Impaired Insulin Secretion After Prenatal Exposure to the Dutch Famine

OBJECTIVE:--We previously reported that people prenatally exposed to famine during the Dutch Hunger Winter of 1944-1945 have higher 2-h glucose concentrations after an oral glucose tolerance test in later life. We aimed to determine whether this association is mediated through alterations in insulin...

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Veröffentlicht in:Diabetes care 2006-08, Vol.29 (8), p.1897-1901
Hauptverfasser: Rooij, Susanne R. de, Painter, Rebecca C, Phillips, David I.W, Osmond, Clive, Michels, Robert P.J, Godsland, Ian F, Bossuyt, Patrick M.M, Bleker, Otto P, Roseboom, Tessa J
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container_end_page 1901
container_issue 8
container_start_page 1897
container_title Diabetes care
container_volume 29
creator Rooij, Susanne R. de
Painter, Rebecca C
Phillips, David I.W
Osmond, Clive
Michels, Robert P.J
Godsland, Ian F
Bossuyt, Patrick M.M
Bleker, Otto P
Roseboom, Tessa J
description OBJECTIVE:--We previously reported that people prenatally exposed to famine during the Dutch Hunger Winter of 1944-1945 have higher 2-h glucose concentrations after an oral glucose tolerance test in later life. We aimed to determine whether this association is mediated through alterations in insulin secretion, insulin sensitivity, or a combination of both. RESEARCH DESIGN AND METHODS--We performed a 15-sample intravenous glucose tolerance test in a subsample of 94 normoglycemic men and women from the Dutch Famine Birth Cohort. We used the disposition index, derived as the product of insulin sensitivity and the first-phase insulin response to glucose as a measure of the activity of the β-cells adjusted for insulin resistance. In all analyses, we adjusted for sex and BMI. RESULTS:--Glucose tolerance was impaired in people who had been prenatally exposed to famine compared with people unexposed to famine (difference in intravenous glucose tolerance test Kg value -21% [95% CI -41 to -4]). People exposed to famine during midgestation had a significantly lower disposition index (-53% [-126 to -3]) compared with people unexposed to famine. Prenatal exposure to famine during early gestation was also associated with a lower disposition index, but this difference did not reach statistical significance. CONCLUSIONS:--Impaired glucose tolerance after exposure to famine during mid-gestation and early gestation seems to be mediated through an insulin secretion defect.
doi_str_mv 10.2337/dc06-0460
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We aimed to determine whether this association is mediated through alterations in insulin secretion, insulin sensitivity, or a combination of both. RESEARCH DESIGN AND METHODS--We performed a 15-sample intravenous glucose tolerance test in a subsample of 94 normoglycemic men and women from the Dutch Famine Birth Cohort. We used the disposition index, derived as the product of insulin sensitivity and the first-phase insulin response to glucose as a measure of the activity of the β-cells adjusted for insulin resistance. In all analyses, we adjusted for sex and BMI. RESULTS:--Glucose tolerance was impaired in people who had been prenatally exposed to famine compared with people unexposed to famine (difference in intravenous glucose tolerance test Kg value -21% [95% CI -41 to -4]). People exposed to famine during midgestation had a significantly lower disposition index (-53% [-126 to -3]) compared with people unexposed to famine. Prenatal exposure to famine during early gestation was also associated with a lower disposition index, but this difference did not reach statistical significance. CONCLUSIONS:--Impaired glucose tolerance after exposure to famine during mid-gestation and early gestation seems to be mediated through an insulin secretion defect.</description><identifier>ISSN: 0149-5992</identifier><identifier>EISSN: 1935-5548</identifier><identifier>DOI: 10.2337/dc06-0460</identifier><identifier>PMID: 16873799</identifier><identifier>CODEN: DICAD2</identifier><language>eng</language><publisher>Alexandria, VA: American Diabetes Association</publisher><subject>Apoptosis ; Biological and medical sciences ; Birth weight ; Blood Glucose - metabolism ; Diabetes ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Female ; Fertility ; Fetal malnutrition ; Fetuses ; Glucose ; Glucose Tolerance Test ; Glucose tolerance tests ; Health aspects ; Humans ; Insulin ; Insulin - blood ; Insulin - metabolism ; Insulin Secretion ; Male ; Medical sciences ; Middle Aged ; Mortality ; Mothers ; Netherlands ; Netherlands - epidemiology ; Pregnancy ; Prenatal exposure ; Prenatal Nutritional Physiological Phenomena ; Risk factors ; Starvation - epidemiology ; Victims of famine</subject><ispartof>Diabetes care, 2006-08, Vol.29 (8), p.1897-1901</ispartof><rights>2006 INIST-CNRS</rights><rights>COPYRIGHT 2006 American Diabetes Association</rights><rights>Copyright American Diabetes Association Aug 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c577t-6eaac8f1a1f331e541c4297a7888abf7d296c426b1b871ff0a5c3279517efaa23</citedby><cites>FETCH-LOGICAL-c577t-6eaac8f1a1f331e541c4297a7888abf7d296c426b1b871ff0a5c3279517efaa23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=18002019$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16873799$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rooij, Susanne R. de</creatorcontrib><creatorcontrib>Painter, Rebecca C</creatorcontrib><creatorcontrib>Phillips, David I.W</creatorcontrib><creatorcontrib>Osmond, Clive</creatorcontrib><creatorcontrib>Michels, Robert P.J</creatorcontrib><creatorcontrib>Godsland, Ian F</creatorcontrib><creatorcontrib>Bossuyt, Patrick M.M</creatorcontrib><creatorcontrib>Bleker, Otto P</creatorcontrib><creatorcontrib>Roseboom, Tessa J</creatorcontrib><title>Impaired Insulin Secretion After Prenatal Exposure to the Dutch Famine</title><title>Diabetes care</title><addtitle>Diabetes Care</addtitle><description>OBJECTIVE:--We previously reported that people prenatally exposed to famine during the Dutch Hunger Winter of 1944-1945 have higher 2-h glucose concentrations after an oral glucose tolerance test in later life. We aimed to determine whether this association is mediated through alterations in insulin secretion, insulin sensitivity, or a combination of both. RESEARCH DESIGN AND METHODS--We performed a 15-sample intravenous glucose tolerance test in a subsample of 94 normoglycemic men and women from the Dutch Famine Birth Cohort. We used the disposition index, derived as the product of insulin sensitivity and the first-phase insulin response to glucose as a measure of the activity of the β-cells adjusted for insulin resistance. In all analyses, we adjusted for sex and BMI. RESULTS:--Glucose tolerance was impaired in people who had been prenatally exposed to famine compared with people unexposed to famine (difference in intravenous glucose tolerance test Kg value -21% [95% CI -41 to -4]). People exposed to famine during midgestation had a significantly lower disposition index (-53% [-126 to -3]) compared with people unexposed to famine. Prenatal exposure to famine during early gestation was also associated with a lower disposition index, but this difference did not reach statistical significance. CONCLUSIONS:--Impaired glucose tolerance after exposure to famine during mid-gestation and early gestation seems to be mediated through an insulin secretion defect.</description><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Birth weight</subject><subject>Blood Glucose - metabolism</subject><subject>Diabetes</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. 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We aimed to determine whether this association is mediated through alterations in insulin secretion, insulin sensitivity, or a combination of both. RESEARCH DESIGN AND METHODS--We performed a 15-sample intravenous glucose tolerance test in a subsample of 94 normoglycemic men and women from the Dutch Famine Birth Cohort. We used the disposition index, derived as the product of insulin sensitivity and the first-phase insulin response to glucose as a measure of the activity of the β-cells adjusted for insulin resistance. In all analyses, we adjusted for sex and BMI. RESULTS:--Glucose tolerance was impaired in people who had been prenatally exposed to famine compared with people unexposed to famine (difference in intravenous glucose tolerance test Kg value -21% [95% CI -41 to -4]). People exposed to famine during midgestation had a significantly lower disposition index (-53% [-126 to -3]) compared with people unexposed to famine. Prenatal exposure to famine during early gestation was also associated with a lower disposition index, but this difference did not reach statistical significance. CONCLUSIONS:--Impaired glucose tolerance after exposure to famine during mid-gestation and early gestation seems to be mediated through an insulin secretion defect.</abstract><cop>Alexandria, VA</cop><pub>American Diabetes Association</pub><pmid>16873799</pmid><doi>10.2337/dc06-0460</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
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subjects Apoptosis
Biological and medical sciences
Birth weight
Blood Glucose - metabolism
Diabetes
Diabetes. Impaired glucose tolerance
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Female
Fertility
Fetal malnutrition
Fetuses
Glucose
Glucose Tolerance Test
Glucose tolerance tests
Health aspects
Humans
Insulin
Insulin - blood
Insulin - metabolism
Insulin Secretion
Male
Medical sciences
Middle Aged
Mortality
Mothers
Netherlands
Netherlands - epidemiology
Pregnancy
Prenatal exposure
Prenatal Nutritional Physiological Phenomena
Risk factors
Starvation - epidemiology
Victims of famine
title Impaired Insulin Secretion After Prenatal Exposure to the Dutch Famine
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