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). Unlike their old male counterparts and young females, the old peri- and post-menopausal females had relatively constant levels of plasma leptin across the day and night. However, this aging-related sexual dimorphism was not evident in all of the old
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1991 ). Sexual dimorphism in corticosterone secretion is well established: female rodents display elevated corticosterone secretion in basal and some stress conditions relative to males ( Critchlow et al. 1963 ). Furthermore, estrogen exerts
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glucose homeostasis in the BAT, WAT, and livers of Gpbar1 −/− and Gpbar1 + / + mice on HFD did not reveal more than 2.5-fold changes between KO and WT control mice ( Supplementary Figures 1B, C and 2 ). Sexual dimorphism in HFD-induced obesity and
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humans . American Journal of Physiology. Endocrinology and Metabolism 283 1008 – 1015 . ( doi:10.1152/ajpendo.00513.2001 ) Jansson JO Edén S Isaksson O 1985 Sexual dimorphism in the control of growth hormone secretion . Endocrine Reviews
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arrangement and development of kisspeptin neurons using male and female mice. They found that kisspeptin neuronal cell bodies existed primarily in the ARC and RP3V. They also noticed a sexual dimorphism in the number of kisspeptin neurons present in the RP3V
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higher incidence of thyroid dysfunction and carcinomas than men ( Ron et al . 1987 ). However, elderly men with thyroid carcinomas have much worse prognosis than women ( Morganti et al . 2005 ). In animal models, rats in particular, sexual dimorphism is
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Physiology and Pharmacology,
Paediatrics, University of Western Ontario, London, Ontario, Canada N6A 4V2
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Departments of Medicine,
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Departments of Medicine,
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Departments of Medicine,
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the adults at age 50 with a profound sexual dimorphism, the relative obesity being seen in the females but not in the males ( Ravelli et al. 1999 ). Dietary modifications in early life, such as altered composition, excess or restricted intake
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progressive hyperglycemia, accompanied by lymphocytic infiltration of pancreatic islets. In some basic aspects, this model mimics recent-onset IDDM in human patients ( O’Brien et al. 1996 ). There is evidence of sexual dimorphism in the incidence and
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at PND 8–10 corresponds with the reduction in GH at PND 8 in those females. Since Pou1f1 is also reduced at PND 15, we need to investigate whether or not Pou1f1 remains down throughout development in this model. We do see sexual dimorphism of Pou1f1
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putative physiopathological implications . Peptides 30 139 – 145 doi:10.1016/j.peptides.2008.06.007 . Clarkson J Herbison AE 2006 Postnatal development of kisspeptin neurons in mouse hypothalamus; sexual dimorphism and projections to