Adipose Tissue Biology and Effect of Weight Loss in Women With Lipedema

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)

Lipedema is a lipodystrophic disease that is typically characterized by a marked increase in lower-body subcutaneous adipose tissue that is purported to have increased inflammation and fibrosis, have impaired microvascular/lymphatic circulation, and be resistant to reduction by weight loss therapy. However, these outcomes have not been adequately studied. We evaluated body composition, insulin sensitivity, metabolic health, and adipose tissue biology in women with obesity and lipedema (Obese-LIP) before and after moderate (∼9%) diet-induced weight loss. At baseline, people with Obese-LIP had ∼23% greater leg fat mass, ∼11% lower android-to-gynoid ratio, and ∼48% greater insulin sensitivity (all P Article highlights We sought to increase our understanding of the pathophysiology of lipedema and the effects of weight loss. We examined whether there are differences in upper- and lower-body adipose tissue biology in lipedema and whether adipose tissue is affected by weight loss. Women with obesity and lipedema have decreased expression of genes related to lymphatic/vascular function and increased expression of genes related to fibrosis and inflammation in thigh compared with abdominal subcutaneous adipose tissue; weight loss increased insulin sensitivity and decreased leg fat but did not affect adipose tissue inflammation or fibrosis. Weight loss should be the first-line therapy for

Evidence level

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

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