The etiology of Autism Spectrum Disorders (ASD) includes a strong genetic component and a complicated environmental component. Recent evidence indicates that maternal diabetes, including gestational diabetes, is associated with an increased prevalence of ASD. While previous studies have looked into possible roles for maternal diabetes in neurodevelopment, there are few studies into how gestational diabetes, with no previous diabetic or metabolic phenotype, may affect neurodevelopment. In this study, we have specifically induced gestational diabetes in mice, followed by behavioral and molecular phenotyping of the mice offspring. Pregnant mice were injected with STZ a day after initiation of pregnancy. Glucose levels increased to diabetic levels between E7 and E14 in pregnancy in a subset of the pregnant animals. Male offspring of Gestational Diabetic mothers displayed increased repetitive behaviors with no dysregulation in the three-chambered social interaction test. RNA-seq analysis revealed a dysregulation in genes related to forebrain development in the frontal cortex and a dysregulation of a network of neurodevelopment and immune related genes in the striatum. Together, these results give evidence that gestational diabetes can induce changes in adulthood behavior and gene transcription in the brain.

: Cells are mainly dependent on glucose as their energy source. Multicellular organisms need to adequately control individual glucose uptake by the cells, and the insulin-glucagon endocrine system serves as the key glucose regulation mechanism. Insulin allows for effective glucose entry into the cells when blood glucose levels are high, and glucagon acts as its opponent, balancing low blood glucose levels. A lack of insulin will prevent glucose entry to the cells, resulting in glucose accumulation in the bloodstream. Diabetes is a disease which is characterized by elevated blood glucose levels. All diabetes types are characterized by an inefficient insulin signaling mechanism. This could be the result of insufficient insulin secretion as in the case of type I diabetes and progressive incidents of type II diabetes or due to insufficient response to insulin (known as insulin resistance). We emphasize here, that Diabetes is actually a disease of starved tissues, unable to absorb glucose (and other nutrients), and not a disease of high glucose levels. Indeed, diabetic patients, prior to insulin discovery, suffered from glucose malabsorption. In this mini-review, we will define diabetes, discuss the current status of diabetes treatments, review the current knowledge of the different hormones that participate in glucose homeostasis and the employment of different modulators of these hormones. As this issue deals with peptide therapeutics, special attention will be given to synthetic peptide analogs, peptide agonists as well as antagonists.

No abstract

No abstract