Читать книгу Clinical Obesity in Adults and Children - Группа авторов - Страница 67

Obesity arises from the interaction between genetic, environmental, and behavioral factors acting through the physiologic mediators of energy intake and energy expenditure. Body weight is the archetypal polygenic trait, a quantitative phenotype that usually fails to display a Mendelian pattern of inheritance because it is influenced by many different regions of the genome [1]. The concept that environmental factors operate on an underlying pool of genes that contribute to obesity susceptibility has important implications for our approach to the prevention and treatment of obesity. If some environmental variables manifest themselves only on certain genotypes, efforts to prevent obesity at a public health level can be focused on recognition and counseling of susceptible individuals. In addition, appreciating the importance of genetic variation as an underlying cause helps to dispel the notion that obesity represents an individual fault in behavior and provides a starting point for efforts to identify the genes involved.

In the last 20 years, several single‐gene defects causing severe human obesity have been identified. Studies of patients with mutations in these molecules have shed light on the physiologic role of such molecules in the regulation of body weight in humans and provided new treatment for subgroups of people with severe obesity.