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Noncanonical CDK4 signaling rescues diabetes in a mouse model by promoting β cell differentiation
Expanding β cell mass is a critical goal in the fight against diabetes. CDK4, an extensively characterized cell cycle activator, is required to establish and maintain β cell number. β cell failure in the IRS2-deletion mouse type 2 diabetes model is, in part, due to loss of CDK4 regulator cyclin D2. We set out to determine whether replacement of endogenous CDK4 with the inhibitor-resistant mutant CDK4-R24C rescued the loss of β cell mass in IRS2-deficient mice. Surprisingly, not only β cell mass but also β cell dedifferentiation was effectively rescued, despite no improvement in whole body insulin sensitivity. Ex vivo studies in primary islet cells revealed a mechanism in which CDK4 intervened downstream in the insulin signaling pathway to prevent FOXO1-mediated transcriptional repression of critical β cell transcription factor
Pdx1
. FOXO1 inhibition was not related to E2F1 activity, to FOXO1 phosphorylation, or even to FOXO1 subcellular localization, but rather was related to deacetylation and reduced FOXO1 abundance. Taken together, these results demonstrate a differentiation-promoting activity of the classical cell cycle activator CDK4 and support the concept that β cell mass can be expanded without compromising function.
Journal Article
Fat for fuel : a revolutionary diet to combat cancer, boost brain power, and increase your energy
\"For over a century, we've accepted the scientific consensus that cancer results from genetic disease due to chromosomal damage in cell nuclei. But what if cancer isn't a genetic disease after all? What if scientists are chasing a flawed paradigm, and cancer isn't a disease of damaged DNA but rather of defective metabolism as a result of mitochondrial dysfunction? What if that [theory] could revolutionize our understanding of other diseases as well--and show us a radical new path to optimal health?\"-- Provided by publisher.
Book
Clinical and molecular diagnosis, screening and management of Beckwith–Wiedemann syndrome: an international consensus statement
Beckwith–Wiedemann syndrome(BWS), a human genomic imprinting disorder is characterised by phenotypic variability that might include overgrowth, macroglossia, abdominal wall defects, neonatal hypoglycaemia, lateralised overgrowth and predisposition to embryonal tumours. Delineation of the molecular defects within the imprinted 11p15.5 region can predict familial recurrence risks and the risk (and type) of embryonal tumour. Despite recent advances in knowledge, there is marked heterogeneity in clinical diagnostic criteria and care. As detailed in this Consensus Statement, an international consensus group agreed 72 recommendations for the clinical and molecular diagnosis and management of BWS, including comprehensive protocols for the molecular investigation, care and treatment from the prenatal period to adulthood. The consensus recommendations apply to patients with Beckwith–Wiedemann spectrum (BWSp) covering classical BWS without a molecular diagnosis and BWS-related phenotypes with an 11p15.5 molecular anomaly. Although the consensus group recommend a tumour surveillance programme targeted by molecular subgroups, surveillance might differ according to the local healthcare system (for example, in the United States), and the results of targeted and universal surveillance should be evaluated prospectively. International collaboration, including prospective audit of the results of implementing these consensus recommendations, is required to expand the evidence base for the design of optimum care pathways.
Beckwith–Wiedemann syndrome is an overgrowth disorder characterized by variable clinical phenotypes and a complex molecular aetiology. This Consensus Statement summarises recommendations for clinical indications, molecular diagnosis and management of the newly defined Beckwith–Wiedemann spectrum.
Journal Article
COVID‐19–Related School Closings and Risk of Weight Gain Among Children
[...]we anticipate that the COVID-19 pandemic will likely double out-of-school time this year for many children in the United States and will exacerbate the risk factors for weight gain associated with summer recess. While parks and playgrounds remain open in some cities, there is widespread appreciation that it is not possible to keep the playgrounds clean and children will have difficulty maintaining social distance. [...]urban families may, understandably, elect not to use these spaces, exacerbating the disparity between those who can/ cannot remain physically active outdoors. [...]the National Institutes of Health's Environmental Influences on Child Health Outcomes program (ECHO; https://www.nih.gov/research-training/environmentalinfluences-child-health-outcomes-echo-program) includes 70 cohorts that are studying childhood obesity and is a resource that can be used to study the obesity-related consequences of extended school closure.O Funding agencies: Wang is funded by National Heart, Lung, and Blood Institute of National Institutes of Health (grant R01HL141427 \"Assessment of Policies Through Prediction of Long-Term Effects on Cardiovascular Disease Using Simulation [APPLE CDS]\").
Journal Article