Scholarlink

<p>Monogenic early-onset obesity can be triggered by alterations in genes which mostly code for components of the leptin-melanocortin signalling pathway, alter its physiological function in the hypothalamus and lead to a&#xa0;lack of a&#xa0;feeling of satiety and a&#xa0;constant feeling of hunger (hyperphagia). Consequently, most affected individuals experience a&#xa0;massive gain in body weight even in early childhood. The manifestation of hyperphagia should be particularly considered in the treatment as traditional methods, such as life-style modifications, metabolic or bariatric surgery do not sufficiently address the hyperphagia. In the clinical practice, the distinction between monogenic and multifactorial forms of obesity can often be challenging. Phenotypic features, such as the typical early childhood weight trajectory, hyperphagia and/or additional symptoms can provide important clues pointing to a&#xa0;monogenic form, which should lead to the initiation of genetic testing. For some monogenic forms of obesity specific mechanism-based pharmacological treatment options are now available, which directly target the leptin-melanocortin pathway and minimize hyperphagia. Such personalized pharmacological treatment options represent an increasingly more important part of individualized multimodal treatment concepts for children and adolescents with monogenic obesity.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Monogene Adipositas

  • 期刊论文

  • 发表日期：

    2025年3月27日

查看全文
  • Joanna Lerner,
  • Stefanie Zorn,
  • Julia von Schnurbein,
  • Susanna Wiegand,
  • Peter Kühnen,
  • Reiner Siebert,
  • Martin Wabitsch

摘要

Monogenic early-onset obesity can be triggered by alterations in genes which mostly code for components of the leptin-melanocortin signalling pathway, alter its physiological function in the hypothalamus and lead to a lack of a feeling of satiety and a constant feeling of hunger (hyperphagia). Consequently, most affected individuals experience a massive gain in body weight even in early childhood. The manifestation of hyperphagia should be particularly considered in the treatment as traditional methods, such as life-style modifications, metabolic or bariatric surgery do not sufficiently address the hyperphagia. In the clinical practice, the distinction between monogenic and multifactorial forms of obesity can often be challenging. Phenotypic features, such as the typical early childhood weight trajectory, hyperphagia and/or additional symptoms can provide important clues pointing to a monogenic form, which should lead to the initiation of genetic testing. For some monogenic forms of obesity specific mechanism-based pharmacological treatment options are now available, which directly target the leptin-melanocortin pathway and minimize hyperphagia. Such personalized pharmacological treatment options represent an increasingly more important part of individualized multimodal treatment concepts for children and adolescents with monogenic obesity.