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.
Taken together with the observations that SPARC deficiency had protective effects on hepatocytes via a favorable inhibition profile, functional knowledge of SPARC may offer a unique therapeutic approach to preserve hepatocellular fate decisions in diabetes.
Our data suggest that levels of SPARC are reduced in islets from donors with diabetes and that it has a role in insulin secretion, an effect which appears independent of SPARC's modulation of obesity-induced insulin resistance in adipose tissue.