Why the study?
Despite focus on SCD1 in vascular disorders, the relationship between SCD1 and perivascular adipose tissue under high-fat diet conditions remains poorly understood.
SCD1 deficiency in mice on a high-fat diet alters perivascular adipose tissue metabolism and increases inflammation, highlighting its role in vascular homeostasis.
SCD1 targeting in obesity warrants caution before human translation; hypothesis-generating for perivascular inflammation and needs clinical validation.
The dysregulation of perivascular adipose tissue (PVAT) is a key contributor to obesity‐induced vascular dysfunction. Mouse periaortic adipose tissue is divided into two parts: thoracic perivascular adipose tissue (TPVAT) and abdominal perivascular adipose tissue (APVAT). These two parts have different physiological properties, which translate into different effects on the vascular wall in the onset of metabolic syndrome. Stearoyl‐CoA desaturase 1 (SCD1) is an enzyme that is involved in the synthesis of monounsaturated fatty acids and has been shown to play an important role in metabolic syndrome, including vascular homeostasis. Despite a considerable focus on the role of SCD1 in the development of vascular disorders, there is currently a lack of knowledge of the relationship between SCD1 and PVAT. The present study investigated effects of SCD1 deficiency on lipolysis, β‐oxidation, mitochondrial dynamics, and inflammation in mouse TPVAT and APVAT under high‐fat diet (HFD) feeding conditions. We found lower triglyceride levels in PVAT in SCD1 −/− mice both in vitro and in vivo compared with wildtype perivascular adipocytes, attributable to activated lipolysis and β‐oxidation. Moreover, PVAT in HFD‐fed SCD1 −/− mice was characterized by higher levels of oxidative phosphorylation complexes and mitochondrial respiratory potential and alterations of mitochondrial morphology compared with wildtype mice. Furthermore, TPVAT and APVAT in SCD1 −/− mice showed signs of greater pro‐inflammatory macrophage polarization and higher inflammatory markers that were induced by a HFD. This may be related to the accumulation free fatty acids and diacylglycerols, which are enriched in saturated fatty acids. These findings elucidate the role of SCD1 in maintaining vascular integrity.
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Sówka et al. (2025) studied this question.
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