{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T04:38:04Z","timestamp":1790483884483,"version":"4.1.0"},"reference-count":56,"publisher":"Wiley","issue":"23","license":[{"start":{"date-parts":[[2019,11,13]],"date-time":"2019-11-13T00:00:00Z","timestamp":1573603200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001794","name":"University of Queensland","doi-asserted-by":"publisher","award":["ECRScheme"],"award-info":[{"award-number":["ECRScheme"]}],"id":[{"id":"10.13039\/501100001794","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","award":["APP1078164"],"award-info":[{"award-number":["APP1078164"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Prenatal alcohol exposure has the potential to affect fetal development and programme chronic disease in offspring.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Previous preclinical models typically use high, chronic doses of alcohol throughout pregnancy to examine effects on offspring, particularly on the brain and behaviour.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>In this study we use a rat model of moderate, acute, prenatal alcohol exposure to determine if this can be detrimental to maintenance of glucose homeostasis in adolescent and adult offspring.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Although female offspring were relatively unaffected, there was evidence of insulin resistance in 6\u2010month\u2010old male offspring exposed to prenatal alcohol, suggestive of a pre\u2010diabetic state.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>This result suggests that even a relatively low\u2010dose, acute exposure to alcohol during pregnancy can still programme metabolic dysfunction in a sex\u2010specific manner.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Alcohol consumption is highly prevalent amongst women of reproductive age. Given that approximately 50% of pregnancies are unplanned, alcohol has the potential to affect fetal development and programme chronic disease in offspring. We examined the effect of an acute but moderate prenatal alcohol exposure (PAE) on glucose metabolism, lipid levels and dietary preference in adolescent and\/or adult rat offspring. Pregnant Sprague\u2013Dawley rats received an oral gavage of ethanol (1\u00a0g\u00a0kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      maternal body weight,\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a09 dams) or an equivalent volume of saline (control,\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a08 dams) at embryonic days 13.5 and 14.5. PAE resulted in a blood alcohol concentration of 0.05\u20130.06% 1\u00a0h post\u2010gavage in dams. Fasting blood glucose concentration was not affected by PAE in offspring at any age, nor were blood glucose levels during a glucose tolerance test (GTT) in 6\u2010month\u2010old offspring (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      &gt;\u00a00.5). However, there was evidence of insulin resistance in PAE male offspring at 6\u00a0months of age, with significantly elevated fasting plasma insulin (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\u00a00.001), a tendency for increased first phase insulin secretion during the GTT and impaired glucose clearance following an insulin challenge (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\u00a00.007). This was accompanied by modest alterations in protein kinase B (AKT) signalling in adipose tissue. PAE also resulted in reduced calorie consumption by offspring compared to controls (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\u00a00.04). These data suggest that a relatively low\u2010level, acute PAE programmes metabolic dysfunction in offspring in a sex\u2010specific manner. These results highlight that alcohol consumption during pregnancy has the potential to affect the long\u2010term health of offspring.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp278531","type":"journal-article","created":{"date-parts":[[2019,10,8]],"date-time":"2019-10-08T21:08:36Z","timestamp":1570568916000},"page":"5619-5637","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["Prenatal alcohol exposure programmes offspring disease: insulin resistance in adult males in a rat model of acute exposure"],"prefix":"10.1113","volume":"597","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2422-7771","authenticated-orcid":false,"given":"Tam M. 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