causes insulin-deficient diabetes and Cdk4 activation results in beta-islet cell hyperplasia
31. Beta-cell apoptosis is responsible for the development of IDDM in the multiple low-dose streptozotocin model
32. Increased susceptibility to streptozotocin-induced beta-cell apoptosis and delayed autoimmune diabetes in alkylpurine-DNA-N-glycosylase-deficient mice
33. Streptozotocin interactions with pancreatic beta cells and the induction of insulin-dependent diabetes