Objective: To describe the antiobesity drug-prescribing patterns of US physicians over the past decade. Methods: Data for adult patients were obtained from the National Ambulatory Medical Care Survey and the National Hospital Ambulatory Medical Care Survey. Obesity was identified using ICD-9 codes, BMI values, and a chronic-obesity-condition variable. For patients with obesity, a logistic-regression model was estimated to determine the odds of receiving pharmacotherapy. Results: Of the 987 million visits by patients with obesity from 2005 to 2010, 2.0% mentioned an antiobesity drug. Additionally, there were 6.5 million visits by patients without obesity but with an antiobesity drug mention. Visits made by females (OR 5 2.89; 95% CI: 2.08-4.03), by white patients (OR 5 1.55; 95% CI: 1.08-2.24), by younger adults (OR 5 1.71; 95% CI: 1.34-2.20), and in the South (OR 5 3.39; 95% CI: 1.49-7.72) were more likely to involve an antiobesity drug prescription. Conclusions: Only 1 in 50 patients with obesity received a prescription for an antiobesity medication. Moreover, in contrast to what the 1998 Guidelines suggested, physicians tended to prescribe antiobesity medications to self-paying, young, white females, many of whom lived in the South, and not all of whom had obesity.
Epithelial development starts with stem cell commitment to ectoderm followed by differentiation to basal keratinocytes. The basal keratinocytes, first committed in embryogenesis, constitute the basal layer of the epidermis. They have robust proliferation and differentiation potential, giving rise to suprabasal cells, and are responsible for expansion, maintenance and regeneration of the epidermis. We generated basal epithelial cells in vitro through differentiation of mouse embryonic stem cells (mESCs). Early on in differentiation, the expression of stem cell markers, Oct4 and Nanog, decreased rapidly along with increased ectoderm marker keratin (Krt) 18. Later on, Krt 18 expression was subdued when cells displayed basal keratinocyte characteristics, including regular polygonal shape, adherent and tight junctions and Krt 14 expression. Using Map3k1 mutant mESCs and environmental dioxin, we examined the gene and environment effects on differentiation. Neither Map3k1 mutation nor dioxin altered mESC differentiation to ectoderm and basal keratinocytes, but they, individually and in combination, potentiated Krt 1 expression and basal to spinous differentiation. Similar gene-environment effects were observed in vivo where dioxin exposure increased Krt 1 more substantially in the epithelium of Map3k1+/− than wild type embryos. Thus, the in vitro model of epithelial differentiation can detect genetic and environmental effects on epidermal development.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.