Research reportStabilization of tubulin mRNAs by insulin and insulin-like growth factor I during neurite formation
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Secreted amyloid precursor protein alpha activates neuronal insulin receptors and prevents diabetes-induced encephalopathy
2018, Experimental NeurologyCitation Excerpt :Dimerized insulin or IGF1 receptor (IGF1R) complexes are activated at the plasma membrane following ligand binding at the active site, leading to recruitment of kinases including PI3K and AKT to initiate signal transduction. Insulin increases neuronal outgrowth in vitro in a dose dependent manner (Wang et al., 1992; Mill et al., 1985; Recio-Pinto and Ishii, 1984; Fernyhough et al., 1989) and prevents cell death through pro-apoptotic protein inhibition by PI3K-induced AKT activation (Cardone et al., 1998; Datta et al., 1996; Datta et al., 1997). Insulin also modulates synaptic plasticity in vitro (Man et al., 2003; Liu et al., 1995) indicating a role for insulin in memory formation.
Insulin prevents aberrant mitochondrial phenotype in sensory neurons of type 1 diabetic rats
2017, Experimental NeurologyCitation Excerpt :We used a physiologically relevant concentration (10 nM) of insulin in all cell culture experiments to minimize confounding effects deriving from potential cross-occupation of insulin-like growth factor receptors by excess insulin (Benyoucef et al., 2007; Kleinridders, 2016; Recio-Pinto and Ishii, 1988). Other reported consequences of insulin stimulation of sensory neurons include increased transcription and synthesis of cytoskeletal proteins, such as tubulin and neurofilament (Fernyhough et al., 1989; Wang et al., 1992) that are essential for axonal growth, regeneration and structural stability. Demonstration that exogenous insulin also dose-dependently enhanced neurite outgrowth of sensory neurons is consistent with prior studies (Fernyhough et al., 1993; Recio-Pinto et al., 1986) and highlights the direct neurotrophic properties of insulin in sensory neurons.
Diabetes and the plasticity of sensory neurons
2015, Neuroscience LettersCitation Excerpt :Since, polyneuropathy is now recognized in ‘prediabetic’ patients with metabolic syndrome alone, it is possible that high circulating insulin exposure might generate resistance, downregulation of neuronal growth transduction pathways and neuropathy. Adult sensory neurons treated with insulin in the nanomolar range have enhanced neurite outgrowth [76]. However, we noted that adult sensory neurons exposed to higher, micromolar doses of insulin continuosly or briefly or chronically exposed to picomolar doses lost their trophic response [74].
Corneal nerves in health and disease
2014, Survey of OphthalmologyMechanisms of diabetic neuron damage: Molecular pathways
2014, Handbook of Clinical NeurologyCitation Excerpt :The possibility that diabetic neuropathy might arise from failed trophic factor signaling has been considered by several groups (Apfel et al., 1994; Brewster et al., 1994c; Apfel and Kessler, 1995; Christianson et al., 2003). Insulin itself is an important consideration since it acts as a neurotrophic factor and its receptors are widely expressed on most peripheral neurons (Fernyhough et al., 1989; Ishii, 1993, 1995; Sugimoto et al., 2000, 2002). That insulin deficiency or resistance might be linked to neuropathy may appear to be an obvious conclusion, yet it has only recently garnered support.
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Present address: Cell Biophysics Unit, Medical Research Council, Kings College, London, U.K.