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Curcumin modulates the adipose FBN1-Asprosin axis and improves metabolic dysfunction in a rat model of type 2
Abdolvahed Safarzaei1, Hamid Hafezinouri2, Hamed Fanaei3,4
1Pharmacology Research Center, Zahedan University of Medical Sciences, Zahedan, Iran.
Background:
Asprosin, a glucogenic adipokine derived from the C-terminal region of profibrillin-1 encoded by FBN1, has emerged as a potential regulator of glucose homeostasis and insulin resistance. However, the effects of curcumin on the adipose FBN1-asprosin axis in type 2 diabetes mellitus (T2DM) remain unclear. This study investigated whether curcumin supplementation modulates adipose tissue FBN1 expression and circulating asprosin in a rat model of T2DM.
Methods:
Forty male Wistar rats were randomly allocated to four groups (n = 10/group): control, curcumin, T2DM, and T2DM + curcumin. T2DM was induced by high-fat diet feeding followed by low-dose streptozotocin administration. Diabetic rats received curcumin (300 mg/kg/day) by oral gavage for eight weeks. Body weight, fasting blood glucose, fasting insulin, and homeostatic model assessment of insulin resistance (HOMA-IR) were assessed. Serum asprosin concentrations were determined using ELISA, and FBN1 gene expression in subcutaneous adipose tissue was quantified using real-time PCR.
Results:
Compared with controls, diabetic rats exhibited significantly higher body weight, fasting blood glucose, fasting insulin, HOMA-IR, adipose tissue FBN1 expression, and serum asprosin concentrations (all P < 0.0001). Curcumin supplementation significantly reduced body weight, fasting blood glucose, fasting insulin, and HOMA-IR in diabetic rats (P < 0.05). Moreover, curcumin significantly attenuated adipose tissue FBN1 expression (P = 0.0028) and circulating asprosin levels (P = 0.0014) compared with untreated diabetic rats.
Conclusion:
Curcumin supplementation improves metabolic abnormalities and attenuates the adipose FBN1-asprosin axis in experimental T2DM. These findings suggest that modulation of FBN1-asprosin signaling may contribute to the metabolic effects of curcumin and warrants further mechanistic investigation.