Puberty and type 1 diabetes
Various data on type 1 diabetes mellitus (T1DM) have showed that the incidence of T1DM peaks at puberty. However, diabetes control and complications could be adversely affected by the physiological changes of puberty. In early years of insulin therapy, severe growth retardation with pubertal delay,...
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Medknow Publications & Media Pvt Ltd
2015
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4413391/ |
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pubmed-44133912015-05-04 Puberty and type 1 diabetes Chowdhury, Subhankar Brief Communication Various data on type 1 diabetes mellitus (T1DM) have showed that the incidence of T1DM peaks at puberty. However, diabetes control and complications could be adversely affected by the physiological changes of puberty. In early years of insulin therapy, severe growth retardation with pubertal delay, like in Mauriac syndrome, have been reported. Insulin and leptin are metabolic factors, circulating in the periphery, which participate in the hypothalamic control of metabolism and reproduction. Insulin may be an important regulator of leptin in humans. Increased levels of advanced glycation end products suppress activation of the gonadotropin-releasing hormone (GnRH) pulse generator, resulting in pubertal delay. Glycemic control deteriorates during puberty as the lean body mass doubles mainly over a period of 25 years, which increases insulin requirement. There is also an increase in insulin resistance over the period of puberty. In normal individuals, fasting and postprandial insulin concentrations reach a peak in both sexes in mid to late puberty. Puberty, at all stages, has the worst insulin resistance. It has been observed that an excessive GH secretion in T1DM during puberty has significant effects on ketogenesis. Adolescent T1DM tends to decompensate very rapidly and develop ketoacidosis when the late night insulin dose is omitted. Adolescence is a critical developmental phase that presents unique challenges and opportunities to individuals with diabetes, their families and their healthcare providers. Medknow Publications & Media Pvt Ltd 2015-04 /pmc/articles/PMC4413391/ /pubmed/25941652 http://dx.doi.org/10.4103/2230-8210.155402 Text en Copyright: © Indian Journal of Endocrinology and Metabolism http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Chowdhury, Subhankar |
| spellingShingle |
Chowdhury, Subhankar Puberty and type 1 diabetes |
| author_facet |
Chowdhury, Subhankar |
| author_sort |
Chowdhury, Subhankar |
| title |
Puberty and type 1 diabetes |
| title_short |
Puberty and type 1 diabetes |
| title_full |
Puberty and type 1 diabetes |
| title_fullStr |
Puberty and type 1 diabetes |
| title_full_unstemmed |
Puberty and type 1 diabetes |
| title_sort |
puberty and type 1 diabetes |
| description |
Various data on type 1 diabetes mellitus (T1DM) have showed that the incidence of T1DM peaks at puberty. However, diabetes control and complications could be adversely affected by the physiological changes of puberty. In early years of insulin therapy, severe growth retardation with pubertal delay, like in Mauriac syndrome, have been reported. Insulin and leptin are metabolic factors, circulating in the periphery, which participate in the hypothalamic control of metabolism and reproduction. Insulin may be an important regulator of leptin in humans. Increased levels of advanced glycation end products suppress activation of the gonadotropin-releasing hormone (GnRH) pulse generator, resulting in pubertal delay. Glycemic control deteriorates during puberty as the lean body mass doubles mainly over a period of 25 years, which increases insulin requirement. There is also an increase in insulin resistance over the period of puberty. In normal individuals, fasting and postprandial insulin concentrations reach a peak in both sexes in mid to late puberty. Puberty, at all stages, has the worst insulin resistance. It has been observed that an excessive GH secretion in T1DM during puberty has significant effects on ketogenesis. Adolescent T1DM tends to decompensate very rapidly and develop ketoacidosis when the late night insulin dose is omitted. Adolescence is a critical developmental phase that presents unique challenges and opportunities to individuals with diabetes, their families and their healthcare providers. |
| publisher |
Medknow Publications & Media Pvt Ltd |
| publishDate |
2015 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4413391/ |
| _version_ |
1613217021297688576 |