کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5554240 | 1558111 | 2017 | 6 صفحه PDF | دانلود رایگان |
- Subcutaneous adipose tissue dysfunction is central for development of insulin resistance.
- Psoriasis is an independent risk-factor for development of T2D.
- Skin-specific transgenic mice display altered whole-body glucose and lipid homeostasis.
- Subcutaneous adipose tissue function is impaired directly below psoriatic skin lesions.
- The skin secretes proteins and peptides which can enhance or impair metabolic control.
Prevalence of obesity and related complications such as type 2 diabetes (T2D) has increased dramatically in recent decades. Metabolic complications of obesity arise in part due to subcutaneous adipose tissue (SAT) dysfunction. However, it is currently unclear why some obese individuals develop insulin resistance and T2D and others do not. In this review, we discuss the role of the skin in regulating SAT function, and whether presence of inflammatory skin diseases such as psoriasis represent a novel risk mechanism mediating development of obesity-related complications.
Journal: Current Opinion in Pharmacology - Volume 37, December 2017, Pages 59-64