FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2098789212> ?p ?o ?g. }

• W2098789212 endingPage "1569" @default.
• W2098789212 startingPage "1566" @default.
• W2098789212 abstract "During pregnancy there is an enhanced need for insulin to accommodate the growing fetal compartment as well as the substantial increase in insulin resistance. Failure of the islets to adapt to this increased demand for insulin leads to gestational diabetes. The report by Huang et al. (1), using an in vivo model of prolactin (PRL) receptor deficiency, provides an important validation of the hypothesis that -cell PRL receptors are central to mechanisms whereby islets adapt to pregnancy (Fig. 1). This study showed not only that PRL receptor deficiency leads to gestational diabetes, but the genetic phenotype of the mother influences the outcome of islet development in the fetus. That islets undergo changes during pregnancy was observed as early as 1930 (2), when Cramer concluded that islets are a very plastic tissue that undergo considerable changes, especially during pregnancy. The changes he observed included increased secretory activity, islet growth, and neogenesis. Direct evidence for functional changes in islets did not occur until the development of a sensitive insulin assay in the 1960s, when it was reported that there was a progressive increase in both fasting and glucosestimulated insulin secretion throughout the course of human pregnancy (3). This and subsequent research led to the characterization of pregnancy as a condition of elevated serum insulin levels, slightly lower blood glucose levels, and peripheral insulin resistance. The short-term regulation of insulin secretion is achieved by elevating blood glucose. However, if this were the only mechanism available for increasing insulin secretion during pregnancy, there would be a need for persistent hyperglycemia, a condition detrimental both to the mother and the developing fetus. Thus, when there is an increased need for insulin over a prolonged period of time, such as occurs in pregnancy, islets must undergo adaptive changes. The outcome of the up-regulation must be such that there is enhanced insulin secretion at normal glucose levels. There are three basic mechanisms whereby one can increase insulin secretion at normal glucose concentrations: increase the islet -cell mass, increase the sensitivity of insulin secretion in response to glucose, or both. Evidence that there is an increase islet/ -cell mass comes from a number of studies (4–7). These studies indicate that there is an approximate 2-fold increase in islet mass. DNA content per islet also indicates an increase in islet mass, and both morphometric and DNA to protein ratio methods indicate -cell hypertrophy as well as -cell hyperplasia (8– 12). Evidence for increased -cell mitosis comes from tritiated thymidine and bromodeoxyuridine labeling of islets during pregnancy (4, 13, 14). Overall, these reports indicate that islet mass doubles, and the increase is a consequence of new -cell formation as well as an increase in -cell size. There is less information on whether islet neogenesis occurs during pregnancy. One report failed to detect evidence for islet neogenesis during pregnancy but did show that another condition of persistent hyperlactogenemia may result in islet neogenesis (15). There is also evidence for an increase in glucose-sensitive insulin secretion. During rodent pregnancy, fasting serum insulin levels are increased, and glucose levels are decreased (8, 16, 17), similar to that observed in human pregnancy. Green and Taylor (9) showed a leftward shift of the glucose-stimulated insulin secretion response curve in islets isolated from pregnant rats. In a similar study, we used perfused pancreas preparations to examine insulin secretion throughout rat pregnancy. A leftward shift in glucose-responsive insulin secretion as well as above-threshold insulin release was first noted on d 10 and peaked by d 15 (4). The threshold for glucose-stimulated insulin secretion decreased from 5.7–3.3 mM by d 15 pregnancy. The lowering of the threshold for glucose-stimulated insulin secretion is a key feature of islets as they adapt to pregnancy. It is through this maneuver that a large increase in insulin secretion can be achieved at fasting blood glucose levels, as is seen during pregnancy. The most important changes in islet adaptation to pregnancy are enhanced insulin secretion and enhanced -cell mass. Candidate hormones must be shown to induce these changes. Although a variety of hormones increase during pregnancy, only PRL and placental lactogen, which acts through PRL receptors, are capable of inducing the changes that occur in islets during" @default.
• W2098789212 created "2016-06-24" @default.
• W2098789212 creator A5015761283 @default.
• W2098789212 creator A5054209702 @default.
• W2098789212 date "2009-04-01" @default.
• W2098789212 modified "2023-10-02" @default.
• W2098789212 title "Prolactin Receptors Are Critical to the Adaptation of Islets to Pregnancy" @default.
• W2098789212 cites W1492153103 @default.
• W2098789212 cites W180739046 @default.
• W2098789212 cites W1968856585 @default.
• W2098789212 cites W1969459168 @default.
• W2098789212 cites W1972212762 @default.
• W2098789212 cites W1981235241 @default.
• W2098789212 cites W1981564790 @default.
• W2098789212 cites W1986298296 @default.
• W2098789212 cites W1987908541 @default.
• W2098789212 cites W1989955420 @default.
• W2098789212 cites W1996310923 @default.
• W2098789212 cites W1999585523 @default.
• W2098789212 cites W2000412931 @default.
• W2098789212 cites W2006359547 @default.
• W2098789212 cites W2019277645 @default.
• W2098789212 cites W2024331279 @default.
• W2098789212 cites W2035940741 @default.
• W2098789212 cites W2037781012 @default.
• W2098789212 cites W2041165229 @default.
• W2098789212 cites W2048157375 @default.
• W2098789212 cites W2050185190 @default.
• W2098789212 cites W2058917386 @default.
• W2098789212 cites W2064496466 @default.
• W2098789212 cites W2069438759 @default.
• W2098789212 cites W2074637447 @default.
• W2098789212 cites W2080124386 @default.
• W2098789212 cites W2098197630 @default.
• W2098789212 cites W2118884708 @default.
• W2098789212 cites W2125858776 @default.
• W2098789212 cites W2131401263 @default.
• W2098789212 cites W2132051907 @default.
• W2098789212 cites W2140439271 @default.
• W2098789212 cites W2146296317 @default.
• W2098789212 cites W2147891161 @default.
• W2098789212 cites W2148486284 @default.
• W2098789212 cites W2148583270 @default.
• W2098789212 cites W2150388470 @default.
• W2098789212 cites W2152699028 @default.
• W2098789212 cites W2154630029 @default.
• W2098789212 cites W2161092753 @default.
• W2098789212 cites W2168932510 @default.
• W2098789212 cites W2173560213 @default.
• W2098789212 cites W2418044337 @default.
• W2098789212 doi "https://doi.org/10.1210/en.2008-1710" @default.
• W2098789212 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19307419" @default.
• W2098789212 hasPublicationYear "2009" @default.
• W2098789212 type Work @default.
• W2098789212 sameAs 2098789212 @default.
• W2098789212 citedByCount "61" @default.
• W2098789212 countsByYear W20987892122012 @default.
• W2098789212 countsByYear W20987892122013 @default.
• W2098789212 countsByYear W20987892122014 @default.
• W2098789212 countsByYear W20987892122015 @default.
• W2098789212 countsByYear W20987892122016 @default.
• W2098789212 countsByYear W20987892122018 @default.
• W2098789212 countsByYear W20987892122019 @default.
• W2098789212 countsByYear W20987892122020 @default.
• W2098789212 countsByYear W20987892122021 @default.
• W2098789212 countsByYear W20987892122022 @default.
• W2098789212 countsByYear W20987892122023 @default.
• W2098789212 crossrefType "journal-article" @default.
• W2098789212 hasAuthorship W2098789212A5015761283 @default.
• W2098789212 hasAuthorship W2098789212A5054209702 @default.
• W2098789212 hasBestOaLocation W20987892121 @default.
• W2098789212 hasConcept C126322002 @default.
• W2098789212 hasConcept C134018914 @default.
• W2098789212 hasConcept C139807058 @default.
• W2098789212 hasConcept C169760540 @default.
• W2098789212 hasConcept C170493617 @default.
• W2098789212 hasConcept C2779064019 @default.
• W2098789212 hasConcept C2779234561 @default.
• W2098789212 hasConcept C54355233 @default.
• W2098789212 hasConcept C71315377 @default.
• W2098789212 hasConcept C71924100 @default.
• W2098789212 hasConcept C86803240 @default.
• W2098789212 hasConceptScore W2098789212C126322002 @default.
• W2098789212 hasConceptScore W2098789212C134018914 @default.
• W2098789212 hasConceptScore W2098789212C139807058 @default.
• W2098789212 hasConceptScore W2098789212C169760540 @default.
• W2098789212 hasConceptScore W2098789212C170493617 @default.
• W2098789212 hasConceptScore W2098789212C2779064019 @default.
• W2098789212 hasConceptScore W2098789212C2779234561 @default.
• W2098789212 hasConceptScore W2098789212C54355233 @default.
• W2098789212 hasConceptScore W2098789212C71315377 @default.
• W2098789212 hasConceptScore W2098789212C71924100 @default.
• W2098789212 hasConceptScore W2098789212C86803240 @default.
• W2098789212 hasIssue "4" @default.
• W2098789212 hasLocation W20987892121 @default.
• W2098789212 hasLocation W20987892122 @default.
• W2098789212 hasOpenAccess W2098789212 @default.
• W2098789212 hasPrimaryLocation W20987892121 @default.

• next