The plasminogen receptor Plg-R KT regulates adipose function and metabolic homeostasis

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)

Background Plg-R KT , a unique transmembrane plasminogen receptor, enhances the activation of plasminogen to plasmin, and localizes the proteolytic activity of plasmin on the cell surface. Objectives We investigated the role of Plg-R KT in adipose function, metabolic homeostasis, and obesity. Methods We used adipose tissue (AT) sections from bariatric surgery patients and from high fat diet (HFD)-induced obese mice together with immunofluorescence and real-time polymerase chain reaction to study adipose expression of Plg-R KT . Mice genetically deficient in Plg-R KT and littermate controls fed a HFD or control low fat diet (LFD) were used to determine the role of Plg-R KT in insulin resistance, glucose tolerance, type 2 diabetes, and associated mechanisms including adipose inflammation, fibrosis, and ectopic lipid storage. The role of Plg-R KT in adipogenesis was determined using 3T3-L1 preadipocytes and primary cultures established from Plg-R KT -deficient and littermate control mice. Results Plg-R KT was highly expressed in both human and mouse AT, and its levels dramatically increased during adipogenesis. Plg-R KT -deficient mice, when fed a HFD, gained more weight, developed more hepatic steatosis, and were more insulin resistant/glucose intolerant than HFD-fed wild-type littermates. Mechanistically, these metabolic defects were linked with increased AT inflammation, AT mac

Evidence level

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

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