Joint international consensus statement for ending stigma of obesity.

People with obesity commonly face a pervasive, resilient form of social stigma. They are often subject to discrimination in the workplace as well as in educational and healthcare settings. Research indicates that weight stigma can cause physical and psychological harm, and that affected individuals are less likely to receive adequate care.

Pharmacotherapy for Patients with Obesity.

Background: Although pharmacotherapy is not the cornerstone of obesity treatment, it is a valuable tool that could be considered for patients who have not had adequate benefit from lifestyle interventions or who have difficulty maintaining initial weight loss over longer periods.

Content: This review focuses on the role of antiobesity drugs, the mechanisms by which the drugs work, potential pharmacological targets in the neural control of food intake and regulation of body weight, the history of antiobesity drugs, a summary of efficacy and safety data from clinical trials, and the clinical application of pharmacotherapy. Currently, 5 approved drug therapies are available in the US for long-term weight management, with only 2 of these meeting the stronger Food and Drug Administration (FDA) criteria of 5% weight loss relative to a placebo after 1 year and others receiving approval based on the categorical criterion of the proportions of patients achieving 5% weight loss.

Monoclonal antibody targeting of fibroblast growth factor receptor 1c ameliorates obesity and glucose intolerance via central mechanisms.

We have generated a novel monoclonal antibody targeting human FGFR1c (R1c mAb) that caused profound body weight and body fat loss in diet-induced obese mice due to decreased food intake (with energy expenditure unaltered), in turn improving glucose control. R1c mAb also caused weight loss in leptin-deficient ob/ob mice, leptin receptor-mutant db/db mice, and in mice lacking either the melanocortin 4 receptor or the melanin-concentrating hormone receptor 1. In addition, R1c mAb did not change hypothalamic mRNA expression levels of Agrp, Cart, Pomc, Npy, Crh, Mch, or Orexin, suggesting that R1c mAb could cause food intake inhibition and body weight loss via other mechanisms in the brain.