Genetic control of pubertal timing

Kaminski, Beth; Palmert, Mark R.

doi:10.1097/mop.0b013e3283060ed4

Cited by 14 publications

(6 citation statements)

References 75 publications

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“…LEP, the gene encoding the protein leptin, is located approximately 10 cM from CFTR and has been previously shown to be linked to CFTR (44)(45)(46)(47)(48)(49). Leptin plays an important role in pubertal timing and in the overall function of the HPG axis, therefore, a potential link between CFTR and ovarian function through leptin might also warrant further investigation (50)(51)(52)(53).…”

Section: Discussionmentioning

confidence: 99%

Female cystic fibrosis mutation carriers and assisted reproductive technology: does carrier status affect reproductive outcomes?

VanWort

Lee

Karvir³

et al. 2014

Fertility and Sterility

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Section: Discussionmentioning

confidence: 99%

Female cystic fibrosis mutation carriers and assisted reproductive technology: does carrier status affect reproductive outcomes?

VanWort

Lee

Karvir³

et al. 2014

Fertility and Sterility

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“…This delay is associated with decreased bone density and may result in a loss of final height potential (1), underscoring the clinical importance of determining the mechanisms behind delayed puberty in IBD. One proposed mechanism for this delay is that IBD causes decreased food intake and poor weight gain, leading to low levels of leptin—a hormone necessary for the onset of puberty (1,8-10). As a means of investigating this issue, we have used a model of DSS colitis in prepubertal male mice to demonstrate that these mice have a delay in puberty relative to mice that were FR to maintain the same weight as the DSS group.…”

Section: Discussionmentioning

confidence: 99%

“…Leptin is known to be necessary for pubertal progression, as evidenced by a lack of pubertal progression in rodent (7) and human (8,9) males with leptin deficiency. Thus, one potential mechanism for pubertal delay in males with colitis could be decreased fat stores leading to lower leptin levels (10). …”

mentioning

confidence: 99%

Puberty Is Delayed in Male Mice With Dextran Sodium Sulfate Colitis Out of Proportion to Changes in Food Intake, Body Weight, and Serum Levels of Leptin

DeBoer

2011

Pediatr Res

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ABSTRACT:In boys, inflammatory bowel disease often results in delayed puberty associated with decreased bone mineral density and decreased linear growth. Our goal was to investigate whether pubertal timing and levels of leptin differed between prepubertal male mice with colitis and food-restricted (FR) mice maintained at a similar weight. We induced colitis in 32-d-old male mice using dextran sodium sulfate (DSS), resulting in 10 d of worsening colitis. We followed up these mice for separation of the prepuce from the glans penis as a marker of pubertal progression. Compared with freefeeding control mice, DSS and FR mice had significantly lower weight on d 7-10 of treatment. DSS mice had later puberty than control and FR mice. DSS mice also had smaller testes, lower FSH levels, increased systemic cytokines, and increased colonic inflammation by histology. Leptin levels were similar between DSS and FR mice, whereas both had decreases in leptin compared with controls. We conclude that DSS colitis causes delayed puberty in sexually immature male mice beyond what is seen among FR mice of similar weight, food intake, and leptin levels. These experiments provide support for the hypothesis that pubertal delay in colitis is influenced by factors beyond poor weight gain alone. (Pediatr Res 69: 34-39, 2011)

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“…These effects of IBD on HPG axis function have been postulated to be caused by two primary mechanisms. The first of these is poor weight gain, with subsequent decrease in fat mass and decrease in levels of leptin, an adipocyte-derived hormone that is essential for the normal timing of puberty [10, 11]. The second mech- anism by which IBD may affect HPG function relates to increased systemic inflammation, given the known effects of inflammatory cytokines on levels of gonadotropins [9,12–14].…”

Section: Introductionmentioning

confidence: 99%

Partial normalization of pubertal timing in female mice with DSS colitis treated with anti-TNF-α antibody

DeBoer

Steinman

2012

J Gastroenterol

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Background Inflammatory bowel disease (IBD) and resultant colitis occurring prior to puberty are frequently associated with delayed puberty and losses of growth and bone mineralization. Some of this delay may be due to colonic inflammation and associated systemic inflamma- tion. To date no treatments for IBD have been shown to normalize the timing of puberty. Our objective in this study was to determine whether there is a normalization of the timing of puberty during treatment of colitis using mono- clonal antibodies (abs) to tumor necrosis factor (TNF)-α. Methods We induced colitis in 23-day-old C57Bl6 female mice using 3% dextran sodium sulfate (DSS) for 7 days, followed by removal of DSS for an additional 3 days, resulting in 10 days of worsening colitis. DSS- treated mice received either TNF-α ab or Control ab on days 4 and 8 of colitis, while non-colitic Control mice received injections of TNF-α ab (Control + TNF-α ab). All groups were followed for the timing of vaginal opening until day of life 33, when they were euthanized for serum and colon collection. Results The DSS + TNF-α ab group had lower levels of systemic interleukin (IL)-6 and a partial normalization of the timing of vaginal opening compared to the DSS + Control ab group. There were no differences in weight gain, growth, or colon histological inflammatory scores between the DSS + TNFa ab and DSS + Control ab groups over the course of the experiment. Conclusions We conclude that anti-TNF-α ab treatment causes a partial normalization of pubertal timing coincident with decreased systemic inflammation in DSS colitis. These data may have implications regarding growth and bone mineralization outcomes in pediatric IBD.

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Genetic control of pubertal timing

Abstract: This review summarizes recent advances regarding the genetic control of pubertal timing and presents areas for future investigation.

Cited by 14 publications

References 75 publications

Female cystic fibrosis mutation carriers and assisted reproductive technology: does carrier status affect reproductive outcomes?

Female cystic fibrosis mutation carriers and assisted reproductive technology: does carrier status affect reproductive outcomes?

Puberty Is Delayed in Male Mice With Dextran Sodium Sulfate Colitis Out of Proportion to Changes in Food Intake, Body Weight, and Serum Levels of Leptin

Partial normalization of pubertal timing in female mice with DSS colitis treated with anti-TNF-α antibody

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