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Our group has previously reported that lack of adipose tissue (lipodystrophy) leads to glucose intolerance and impaired endothelial-dependent vasorelaxation (EDR) via reduced signaling of the adipokine, leptin in the endothelium. However, the identity of the adipose depot responsible for endothelial leptin signaling activation and the underlying mechanism remains ill-defined. Our new data indicate that the perivascular adipose tissue (PVAT) is an important source of leptin. Thus, we hypothesized that leptin specifically derived from PVAT restores EDR and glucose tolerance in a mouse model with global deficiency in adipose tissue (lipodystrophic, BSCL2^-/-). Restoration of PVAT in BSCL2^-/- mice corrected systemic glycemic status (GTT AUC, BSCL2^-/- + PVAT 635.3 ± 31.28 vs sham 741.6 ± 45.87, p<0.05). Moreover, PVAT transplantation restored EDR locally (abdominal aorta EDR AUC, BSCL2^-/- + PVAT 224.9 …