Journal
ENDOCRINOLOGY
Volume 154, Issue 3, Pages 1337-1348Publisher
ENDOCRINE SOC
DOI: 10.1210/en.2012-2056
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Funding
- Eunice Kennedy Shriver National Institute of Child Health and Human Development/National Institutes of Health (SCCPIR) [U54-HD28934]
- National Institutes of Health [R00HD056491, R21HD071529]
- deArce-Koch Fund
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Pubertal onset only occurs in a favorable, anabolic hormonal environment. The neuropeptide kisspeptin, encoded by the Kiss1 gene, modifies GnRH neuronal activity to initiate puberty and maintain fertility, but the factors that regulate Kiss1 neurons and permit pubertal maturation remain to be clarified. The anabolic factor insulin may signal nutritional status to these neurons. To determine whether insulin sensing plays an important role in Kiss1 neuron function, we generated mice lacking insulin receptors in Kiss1 neurons (IR Delta Kiss mice). IR Delta Kiss females showed a delay in vaginal opening and in first estrus, whereas IR Delta Kiss males also exhibited late sexual maturation. Correspondingly, LH levels in IR Delta Kiss mice were reduced in early puberty in both sexes. Adult reproductive capacity, body weight, fat composition, food intake, and glucose regulation were comparable between the 2 groups. These data suggest that impaired insulin sensing by Kiss1 neurons delays the initiation of puberty but does not affect adult fertility. These studies provide insight into the mechanisms regulating pubertal timing in anabolic states. (Endocrinology 154: 1337-1348, 2013)
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