Role of hypertrophic adipocytes, collagen VI, and CD38 in adipose tissue fibrosis in obesity

Early human evidence such as case series or small samples is exploring possible benefits.

• 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)

Adipose tissue fibrosis is associated with metabolic alterations in patients with obesity and involves three major collagen types: fibrillar collagens I and III and non-fibrillar collagen VI. In this study, fibrosis was found to be significantly increased only in visceral adipose tissue in patients with obesity (4.7% vs. 2.5% in controls, p < 0.001), whereas no significant difference was observed in subcutaneous adipose tissue. Transmission electron microscopy and high-resolution scanning electron microscopy suggested that hypertrophic adipocytes may contribute to the production of fibrillar collagens I and III. In vitro data were consistent with this interpretation. Expression of the COL6 gene, which encodes the non-fibrillar collagen VI, was reduced in adipose tissue from obese patients. Notably, patients carrying mutations in COL6 genes displayed increased fibrosis even in subcutaneous fat, approximately 6.5-fold higher than controls in the patient with the severe form (Ullrich) and 2.8-fold higher in two patients with the milder form (Bethlem). Approximately 15% of adipocytes in obese tissue appeared stressed or dead (perilipin-1 negative), and the associated infiltrating macrophages exhibited increased expression of CD38, an ectoenzyme implicated in systemic fibrosis. Correlations with gene expression also indicated the importance of myofibroblasts and the extracellular-ma

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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