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Puberty in Female Mice Is Not Associated with Increases in Either Body Fat or Leptin

Section of Integrative Biology, School of Biological Sciences, University of Texas, Austin, Texas 78712

Address all correspondence and requests for reprints to: Dr. F. H. Bronson, Section of Integrative Biology, School of Biological Sciences, University of Texas, Austin, Texas 78712. E-mail: bronson{at}mail.utexas.edu

It has been hypothesized that puberty is triggered when body fat and hence circulating levels of leptin exceed critical thresholds. Four kinds of experiments tested that hypothesis in female mice. When age was the independent variable, body fat and circulating levels of leptin decreased rather than increased before the onset of puberty. When stage of reproductive development was the independent variable, neither body fat nor circulating levels of leptin correlated with the onset of puberty. In sharp contrast, reproductive development was well correlated with body weight. A significant nocturnal peak in circulating levels of leptin was seen before and at all stages of reproductive development, but the highest levels were seen after rather than before the first estrous cycle was initiated. Neither acceleration nor deceleration of puberty by varying the female’s social environment had any effect on either body fat or leptin. There is no support in any of these experiments for the hypothesis that an increase in body fat and thus an increase in circulating levels of leptin triggers puberty in female mice.

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