Fibrillin-1 regulates white adipose tissue development, homeostasis, and function.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Fibrillin-1 is an extracellular glycoprotein present throughout the body. Mutations in fibrillin-1 cause a wide spectrum of type I fibrillinopathies, including Marfan syndrome characterized by clinical manifestations in adipose tissues, among others. This study addresses the hypothesis that fibrillin-1 regulates adipocyte development and plays a vital role in adipose tissue homeostasis. We employed two mouse models - Fbn1 mgR/mgR (20-25% of normal fibrillin-1) and Fbn1 C1041G/+ (missense mutation in fibrillin-1) to examine the role of fibrillin-1 in adipose tissue development and homeostasis. Fibrillin-1 was detected around mature adipocytes in both mouse and human white adipose tissues. As expected, Fbn1 mgR/mgR mice displayed a significant reduction of fibrillin-1 in white adipose tissue, and no change was observed for Fbn1 C1041G/+ mice, each compared to their respective littermates. Male Fbn1 mgR/mgR mice had more white and brown adipose tissues, whereas female Fbn1 mgR/mgR and both male and female Fbn1 C1041G/+ showed no difference compared to their respective wild-type littermates. Consistent with this data, male Fbn1 mgR/mgR mice displayed hyperinsulinemia and an insulin resistance phenotype with higher levels of cholesterol and high-density lipoproteins in the serum. Fibrillin-1 deficiency in male Fbn1 mgR/mgR mice also promoted adipogenic gene expression and led to hyp

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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