Prenatal Testosterone Exposure Disrupts Insulin Secretion And Promotes Insulin Resistance
Hyperandrogenemia and metabolic disturbances during postnatal life are strongly linked both to polycystic ovary syndrome and other conditions that arise from prenatal exposure to androgen excess. In an animal model of this condition, we reported that insulin sensitivity (IS) was lower in young femal...
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| Veröffentlicht in: | Scientific reports 2020-01, Vol.10 (1), p.404, Article 404 |
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| description | Hyperandrogenemia and metabolic disturbances during postnatal life are strongly linked both to polycystic ovary syndrome and other conditions that arise from prenatal exposure to androgen excess. In an animal model of this condition, we reported that insulin sensitivity (IS) was lower in young female sheep born to testosterone-treated mothers versus sheep born to non-exposed mothers (control). This lower insulin sensitivity remains throughout reproductive life. However, it is unknown whether abnormal postnatal levels of testosterone (T) further decrease IS derived from prenatal exposure to testosterone. Therefore, we assessed the effects of an acute testosterone administration (40 mg) on IS and insulin secretion during an intravenous glucose tolerance test performed at 40 weeks of age (adulthood) in previously ovariectomized sheep at 26 weeks of age (prepuberty), that were either prenatally exposed to testosterone (T-females, n = 6) or not (C-females, n = 6). The incremental area under the curve of insulin was greater in C-females both with or without the acute testosterone treatment (P |
| doi_str_mv | 10.1038/s41598-019-57197-x |
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In an animal model of this condition, we reported that insulin sensitivity (IS) was lower in young female sheep born to testosterone-treated mothers versus sheep born to non-exposed mothers (control). This lower insulin sensitivity remains throughout reproductive life. However, it is unknown whether abnormal postnatal levels of testosterone (T) further decrease IS derived from prenatal exposure to testosterone. Therefore, we assessed the effects of an acute testosterone administration (40 mg) on IS and insulin secretion during an intravenous glucose tolerance test performed at 40 weeks of age (adulthood) in previously ovariectomized sheep at 26 weeks of age (prepuberty), that were either prenatally exposed to testosterone (T-females, n = 6) or not (C-females, n = 6). The incremental area under the curve of insulin was greater in C-females both with or without the acute testosterone treatment (P < 0.05). The ISI-Composite was lower after an acute testosterone treatment, only in T-females. We conclude that prenatal exposure to testosterone disrupts pancreatic insulin secretion in response to glucose and that in this setting further hyperandrogenemia may predispose to lower insulin sensitivity.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-57197-x</identifier><identifier>PMID: 31941959</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>692/163/2743/137/773 ; 692/699/2743/137/773 ; Animal models ; Animals ; Embryonic Development - drug effects ; Female ; Females ; Glucose ; Glucose tolerance ; Humanities and Social Sciences ; Insulin ; Insulin Resistance ; Insulin secretion ; Insulin Secretion - drug effects ; Intravenous administration ; multidisciplinary ; Ovariectomy ; Pancreas ; Polycystic ovary syndrome ; Pregnancy ; Prenatal experience ; Prenatal exposure ; Prenatal Exposure Delayed Effects - chemically induced ; Prenatal Exposure Delayed Effects - metabolism ; Prenatal Exposure Delayed Effects - pathology ; Science ; Science (multidisciplinary) ; Secretion ; Sheep ; Testosterone ; Testosterone - adverse effects</subject><ispartof>Scientific reports, 2020-01, Vol.10 (1), p.404, Article 404</ispartof><rights>The Author(s) 2020</rights><rights>This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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In an animal model of this condition, we reported that insulin sensitivity (IS) was lower in young female sheep born to testosterone-treated mothers versus sheep born to non-exposed mothers (control). This lower insulin sensitivity remains throughout reproductive life. However, it is unknown whether abnormal postnatal levels of testosterone (T) further decrease IS derived from prenatal exposure to testosterone. Therefore, we assessed the effects of an acute testosterone administration (40 mg) on IS and insulin secretion during an intravenous glucose tolerance test performed at 40 weeks of age (adulthood) in previously ovariectomized sheep at 26 weeks of age (prepuberty), that were either prenatally exposed to testosterone (T-females, n = 6) or not (C-females, n = 6). The incremental area under the curve of insulin was greater in C-females both with or without the acute testosterone treatment (P < 0.05). The ISI-Composite was lower after an acute testosterone treatment, only in T-females. We conclude that prenatal exposure to testosterone disrupts pancreatic insulin secretion in response to glucose and that in this setting further hyperandrogenemia may predispose to lower insulin sensitivity.</description><subject>692/163/2743/137/773</subject><subject>692/699/2743/137/773</subject><subject>Animal models</subject><subject>Animals</subject><subject>Embryonic Development - drug effects</subject><subject>Female</subject><subject>Females</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>Humanities and Social Sciences</subject><subject>Insulin</subject><subject>Insulin Resistance</subject><subject>Insulin secretion</subject><subject>Insulin Secretion - drug effects</subject><subject>Intravenous administration</subject><subject>multidisciplinary</subject><subject>Ovariectomy</subject><subject>Pancreas</subject><subject>Polycystic ovary syndrome</subject><subject>Pregnancy</subject><subject>Prenatal experience</subject><subject>Prenatal exposure</subject><subject>Prenatal Exposure Delayed Effects - 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In an animal model of this condition, we reported that insulin sensitivity (IS) was lower in young female sheep born to testosterone-treated mothers versus sheep born to non-exposed mothers (control). This lower insulin sensitivity remains throughout reproductive life. However, it is unknown whether abnormal postnatal levels of testosterone (T) further decrease IS derived from prenatal exposure to testosterone. Therefore, we assessed the effects of an acute testosterone administration (40 mg) on IS and insulin secretion during an intravenous glucose tolerance test performed at 40 weeks of age (adulthood) in previously ovariectomized sheep at 26 weeks of age (prepuberty), that were either prenatally exposed to testosterone (T-females, n = 6) or not (C-females, n = 6). The incremental area under the curve of insulin was greater in C-females both with or without the acute testosterone treatment (P < 0.05). The ISI-Composite was lower after an acute testosterone treatment, only in T-females. We conclude that prenatal exposure to testosterone disrupts pancreatic insulin secretion in response to glucose and that in this setting further hyperandrogenemia may predispose to lower insulin sensitivity.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31941959</pmid><doi>10.1038/s41598-019-57197-x</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 692/163/2743/137/773 692/699/2743/137/773 Animal models Animals Embryonic Development - drug effects Female Females Glucose Glucose tolerance Humanities and Social Sciences Insulin Insulin Resistance Insulin secretion Insulin Secretion - drug effects Intravenous administration multidisciplinary Ovariectomy Pancreas Polycystic ovary syndrome Pregnancy Prenatal experience Prenatal exposure Prenatal Exposure Delayed Effects - chemically induced Prenatal Exposure Delayed Effects - metabolism Prenatal Exposure Delayed Effects - pathology Science Science (multidisciplinary) Secretion Sheep Testosterone Testosterone - adverse effects |
| title | Prenatal Testosterone Exposure Disrupts Insulin Secretion And Promotes Insulin Resistance |
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