The Pathophysiology of Gestational Diabetes Mellitus
Gestational diabetes mellitus (GDM) is a serious pregnancy complication, in which women without previously diagnosed diabetes develop chronic hyperglycemia during gestation. In most cases, this hyperglycemia is the result of impaired glucose tolerance due to pancreatic β-cell dysfunction on a backgr...
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Veröffentlicht in: | International journal of molecular sciences 2018-10, Vol.19 (11), p.3342 |
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description | Gestational diabetes mellitus (GDM) is a serious pregnancy complication, in which women without previously diagnosed diabetes develop chronic hyperglycemia during gestation. In most cases, this hyperglycemia is the result of impaired glucose tolerance due to pancreatic β-cell dysfunction on a background of chronic insulin resistance. Risk factors for GDM include overweight and obesity, advanced maternal age, and a family history or any form of diabetes. Consequences of GDM include increased risk of maternal cardiovascular disease and type 2 diabetes and macrosomia and birth complications in the infant. There is also a longer-term risk of obesity, type 2 diabetes, and cardiovascular disease in the child. GDM affects approximately 16.5% of pregnancies worldwide, and this number is set to increase with the escalating obesity epidemic. While several management strategies exist-including insulin and lifestyle interventions-there is not yet a cure or an efficacious prevention strategy. One reason for this is that the molecular mechanisms underlying GDM are poorly defined. This review discusses what is known about the pathophysiology of GDM, and where there are gaps in the literature that warrant further exploration. |
doi_str_mv | 10.3390/ijms19113342 |
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In most cases, this hyperglycemia is the result of impaired glucose tolerance due to pancreatic β-cell dysfunction on a background of chronic insulin resistance. Risk factors for GDM include overweight and obesity, advanced maternal age, and a family history or any form of diabetes. Consequences of GDM include increased risk of maternal cardiovascular disease and type 2 diabetes and macrosomia and birth complications in the infant. There is also a longer-term risk of obesity, type 2 diabetes, and cardiovascular disease in the child. GDM affects approximately 16.5% of pregnancies worldwide, and this number is set to increase with the escalating obesity epidemic. While several management strategies exist-including insulin and lifestyle interventions-there is not yet a cure or an efficacious prevention strategy. One reason for this is that the molecular mechanisms underlying GDM are poorly defined. 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Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). 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In most cases, this hyperglycemia is the result of impaired glucose tolerance due to pancreatic β-cell dysfunction on a background of chronic insulin resistance. Risk factors for GDM include overweight and obesity, advanced maternal age, and a family history or any form of diabetes. Consequences of GDM include increased risk of maternal cardiovascular disease and type 2 diabetes and macrosomia and birth complications in the infant. There is also a longer-term risk of obesity, type 2 diabetes, and cardiovascular disease in the child. GDM affects approximately 16.5% of pregnancies worldwide, and this number is set to increase with the escalating obesity epidemic. While several management strategies exist-including insulin and lifestyle interventions-there is not yet a cure or an efficacious prevention strategy. One reason for this is that the molecular mechanisms underlying GDM are poorly defined. This review discusses what is known about the pathophysiology of GDM, and where there are gaps in the literature that warrant further exploration.</description><subject>Adiponectin - metabolism</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - physiopathology</subject><subject>Animals</subject><subject>Beta cells</subject><subject>Body weight</subject><subject>Cardiovascular diseases</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes, Gestational - diagnosis</subject><subject>Diabetes, Gestational - etiology</subject><subject>Diabetes, Gestational - metabolism</subject><subject>Diabetes, Gestational - physiopathology</subject><subject>Diet</subject><subject>Ethnicity</subject><subject>Family medical history</subject><subject>Fatty acids</subject><subject>Female</subject><subject>Fetuses</subject><subject>Gestational diabetes</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glucose tolerance</subject><subject>Hormones</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Insulin</subject><subject>Insulin Resistance</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>Insulin-Secreting Cells - pathology</subject><subject>Leptin - metabolism</subject><subject>Metabolism</subject><subject>Molecular modelling</subject><subject>Nutrition research</subject><subject>Obesity</subject><subject>Overweight</subject><subject>Oxidative Stress</subject><subject>Pathophysiology</subject><subject>Pregnancy</subject><subject>Pregnancy complications</subject><subject>Resistance factors</subject><subject>Review</subject><subject>Risk analysis</subject><subject>Risk Factors</subject><subject>Westernization</subject><subject>Womens health</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkTFPwzAQhS0EoqWwMaNILAwE7HMcJwsSKlCQimAos3V1ncZVUpc4Qeq_x6ilKkx3p_v0dO8eIeeM3nCe01u7qD3LGeM8gQPSZwlATGkqD_f6HjnxfkEpcBD5MelxyiVnSdonyaQ00Tu2pVuVa29d5ebryBXRyPgWW-uWWEUPFqemNT56NVVl286fkqMCK2_OtnVAPp4eJ8PnePw2ehnej2MtgLUxyiwDQECDWs-QFVpIpnMhTE4FRaYZpkxLpMk006mmACmEQQjJUwpZwgfkbqO76qa1mWmzbBus1KqxNTZr5dCqv5ulLdXcfakUZJLKPAhcbQUa99kFS6q2XgcXuDSu8woYSKCUSgjo5T904bom2A-UyCDjwJkM1PWG0o3zvjHF7hhG1U8caj-OgF_sG9jBv__n34klhRQ</recordid><startdate>20181026</startdate><enddate>20181026</enddate><creator>Plows, Jasmine F</creator><creator>Stanley, Joanna L</creator><creator>Baker, Philip N</creator><creator>Reynolds, Clare M</creator><creator>Vickers, Mark H</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1421-3387</orcidid><orcidid>https://orcid.org/0000-0003-4876-9356</orcidid></search><sort><creationdate>20181026</creationdate><title>The Pathophysiology of Gestational Diabetes Mellitus</title><author>Plows, Jasmine F ; Stanley, Joanna L ; Baker, Philip N ; Reynolds, Clare M ; Vickers, Mark H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c521t-a78822a2aeaccda1fc571c955e9050a1c1a61c7a04b8c6c02262a045573602843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adiponectin - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Plows, Jasmine F</au><au>Stanley, Joanna L</au><au>Baker, Philip N</au><au>Reynolds, Clare M</au><au>Vickers, Mark H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Pathophysiology of Gestational Diabetes Mellitus</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2018-10-26</date><risdate>2018</risdate><volume>19</volume><issue>11</issue><spage>3342</spage><pages>3342-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Gestational diabetes mellitus (GDM) is a serious pregnancy complication, in which women without previously diagnosed diabetes develop chronic hyperglycemia during gestation. In most cases, this hyperglycemia is the result of impaired glucose tolerance due to pancreatic β-cell dysfunction on a background of chronic insulin resistance. Risk factors for GDM include overweight and obesity, advanced maternal age, and a family history or any form of diabetes. Consequences of GDM include increased risk of maternal cardiovascular disease and type 2 diabetes and macrosomia and birth complications in the infant. There is also a longer-term risk of obesity, type 2 diabetes, and cardiovascular disease in the child. GDM affects approximately 16.5% of pregnancies worldwide, and this number is set to increase with the escalating obesity epidemic. While several management strategies exist-including insulin and lifestyle interventions-there is not yet a cure or an efficacious prevention strategy. One reason for this is that the molecular mechanisms underlying GDM are poorly defined. This review discusses what is known about the pathophysiology of GDM, and where there are gaps in the literature that warrant further exploration.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>30373146</pmid><doi>10.3390/ijms19113342</doi><orcidid>https://orcid.org/0000-0002-1421-3387</orcidid><orcidid>https://orcid.org/0000-0003-4876-9356</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Adiponectin - metabolism Adipose Tissue - metabolism Adipose Tissue - physiopathology Animals Beta cells Body weight Cardiovascular diseases Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diabetes, Gestational - diagnosis Diabetes, Gestational - etiology Diabetes, Gestational - metabolism Diabetes, Gestational - physiopathology Diet Ethnicity Family medical history Fatty acids Female Fetuses Gestational diabetes Glucose Glucose - metabolism Glucose tolerance Hormones Humans Hyperglycemia Insulin Insulin Resistance Insulin-Secreting Cells - metabolism Insulin-Secreting Cells - pathology Leptin - metabolism Metabolism Molecular modelling Nutrition research Obesity Overweight Oxidative Stress Pathophysiology Pregnancy Pregnancy complications Resistance factors Review Risk analysis Risk Factors Westernization Womens health |
title | The Pathophysiology of Gestational Diabetes Mellitus |
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