Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKB beta).

By H. Cho, J. Mu, J. Kim, J. L. Thorvaldsen, Q. Chu, E. Crenshaw, Klaus H. Kaestner, M. Bartolomei, Gerald I. Shulman, M. Birnbaum. Science, 2001

841 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/130408caf3c42c6092707b7cd0d91f503f5bfd99

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Citations in the corpus

• Suppressor of Cytokine Signaling 1 (SOCS-1) and SOCS-3 Cause Insulin Resistance through Inhibition of Tyrosine Phosphorylation of Insulin Receptor Substrate Proteins by Discrete Mechanisms (2004, background): “Akt lies downstream of PI 3-kinase and has been shown to play an important role in inhibition of hepatic glucose production (7).”
• PHLPP and a second isoform, PHLPP2, differentially attenuate the amplitude of Akt signaling by regulating distinct Akt isoforms. (2007, background): “For example, studies with knockout mice have implicated Akt2 in glucose homeostasis and Akt1 in growth regulation (Cho et al., 2001a, 2001b).”
• Role for Akt3/Protein Kinase Bγ in Attainment of Normal Brain Size (2005, background): “We have reported previously that at least some of the specificity of Akt signaling, when growth versus metabolism is considered, is conferred by dissimilarities between Akt1 and Akt2 and that differences intrinsic to the Akt proteins contribute to selective signaling (3, 16, 17).”
• Akt stimulates hepatic SREBP1c and lipogenesis through parallel mTORC1-dependent and independent pathways (2011, background): “Genetic mouse models have demonstrated that both of these responses to insulin occur, at least in part, downstream of the protein kinase Akt2 (Cho et al., 2001; Garofalo et al., 2003; Leavens et al., 2009).”
• Proliferation, survival and metabolism: the role of PI3K/AKT/mTOR signalling in pluripotency and cell fate determination (2016, background): “Germline deletion of any of the isoforms alone does not lead to clear embryonic lethality despite the various physiological and pathological defects that these mice exhibit (Chen et al., 2001; Cho et al., 2001; Tschopp et al., 2005).”
• Distinct roles of Akt1 and Akt2 in regulating cell migration and epithelial–mesenchymal transition (2005, background): “Akt1 / mice are small with significant growth defects, and Akt2 / mice are unable to maintain glucose homeostasis (Cho et al., 2001a,b).”
• Akt1 controls macrophage response to LPS by regulating microRNAs (2009, background): “In mammals, the Akt family consists of three isoforms, Akt1 (PKBa), Akt2 (PKBb), and Akt3 (PKBg), which are functionally distinct despite their sequence similarities (Cho et al., 2001; Easton et al., 2005; Mao et al., 2007; Maroulakou et al., 2007; Yang et al., 2005).”
• Sleep Duration and Risk of Type 2 Diabetes: A Meta-analysis of Prospective Studies (2015, background): “AKT signaling plays a central role in insulin-stimulated glucose uptake in both muscle and adipose tissue, which was established in rat and human studies (43,44).”
• PI3K/Akt: getting it right matters (2008, background): “…specific phenotypes: Akt1( / ) mice show placental hypotrophy, accompanied by retardation of growth and reduction of body weight (Chen et al., 2001; Cho et al., 2001b); Akt2( / ) mice become hyperinsulemic and hyperglycemic (Cho et al., 2001a); and Akt3( / ) mice exhibit reduced brain sizes…”
• Association between insulin resistance and the development of cardiovascular disease (2018, background): “The disruption of Akt1 in mice causes no significant perturbations in metabolism, whereas mice knocked-out for Akt2 show insulin resistance, with a phenotype closely resembling type 2 diabetes of humans [41].”
• Current approaches for assessing insulin sensitivity and resistance in vivo: advantages, limitations, and appropriate usage. (2008, methodology): “In addition, various dynamic tests including IVGTT, OGTT, and intra-peritoneal insulin tolerance test (ITT) have been used (23, 34, 73).”
• Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure. (2005, unknown): “…genomes ( Akt1 / PKB α , Akt2 / PKB β , and Akt3 / PKB γ ), and loss of Akt1 gene in mice leads to general growth retardation and spontaneous apoptosis in restricted cell types (14, 15), whereas Akt2 gene disruption results in abnormal glucose metabolism and mild growth deficiency (16, 17).”
• PKB/Akt: a key mediator of cell proliferation, survival and insulin responses? (2001, background): “Exciting new data from Birnbaum and colleagues establishes PKBβ as an essential gene for the maintenance of normal glucose homeostasis (Cho et al., 2001).”