Secreted protein acidic and rich in cysteine and bioenergetics: Extracellular matrix, adipocytes remodeling and skeletal muscle metabolism

• Published in: The international journal of biochemistry & cell biology Vol. 117; p. 105627
• Main Authors: Ghanemi, Abdelaziz, Melouane, Aicha, Yoshioka, Mayumi, St-Amand, Jonny
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Ltd 01.12.2019
• Subjects: Adipose tissue; Energy metabolism homeostasis; Extracellular matrix; Secreted protein acidic and rich in cysteine; Skeletal muscle; Secreted protein acidic and rich in cysteine; Extracellular matrix; Energy metabolism homeostasis; Adipose tissue; Skeletal muscle
• ISSN: 1357-2725; 1878-5875
• DOI: 10.1016/j.biocel.2019.105627

•SPARC is a glycoprotein that provides ECM with metabolic and functional properties.•The ECM remodeling plays important roles in adipocytes shape/expansion remodeling.•SPARC is involved in adipose tissue and skeletal muscle metabolism and remodeling.•Specific therapeutic targeting of SPARC for diseases such as obesity The extracellular matrix (ECM) remodeling plays important roles in both adipocytes shape/expansion remodeling and the skeletal muscle (SM) metabolism. Secreted protein acidic and rich in cysteine (SPARC) is expressed in divers tissues including adipose tissue (AT) and SM where it impacts a variety of remodeling as well as metabolic functions. SPARC, also known as osteonectin or BM-40, is a glycoprotein associated with the ECM. Numerous researches attempted to elucidate the implications of SPARC in these two key metabolic tissues under different conditions. Whereas SPARC deficiency tends to shape the remodeling of the adipocytes and the fat distribution, this deficiency decreases SM metabolic properties. On the other hand, SPARC seems to be an enhancer of the metabolism and a mediator of the exercise-induced adaptation in the SM and as well as an adipogenesis inhibitor. Some findings about the SPARC effects on AT and SM seem “contradictory” in terms of tissue development and energy profile therefore highlighting the mechanistic role of SPARC in both is a priority. Yet, within this review, we expose selected researches and compare the results. We conclude with explanations to “reconcile” the different observations, hypothesize the feedback and regulatory character of SPARC and put its roles within the energetic and structural maps of both adipocytes and myocytes in homeostasis and in situations such as obesity or exercise. These properties explain the modifications and the remodeling seen in AT and SM undergoing adaptive changes (obesity, exercise, etc.) and represent a starting point for precise therapeutic targeting of SPARC-related pathways is conditions such as obesity, sarcopenia and diabetes.