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Increased body fat in mice with a targeted mutation of the paternally expressed imprinted gene Peg3

Peg3 encodes a C2H2 type zinc finger protein that is implicated in a novel physiological pathway regulating core body temperature, feeding behavior, and obesity in mice. Peg3+/− mutant mice develop an excess of abdominal, subcutaneous, and intra‐scapular fat, despite a lifetime of lower food intake than wild‐type animals. However, they start life with reduced fat reserves and are slower to enter puberty. These mice maintain a lower core body temperature, fail to respond to a cold challenge, and have lower metabolic activity as measured by oxygen consumption. Plasma leptin levels are significantly higher than in wild types, and Peg3+/− mice appear to have developed leptin resistance. Administration of exogenous leptin resulted in a significant reduction in food intake in wild‐type mice that was not observed in Peg3+/− mutants. This mutation, which is strongly expressed in hypothalamic tissue during development, has the capacity to regulate multiple events relating to energy homeostasis.