Insulin prevents apoptosis of external granular layer neurons in rat cerebellar slice cultures
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Region-specific association between basal blood insulin and cerebral glucose metabolism in older adults
2019, NeuroImage: ClinicalCitation Excerpt :However, because most of the glucose transporters located in the central nervous system (CNS) are insulin-insensitive (i.e., GLUT-1 and GLUT-3), and GLUT-4 is located in the only restricted area with very low density (Schulingkamp et al., 2000; Shah et al., 2012), other mechanisms not mediated by the direct action of insulin on glucose transporters also needed to be considered. In this context, effects of insulin on neuronal/synaptic activity and integrity via insulin binding with insulin receptors (Chiu et al., 2008; Mielke and Wang, 2011; Tanaka et al., 1995; Zhao et al., 2004) might be involved in a region-specific association between basal blood insulin and CMglu observed in our study. The brain regions where fasting blood insulin was associated with CMglu in our study correspond with the regions enriched with insulin bindings in animal models and postmortem human brains, such as limbic structures (i.e., hippocampus), and neocortices including parietal cortices (Havrankova et al., 1978; Hill et al., 1986; Marks et al., 1990).
Glaucoma - Diabetes of the brain: A radical hypothesis about its nature and pathogenesis
2014, Medical HypothesesCitation Excerpt :IRS is important for insulin induced antiapoptotic activity in neurons [90]. Insulin also inhibits apoptosis in cerebral granule cells [95]. Antiapoptotic activity of insulin may be important for many neuronal cell types which may include those involved in AD, schizophrenia and glaucoma.
Insulin is differentially related to cognitive decline and atrophy in Alzheimer's disease and aging
2012, Biochimica et Biophysica Acta - Molecular Basis of DiseaseCitation Excerpt :The mechanisms underlying these relationships in our early AD cohort remain unclear but emerging data suggests an important and beneficial role for insulin in neurodegenerative disease. Insulin is a neuroprotective [21] and neurotrophic [43] factor that protects neurons from amyloid-beta related toxicity [25]. Individuals with AD have lower insulin levels in the cerebrospinal fluid [17] and reduced insulin signaling in the brain [18] compared to those without dementia.
An inflammatory micro-environment promotes human adipocyte apoptosis
2011, Molecular and Cellular EndocrinologyCitation Excerpt :We have previously shown an anti-apoptotic function of insulin-like growth factor I (IGF-1) in human fat cells (Fischer-Posovszky et al., 2004). Insulin mediates survival in several cell types (Díaz et al., 1999; Tanaka et al., 1995) and has anti-apoptotic effects comparable to IGF-1 in brown adipocytes (Navarro et al., 1998; Tseng et al., 2002). This leads us to hypothesize that insulin resistant adipocytes, where insulin is no longer capable of exerting its survival effects, are sensitive to apoptosis induction.
Interaction of perinatal and pre-pubertal factors with genetic predisposition in the development of neural pathways involved in the regulation of energy homeostasis
2010, Brain ResearchCitation Excerpt :Regardless of the temporal sequences, there are numerous factors that can influence neural development. Importantly, both leptin and insulin have properties that affect neuronal survival (neurotropic) and process outgrowth (neurotrophic) of developing neurons (Bouret et al., 2004b, 2008; Puro and Agardh, 1984; Recio-Pinto et al., 1984; Tanaka et al., 1995; Udagawa et al., 2006). Mice lacking leptin or with deficient leptin signaling have abnormal development of ARC-PVN axonal projections of anabolic neuropeptide Y (NPY/agouti-related peptide (AgRP) and catabolic proopiomelanocortin (POMC) neurons involved in the regulation of energy homeostasis (Bouret et al., 2004b).
Developmental gene × environment interactions affecting systems regulating energy homeostasis and obesity
2010, Frontiers in NeuroendocrinologyCitation Excerpt :Most of these have been studied in depth only in rodent brains. Leptin and insulin are among the most important of such factors because of their well documented roles in the ongoing regulation of energy homeostasis and because they also affect neuronal migration, survival (neurotropic) and process outgrowth (neurotrophic) of developing neurons [89,90,206–209]. Mice lacking leptin (ob/ob) and mice (db/db) and rats (selectively bred “DIO”) with deficient leptin signaling have abnormal development of ARC–PVN axonal projections of anabolic NPY/AgRP and catabolic proopiomelanocortin (POMC) neurons involved in the regulation of energy homeostasis [89,90].