Mouse Embryonic Fibroblasts Protect ob/ob Mice From Obesity and Metabolic Complications.

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)

The global obesity epidemic is fueling alarming rates of diabetes, associated with increased risk of cardiovascular disease and cancer. Leptin is a hormone secreted by adipose tissue that is a key regulator of body weight (BW) and energy expenditure. Leptin-deficient humans and mice are obese, diabetic, and infertile and have hepatic steatosis. Although leptin replacement therapy can alleviate the pathologies seen in leptin-deficient patients and mouse models, treatment is costly and requires daily injections. Because adipocytes are the source of leptin secretion, we investigated whether mouse embryonic fibroblasts (MEFs), capable of forming adipocytes, could be injected into ob/ob mice and prevent the metabolic phenotype seen in these leptin-deficient mice. We performed a single subcutaneous injection of MEFs into leptin-deficient ob/ob mice. The MEF injection formed a single fat pad that is histologically similar to white adipose tissue. The ob/ob mice receiving MEFs (obRs) had significantly lower BW compared with nontreated ob/ob mice, primarily because of decreased adipose tissue mass. Additionally, obR mice had significantly less liver steatosis and greater glucose tolerance and insulin sensitivity. obR mice also manifested lower food intake and greater energy expenditure than ob/ob mice, providing a mechanism underlying their metabolic improvement. Furthermore, obRs have

Evidence level

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

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