https://www.selleckchem.com/products/sch-900776.html Whilst the consequences of weight bias and weight bias internalisation (WBI) have been explored, less is known about the factors contributing to their development. Some research has explored the role of social exposure in weight bias and WBI but has been limited in its definition of exposure and focused solely on western countries. The present study therefore aimed to assess the role of social exposure defined in terms of both population and personal exposure in predicting weight bias and WBI, in an international sample. Participants (N = 1041) from 33 countries, aged 18-85 years completed online measures of demographics, weight bias, WBI, and population and personal social exposure. Population exposure was defined using national obesity prevalence data from the World Health Organisation to classify countries as low (obesity rates ≤19.9%; n = 162), medium (20.0-29.9%; n = 672) or high prevalence (≥30%; n = 192). Personal exposure was defined in terms of personal contact and health and attractiveness normapopulation exposure in predicting both weight bias and WBI. Findings hold implications for improving the wellbeing and lived experiences of those living with overweight and obesity.3T3L1 mouse pre-adipocytes develop into adipocytes differently in response to GALNT2 overexpression or to stimulation with rosiglitazone, a reference inducer of adipogenesis. To investigate the biology of alternative pathways of adipogenesis, we studied lipid droplets (LD) morphology, chromatin organization, and gene expression in GALNT2- versus rosiglitazone-induced 3T3L1 adipogenesis. 3T3L1 overexpressing either GALNT2 (GALNT2) or GFP and treated with rosiglitazone (GFPR) were differentiated into adipocytes. LD and nuclei were profiled measuring their morphological features. The expression of adipogenesis-related genes was measured by RT-PCR. As compared to GFPR, GALNT2 showed smaller and more clustered LD, more nuclei with condensed