growth/size/body
• male mutants gain significantly more weight than Lepob homozygous controls between 4 and 16 weeks
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endocrine/exocrine glands
• in nulliparous females, no ductal development occurs, and gland remains in prepubescent state
• females having had one full-term pregnancy show varying degrees of mammary development; some females show minimal ductal elongation, while others show large areas of lobules with presence of milk
• females are incapable of ensuring survival of offspring due to defects in mammary gland structure and physiology
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• gland is significantly increased in weight compared to Lepob homozygotes, and is comparable to wild-type
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• large empty follicles characteristic of Lepob mice are present
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• Leydig cell density is increased over Lepob homozygotes
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homeostasis/metabolism
N |
• insulin and leptin levels are not increased over Lepob homozygotes
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• levels are significantly increased over levels found in Lepob homozygotes; levels are similar to wild-type
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• hypercorticosteronemia is significantly attenuated compared to Lepob homozygotes
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adipose tissue
• WAT amount is significantly higher than in control Lepob heterozygotes
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reproductive system
• gland is significantly increased in weight compared to Lepob homozygotes, and is comparable to wild-type
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• large empty follicles characteristic of Lepob mice are present
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• Leydig cell density is increased over Lepob homozygotes
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• in infertile females, vaginal orifice is small with cytology similar to Lepob homozygotes
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• sperm density is increased over Lepob homozygotes
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• all males tested produced offspring, while only 4/8 females produced live offspring compared to severely reduced fertility in Lepob homozygous male and female mice
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integument
• in nulliparous females, no ductal development occurs, and gland remains in prepubescent state
• females having had one full-term pregnancy show varying degrees of mammary development; some females show minimal ductal elongation, while others show large areas of lobules with presence of milk
• females are incapable of ensuring survival of offspring due to defects in mammary gland structure and physiology
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