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• W2972003441 abstract "The rapid increase in the prevalence of ASD during the past 40 years is associated with excessive dietary energy intake, particularly fructose, and a concomitant increase in metabolic syndrome (obesity, insulin resistance, and hyperlipidemia). Children born to mothers with metabolic syndrome and/or diabetes are at increased risk for ASD. Studies of humans and animal models suggest that ASD involve accelerated growth of neural progenitor cells and neurons resulting in aberrant development of neuronal circuits characterized by a relative GABAergic insufficiency and consequent neuronal network hyperexcitability. Genes associated with ASD encode proteins involved in protein synthesis, cell growth, and synaptic plasticity, and epigenetic molecular modifications implicated in ASD pathogenesis impact the expression of genes in the same pathways. Intermittent fasting, exercise, and avoidance of fructose prevent metabolic syndrome, normalize neuronal network excitability and ameliorate ASD-like behaviors in animal models. Interventions that prevent and reverse metabolic syndrome in conceiving parents and their offspring may prove beneficial in reducing ASD prevalence and symptom severity. We review evidence that suggests a role for excessive consumption of energy-dense foods, particularly fructose, and consequent obesity and insulin resistance (metabolic syndrome) in the recent increase in prevalence of autism spectrum disorders (ASD). Maternal insulin resistance, obesity, and diabetes may predispose offspring to ASD by mechanisms involving chronic activation of anabolic cellular pathways and a lack of metabolic switching to ketosis resulting in a deficit in GABAergic signaling and neuronal network hyperexcitability. Metabolic reprogramming by epigenetic DNA and chromatin modifications may contribute to alterations in gene expression that result in ASD. These mechanistic insights suggest that interventions that improve metabolic health such as intermittent fasting and exercise may ameliorate developmental neuronal network abnormalities and consequent behavioral manifestations in ASD. We review evidence that suggests a role for excessive consumption of energy-dense foods, particularly fructose, and consequent obesity and insulin resistance (metabolic syndrome) in the recent increase in prevalence of autism spectrum disorders (ASD). Maternal insulin resistance, obesity, and diabetes may predispose offspring to ASD by mechanisms involving chronic activation of anabolic cellular pathways and a lack of metabolic switching to ketosis resulting in a deficit in GABAergic signaling and neuronal network hyperexcitability. Metabolic reprogramming by epigenetic DNA and chromatin modifications may contribute to alterations in gene expression that result in ASD. These mechanistic insights suggest that interventions that improve metabolic health such as intermittent fasting and exercise may ameliorate developmental neuronal network abnormalities and consequent behavioral manifestations in ASD. molecular modifications of DNA, histones, and other chromatin-associated proteins that can result in changes in gene expression; examples include methylation, acetylation. and ubiquitination. feeding pattern that includes periods of time of sufficient length to deplete liver glycogen stores and elevate blood ketone levels. process by which the ketone bodies β-hydroxybutyrate and acetoacetate are produced from fatty acids in hepatocytes during periods of food deprivation/fasting. pathophysiological state that is characterized by insulin resistance and obesity, and aberrant cell growth and disengagement of adaptive cellular stress response pathways including autophagy. serine/threonine protein kinase that is the core component of two different protein complexes that positively regulate protein synthesis and cell growth and negatively regulate autophagy. ability of the nervous system to adapt to stressful environmental conditions so as to maintain and restore and enhance the structure and function of neuronal networks. the most anterior region of the frontal cortex that plays a major role in decision making; it uses information about the current behavioral context to rapidly generate goals based on the current biological needs. extent to which an individual interacts with other individuals and integrates into social groups." @default.
• W2972003441 created "2019-09-12" @default.
• W2972003441 creator A5040485871 @default.
• W2972003441 creator A5083040475 @default.
• W2972003441 date "2019-10-01" @default.
• W2972003441 modified "2023-10-16" @default.
• W2972003441 title "Intergenerational Metabolic Syndrome and Neuronal Network Hyperexcitability in Autism" @default.
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