Ioanna A Paschou, Evangelia Sali, Stavroula A Paschou, Konstantinos I Tsamis, Melpomeni Peppa, Theodora Psaltopoulou, Electra Nicolaidou, Alexander J Stratigos
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引用次数: 0
Abstract
"Ozempic face" and facial aging have been observed as side effects in many patients after glucagon like peptide 1 receptor agonists (GLP-1RA) therapy for type 2 diabetes mellitus (T2DM) and obesity. However, those medications can reduce systemic inflammation and possibly promote skin health. The rapid weight loss observed with GLP-1RA has been implicated in facial aging. However, recent evidence suggests further pathophysiological mechanisms for this side effect. The aim of this article is to review the literature and present available data on the possible mechanisms of GLP-1RA on skin aging. Indeed, GLP-1RA may affect other types of skin cells, which may accelerate the process of skin aging itself. More specifically, GLP-1RA can act on adipose-derived stem cells (ADSC) and fibroblasts, that present GLP-1R on their surface. Stimulation of the receptor reduces the ability of ADSC to produce protective cytokines. The absence of those cytokines promotes the production of reactive oxygen species (ROS) and causes oxidative damage on fibroblasts. GLP-1RA also reduce the glucose intake of the ADSC, leading to reduced production of ATP and apoptosis. Finally, the stimulation of GLP-1R on ADSCs reduces indirectly the production of estrogens from dermal white adipose tissues (DWAT), which reduces stimulation of fibroblasts to produce collagen. GLP-1RA can also affect the process of skin aging through interaction with advanced glycation end products (AGEs) and RAGE (receptors of AGEs) activation. In conclusion, many patients receiving GLP-1RA suffer from "Ozempic face" and facial aging. It seems that this complication is not exclusively related to decreased facial fat, but there are more aging mechanisms that have to be elucidated.
期刊介绍：
Well-established as a major journal in today’s rapidly advancing experimental and clinical research areas, Endocrine publishes original articles devoted to basic (including molecular, cellular and physiological studies), translational and clinical research in all the different fields of endocrinology and metabolism. Articles will be accepted based on peer-reviews, priority, and editorial decision. Invited reviews, mini-reviews and viewpoints on relevant pathophysiological and clinical topics, as well as Editorials on articles appearing in the Journal, are published. Unsolicited Editorials will be evaluated by the editorial team. Outcomes of scientific meetings, as well as guidelines and position statements, may be submitted. The Journal also considers special feature articles in the field of endocrine genetics and epigenetics, as well as articles devoted to novel methods and techniques in endocrinology.
Endocrine covers controversial, clinical endocrine issues. Meta-analyses on endocrine and metabolic topics are also accepted. Descriptions of single clinical cases and/or small patients studies are not published unless of exceptional interest. However, reports of novel imaging studies and endocrine side effects in single patients may be considered. Research letters and letters to the editor related or unrelated to recently published articles can be submitted.
Endocrine covers leading topics in endocrinology such as neuroendocrinology, pituitary and hypothalamic peptides, thyroid physiological and clinical aspects, bone and mineral metabolism and osteoporosis, obesity, lipid and energy metabolism and food intake control, insulin, Type 1 and Type 2 diabetes, hormones of male and female reproduction, adrenal diseases pediatric and geriatric endocrinology, endocrine hypertension and endocrine oncology.
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