Variation in the rate of newly diagnosed mental retardation, attention-deficit/hyperactivity disorder, and autism among children in Taiwan depended on age, birth year, period, and socioeconomic status. The extent of the association linking age with the first diagnosis of mental retardation varies across different urbanicity level and socioeconomic status.

The present study examines urbanicity-related differences in help-seeking process among preschool children with autism and investigates the factors associated with utilization of autism-related services within the year of diagnosis. Using the 1997-2004 National Health Insurance Research Database (NHIRD) in Taiwan, we identified a total of 3495 autistic children born in 1997-1999 and 13964 matched controls. Results indicate that suburban and rural autism tended to receive the diagnosis at an older age and to have a longer diagnosis process as compared with urban counterparts. Male gender, a younger age of diagnosis, and being diagnosed by psychiatric specialty strongly predict subsequent greater utilization of autism-specific services (all p < 0.05). Health policy makers and other service providers should address the needs of children with early-onset neurodevelopmental disorders in rural areas, particularly those from disadvantaged families.

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Exercise enhances numerous signalling pathways and activates substrate metabolism in skeletal muscle. Small molecule compounds that activate these cellular responses have been shown to recapitulate the metabolic benefits of exercise. In this study, a histone deacetylase (HDAC) inhibitor, HC toxin, was investigated as a small molecule compound that activates exercise-induced adaptations. In C2C12 myotubes, HC toxin treatment activated two exercise-stimulated pathways: AMP-activated protein kinase (AMPK) and Akt pathways. HC toxin increased the protein content and phosphorylation of insulin receptor substrate 1 as well as the activation of downstream Akt signalling. The effects of HC toxin on IRS1-Akt signalling were PI3K-dependent as wortmannin abolishes its effects on IRS1 protein accumulation and Akt phosphorylation. HC toxin-induced Akt activation was sufficient to enhance downstream mTOR complex 1 (mTORC1) signalling including p70S6K and S6, which were consistently abolished by PI3K inhibition. Insulin-stimulated glucose uptake, glycolysis, mitochondrial respiration and fatty acid oxidation were also enhanced in HC toxin-treated myotubes. When myotubes were challenged with serum starvation for the induction of atrophy, HC toxin treatment prevented the induction of genes that are involved in autophagy and proteasomal proteolysis. Conversely, IRS1-Akt signalling was not induced by HC toxin in several hepatoma cell lines, providing evidence for a favourable safety profile of this small molecule. These data highlight the potential of HDAC inhibitors as a novel class of small molecules for the induction of exercise-like signalling pathways and metabolism.