The effects of type 1 diabetes on the hypothalamic, pituitary and testes axis
Cell and Tissue Research, ISSN: 0302-766X, Vol: 349, Issue: 3, Page: 839-847
2012
- 96Citations
- 72Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations96
- Citation Indexes96
- 96
- CrossRef25
- Captures72
- Readers72
- 72
Review Description
Type 1 diabetes is an autoimmune disorder characterized by a lack of insulin production by the beta cells of the pancreas. This lack of insulin causes a variety of systemic effects on whole-body metabolism. Poorly managed type 1 diabetes can lead to cardiovascular disease, diabetic neuropathy, and diabetic retinopathy. Increasingly, even well-managed type 1 diabetic patients show damage to peripheral organs related to complications from the disease. The central role of insulin in energy homeostasis also renders it an important signaling factor in the reproductive tract. type 1 diabetes has now been demonstrated to cause defects in sperm and testes. The aim of this review is to present the known effects of insulin's role in the function of the male reproductive tract. These effects might be mediated through hormonal alterations in the hypothalamic pituitary gonadal axis or through the direct interaction of insulin on the testes and sperm cells. Although fertility complications also occur in type 2 diabetic males, this review will focus on the defects specifically linked with the lack of insulin seen in type 1 diabetes. © Springer-Verlag 2012.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84866358516&origin=inward; http://dx.doi.org/10.1007/s00441-012-1387-7; http://www.ncbi.nlm.nih.gov/pubmed/22526620; http://link.springer.com/10.1007/s00441-012-1387-7; https://link.springer.com/article/10.1007%2Fs00441-012-1387-7; http://www.springerlink.com/index/10.1007/s00441-012-1387-7; http://www.springerlink.com/index/pdf/10.1007/s00441-012-1387-7; https://dx.doi.org/10.1007/s00441-012-1387-7; https://link.springer.com/article/10.1007/s00441-012-1387-7; https://link.springer.com/content/pdf/10.1007%2Fs00441-012-1387-7.pdf; http://link.springer.com/article/10.1007%2Fs00441-012-1387-7
Springer Science and Business Media LLC
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