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Cited by 358Pancreatic function and diabetesDiabetes and associated disordersDiabetes Treatment and Management

Expansion of β-cell mass in response to pregnancy

Open access
Rieck, Sebastian, Kaestner, Klaus H.·2010·Trends in Endocrinology & Metabolism
DOI 10.1016/j.tem.2009.11.001PMC PMC3627215
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Abstract

Inadequate β-cell mass can lead to insulin insufficiency and diabetes. During times of prolonged metabolic demand for insulin, the endocrine pancreas can respond by increasing β-cell mass, both by increasing cell size and by changing the balance between β-cell proliferation and apoptosis. In this paper, we review recent advances in our understanding of the mechanisms that control the adaptive expansion of β-cell mass, focusing on the islet’s response to pregnancy, a physiological state of insulin resistance. Functional characterization of factors controlling both β-cell proliferation and survival might not only lead to the development of successful therapeutic strategies to enhance the response of the β-cell to increased metabolic loads, but also improve islet transplantation regimens.

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Crossref · 10.1016/j.tem.2009.11.001

Cites

85 of 85 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 109 cited sources checked · 0 supported · 0 flagged

  • Findingcitation

    Gene expression analysis during the peak of β-cell DNA synthesis identified many genes not previously reported to play a role in β-cell expansion.

    “Gene expression analysis during the peak of β-cell DNA synthesis not only showed induction of Prlr and Cdk4 expression in the islets of pregnant mice, but also identified many genes that had not previously been reported to play a role in β-cell expansion, which we discuss further below [10].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [10] Rieck, 2009, The transcriptional response of the islet to pregnancy in mice, Mol. Endocrinol. source

      Not checked in the free run.

    • Rests on an assumption: Gene expression changes in islets during the peak of DNA synthesis reflect the mechanisms that drive β-cell expansion during pregnancy.
  • Findingcitation

    Both Cish and Socs2 are robustly induced at the transcriptional level in pancreatic islets during pregnancy.

    “Both Cish and Socs2, members of the suppressor of cytokine signaling family of proteins, are robustly induced at the transcriptional level in pancreatic islets during pregnancy [10].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [10] Rieck, 2009, The transcriptional response of the islet to pregnancy in mice, Mol. Endocrinol. source

      Not checked in the free run.

    • Rests on an assumption: Gene expression changes in islets during the peak of DNA synthesis reflect the mechanisms that drive β-cell expansion during pregnancy.
  • Findingcitation

    Birc5 gene expression in islets closely mirrors the proliferative profile reflected by Ki67 mRNA levels throughout pregnancy, obesity and β-cell recovery after injury.

    “Indeed, Birc5 gene expression in islets closely mirrors the proliferative profile as reflected in mRNA levels of Ki67 throughout pregnancy, obesity and β-cell recovery after injury [10].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [10] Rieck, 2009, The transcriptional response of the islet to pregnancy in mice, Mol. Endocrinol. source

      Not checked in the free run.

    • Rests on an assumption: Gene expression changes in islets during the peak of DNA synthesis reflect the mechanisms that drive β-cell expansion during pregnancy.
  • Findingcitation

    During the peak of β-cell proliferation in pregnancy, the antiapoptotic gene Birc5 is upregulated.

    “In this context, it is interesting that during the peak of β-cell proliferation in pregnancy, the antiapoptotic gene Birc5 was upregulated [10].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [10] Rieck, 2009, The transcriptional response of the islet to pregnancy in mice, Mol. Endocrinol. source

      Not checked in the free run.

    • Rests on an assumption: Gene expression changes in islets during the peak of DNA synthesis reflect the mechanisms that drive β-cell expansion during pregnancy.
  • Findingcitation

    In islets of pregnant mice at the peak of β-cell DNA synthesis, Prlr and Cdk4 expression are induced.

    “Gene expression analysis during the peak of β-cell DNA synthesis not only showed induction of Prlr and Cdk4 expression in the islets of pregnant mice, but also identified many genes that had not previously been reported to play a role in β-cell expansion, which we discuss further below [10].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [10] Rieck, 2009, The transcriptional response of the islet to pregnancy in mice, Mol. Endocrinol. source

      Not checked in the free run.

    • Rests on an assumption: Gene expression changes in islets during the peak of DNA synthesis reflect the mechanisms that drive β-cell expansion during pregnancy.
  • May combine two claims. 21
  • Classified as probably not a substantial claim. 4

  • May combine two claims.

    Premisecitation

    People with type 1 or type 2 diabetes have reduced β-cell mass and increased β-cell apoptosis, with loss exceeding growth.

    “Indeed, individuals with either type 1 or type 2 diabetes show decreases in β-cell mass and increases in β-cell apoptosis, outweighing that of β-cell growth [6,7].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [6] Butler, 2003, Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes, Diabetes source

      Not checked in the free run.

    • cites [7] Meier, 2005, Sustained beta cell apoptosis in patients with long-standing type 1 diabetes: indirect evidence for islet regeneration?, Diabetologia source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    In young adult mice, most new β-cells come from replication of pre-existing β-cells, and few if any come from progenitors under normal conditions.

    “Genetic lineage tracing studies performed in the young adult mouse indicate that the great majority of new β-cells are derived through replication of pre-existing β-cells and few, if any, newly formed β-cells stem from progenitor populations under normal circumstances, at least in rodents [23].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [23] Dor, 2004, Adult pancreatic beta-cells are formed by self-duplication rather than stem-cell differentiation, Nature source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    The peak of BrdU incorporation occurs about two-thirds of the way through gestation, and labeling returns to pre-pregnancy levels shortly before parturition.

    “The peak of bromodeoxyuridine (BrdU) incorporation, an indicator of DNA synthesis during S-phase, occurs about two-thirds of the way through the gestational period, with labeling returning to pre-pregnancy levels shortly before parturition.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [9] Parsons, 1992, Adaptation of islets of Langerhans to pregnancy: increased islet cell proliferation and insulin secretion correlates with the onset of placental lactogen secretion, Endocrinology source

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    These genetic data indicate that β-cell proliferation matters at some point during ontogeny, but they do not show when in life it is important.

    “These genetic data together indicate a role for β-cell proliferation at some time during ontogeny; they do not, however, address the question of when in life β-cell proliferation is important.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Maternal IGF-1 levels rise in response to increased growth hormone levels.

    “Placental lactogen and growth hormone increase hepatic gluconeogenesis and lipolysis, and maternal IGF-1 levels increase in response to increased growth hormone levels [2,39].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [2] Sorenson, 1997, Adaptation of islets of Langerhans to pregnancy: beta-cell growth, enhanced insulin secretion and the role of lactogenic hormones, Horm. Metab. Res. source

      Not checked in the free run.

    • cites [39] Alsat, 1997, Human placental growth hormone, Am J. Obstet. Gynecol. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Pancreata from people with long-standing type 1 diabetes show measurable β-cell mass and evidence of β-cell apoptosis.

    “Intriguingly, pancreata from individuals with long-standing type 1 diabetes displayed not only measurable β-cell mass, but also evidence of β-cell apoptosis [7].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [7] Meier, 2005, Sustained beta cell apoptosis in patients with long-standing type 1 diabetes: indirect evidence for islet regeneration?, Diabetologia source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Placental lactogen and growth hormone increase hepatic gluconeogenesis and lipolysis.

    “Placental lactogen and growth hormone increase hepatic gluconeogenesis and lipolysis, and maternal IGF-1 levels increase in response to increased growth hormone levels [2,39].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [2] Sorenson, 1997, Adaptation of islets of Langerhans to pregnancy: beta-cell growth, enhanced insulin secretion and the role of lactogenic hormones, Horm. Metab. Res. source

      Not checked in the free run.

    • cites [39] Alsat, 1997, Human placental growth hormone, Am J. Obstet. Gynecol. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    A cell cycle regulatory module in islets distinguishes diabetes-resistant from diabetes-susceptible leptin-deficient Ob/Ob mouse strains and predicts their predisposition to diabetes.

    “Furthermore, gene expression studies uncovered a cell cycle regulatory module in islets that distinguishes between diabetes-resistant and diabetes-susceptible strains of leptin-deficient Ob/Ob mice, and successfully predicts their predisposition to diabetes [33].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [33] Keller, 2008, A gene expression network model of type 2 diabetes links cell cycle regulation in islets with diabetes susceptibility, Genome Res. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Pregnant mice heterozygous for the prolactin receptor null mutation show reduced β-cell proliferation, decreased β-cell size and mass, and impaired glucose tolerance.

    “The requirement of the prolactin receptor for β-cell adaptation during pregnancy was demonstrated using pregnant mice heterozygous for the prolactin receptor null mutation. These mice exhibited reduced β-cell proliferation, decreased β-cell size and mass, and impaired glucose tolerance [46].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [46] Huang, 2009, Prolactin receptor is required for normal glucose homeostasis and modulation of beta-cell mass during pregnancy, Endocrinology source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Global deletion of the prolactin receptor reduces β-cell mass and mildly impairs insulin secretion.

    “Similarly, global deletion of the prolactin receptor (PRLR), through which both PRL and PL signal, reduces β-cell mass and mildly impairs insulin secretion [45].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [45] Freemark, 2002, Targeted deletion of the PRL receptor: effects on islet development, insulin production, and glucose tolerance, Endocrinology source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Overexpression of placental lactogen in β-cells causes a dramatic increase in β-cell proliferation and β-cell mass, even resulting in hypoglycemia.

    “As a proof of principle for direct regulation of β-cell proliferation by prolactin (PRL) and placental lactogen (PL), overexpression of PL in the β-cell caused a dramatic increase in β-cell proliferation and β-cell mass, even resulting in hypoglycemia [44].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [44] Vasavada, 2000, Targeted expression of placental lactogen in the beta cells of transgenic mice results in beta cell proliferation, islet mass augmentation, and hypoglycemia, J. Biol. Chem. source

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    The pregnancy paradigm is a unique example of rapid and reversible β-cell mass expansion, with distinct bursts of β-cell proliferation and apoptosis in a physiological setting.

    “Although the mechanisms underlying these processes are not yet known, the pregnancy paradigm is a unique example of rapid and reversible β-cell mass expansion, with distinct bursts of both β-cell proliferation and β-cell apoptosis occurring in a physiological setting.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    A subset of obese individuals cannot compensate for insulin resistance and develops type 2 diabetes, partly because of increased β-cell apoptosis.

    “A subset of obese individuals is unable to compensate for insulin resistance, and thus develop type 2 diabetes mellitus, due in part to increased β-cell apoptosis [3,6].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [3] Kloppel, 1985, Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited, Surv. Synth. Pathol. Res.

      Not checked in the free run.

    • cites [6] Butler, 2003, Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes, Diabetes source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Ngfr expression is markedly increased in pancreatic islets during pregnancy and after β-cell ablation.

    “expression of signaling molecules such as the nerve growth factor receptor, Ngfr, is also dramatically upregulated in islets during pregnancy and during recovery after β-cell ablation [10].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [10] Rieck, 2009, The transcriptional response of the islet to pregnancy in mice, Mol. Endocrinol. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Hepatocyte growth factor boosts β-cell proliferation and mass, and enhances islet transplant outcomes in vivo.

    “hepatocyte growth factor, Hgf, increases β-cell proliferation and mass, and improves islet transplant outcomes in vivo [75,76].”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [75] Garcia-Ocana, 2000, Hepatocyte growth factor overexpression in the islet of transgenic mice increases beta cell proliferation, enhances islet mass, and induces mild hypoglycemia, J. Biol. Chem. source

      Not checked in the free run.

    • cites [76] Fiaschi-Taesch, 2008, Hepatocyte growth factor enhances engraftment and function of nonhuman primate islets, Diabetes source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Birc5 has a bifunctional role, controlling both proliferation and inhibition of apoptosis specifically in the β-cell in vivo.

    “A recent study showed a bifunctional role for Birc5 (survivin), controlling both proliferation and inhibition of apoptosis specifically in the β-cell in vivo [59].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [59] Jiang, 2008, Postnatal expansion of the pancreatic beta-cell mass is dependent on survivin, Diabetes source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Serotonin is synthesized within β-cells and stored with insulin in secretory granules.

    “it has been known for a long time that serotonin (5-hydroxytryptamine; 5-HT) is synthesized within β-cells and stored together with insulin in secretory granules [77,78]”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [77] Ekholm, 1971, Monoamines in the pancreatic islets of the mouse. Subcellular localization of 5-hydroxytryptamine by electron microscopic autoradiography, Diabetologia source

      Not checked in the free run.

    • cites [78] Richmond, 1996, Calcium- and barium-dependent exocytosis from the rat insulinoma cell line RINm5F assayed using membrane capacitance measurements and serotonin release, Pflugers Arch. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Foxm1 is required for maintenance of β-cell mass postnatally and during β-cell recovery after partial pancreatectomy.

    “Indeed, Foxm1 is required for the maintenance of β-cell mass postnatally and during β-cell recovery after partial pancreatectomy [64].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [64] Ackermann Misfeldt, 2008, Beta-cell proliferation, but not neogenesis, following 60% partial pancreatectomy is impaired in the absence of FoxM1, Diabetes source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The intrauterine milieu affects glucose homeostasis in the adult.

    “These findings provide a link to the well-known phenomenon that the intrauterine milieu affects glucose homeostasis in the adult (reviewed in [50]).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [50] Pinney, 2009, Epigenetic mechanisms in the development of type 2 diabetes, Trends Endocrinol. Metab.

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    STAT5 has pro-proliferative targets such as Cyclin D2, anti-apoptotic targets such as Bcl-xl and Bcl6, and targets involved in β-cell function.

    “Cish and Socs2 decrease activation of STAT5 [67,68], which has both pro-proliferative (Cyclin D2) [69] and anti-apoptotic (Bcl-xl, Bcl6) targets, as well as targets involved in β-cell function (Figure 3) [56,70].”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [69] Friedrichsen, 2003, Signal transducer and activator of transcription 5 activation is sufficient to drive transcriptional induction of cyclin D2 gene and proliferation of rat pancreatic beta-cells, Mol. Endocrinol. source

      Not checked in the free run.

    • cites [56] Karnik, 2007, Menin controls growth of pancreatic beta-cells in pregnant mice and promotes gestational diabetes mellitus, Science source

      Not checked in the free run.

    • cites [70] Fujinaka, 2007, Lactogens promote beta cell survival through JAK2/STAT5 activation and Bcl-XL upregulation, J. Biol. Chem. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Birc5-deficient animals progressively lose β-cell mass after 2 weeks of age, and Birc5-deficient cells exhibit dysmorphic nuclei consistent with defective cell division.

    “Birc5-deficient animals progressively lose β-cell mass after 2 weeks of age, and Birc5-deficient cells exhibit dysmorphic nuclei, consistent with defective cell division [59].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [59] Jiang, 2008, Postnatal expansion of the pancreatic beta-cell mass is dependent on survivin, Diabetes source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    β-cell-specific overexpression of c-Myc in transgenic mice increases β-cell proliferation and also increases apoptosis, leading to diabetes.

    “On the other hand, β-cell specific overexpression of c-Myc in transgenic mice not only increases β-cell proliferation, but also increases apoptosis, leading to the development of diabetes [61].”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [61] Laybutt, 2002, Overexpression of c-Myc in beta-cells of transgenic mice causes proliferation and apoptosis, downregulation of insulin gene expression, and diabetes, Diabetes source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Activation of STAT5, MAPK, phosphatidylinositol 3-kinase and IRS1/2 enhances β-cell compensation downstream of the prolactin receptor in vitro.

    “Although activation of multiple signaling pathways such as STAT5, MAPK and phosphatidylinositol 3-kinase and IRS1/2 enhances β-cell compensation downstream of the prolactin receptor in vitro [52–54], it is not clear whether PRL and/or PL stimulate these pathways in vivo.”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [52] Brelje, 2004, Distinctive roles for prolactin and growth hormone in the activation of signal transducer and activator of transcription 5 in pancreatic islets of langerhans, Endocrinology source

      Not checked in the free run.

    • cites [53] Amaral, 2004, Participation of prolactin receptors and phosphatidylinositol 3-kinase and MAP kinase pathways in the increase in pancreatic islet mass and sensitivity to glucose during pregnancy, J. Endocrinol. source

      Not checked in the free run.

    • cites [54] Amaral, 2003, Prolactin-signal transduction in neonatal rat pancreatic islets and interaction with the insulin-signaling pathway, Horm. Metab. Res. source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    5-HT is coupled by transglutaminases to two small GTPases, making them constitutively active and promoting insulin secretion.

    “5-HT is coupled via the action of transglutaminases to two small GTPases, rendering the latter constitutively active and promoting insulin secretion.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [79] Paulmann, 2009, Intracellular serotonin modulates insulin secretion from pancreatic beta-cells by protein serotonylation, PLoS Biol. source

      Not checked in the free run.

24 of 24

  • The paper relies on this without support.

    Gene expression changes in islets during the peak of DNA synthesis reflect the mechanisms that drive β-cell expansion during pregnancy.

    “Gene expression analysis during the peak of β-cell DNA synthesis not only showed induction of Prlr and Cdk4 expression in the islets of pregnant mice, but also identified many genes that had not previously been reported to play a role in β-cell expansion, which we discuss further below [10].”

  • The paper relies on this without support.

    β-cell mass is maintained by the balance between cell renewal/growth and cell loss.

    “In adult mammals, β-cell mass is maintained by the balance between cell renewal and growth (cell replication, hypertrophy, neogenesis) and cell loss (cell death, atrophy, autophagy) (Figure 1a).”

  • The paper relies on this without support.

    β-cell mass is normally maintained by a tight equilibrium between growth and loss, and it compensates for higher insulin demand such as in pregnancy.

    “The balance between β-cell growth and loss is tightly regulated and functional β-cell mass normally compensates for increased demands for insulin, for example, during pregnancy.”
3 of 3

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Mechanisms underlying pancreatic β-cell expansion in physiological settings may differ between species.

    “Although the mechanisms underlying pancreatic β-cell expansion in physiological settings may differ between species36,37, age-dependent restriction of β-cell proliferation is a conserved feature in mice and humans9,10.”

    From PDGF signalling controls age-dependent proliferation in pancreatic β-cells (2011) · cites this paper as [37]

Cites

Flagged first, then by citations

Research works printed but not linked: 2

  1. Kloppel, 1985, Islet pathology and the pathogenesis of type 1 and type 2 diabetes mellitus revisited, Surv. Synth. Pathol. Res., 4, 110
  2. Butler, 2003, Increased beta-cell apoptosis prevents adaptive increase in beta-cell mass in mouse model of type 2 diabetes: evidence for role of islet amyloid formation rather than direct action of amyloid, Diabetes, 52, 2304, 10.2337/diabetes.52.9.2304 · DOI · Paper page

Cited by

Sorted by citations

Authors
Rieck, S., & Kaestner, K. H.
Affiliations
University of Pennsylvania (US)
Corresponding author
Kaestner, Klaus H.
ORCID
Kaestner, Klaus H.
Venue
Trends in Endocrinology & Metabolism
Publisher
Elsevier BV
Published
2010-03
Volume
21
Issue
3
Pages
151-158
ISSN
1043-2760 (ISSN-L)
DOI
10.1016/j.tem.2009.11.001
PMC
PMC3627215
OpenAlex
W2011220884
Semantic Scholar
d361f3febb63c8c5345337b00d99d4870139bf79
Cited by
358
References
85
Citations by year
2026: 16 · 2025: 13 · 2024: 20 · 2023: 25 · 2022: 25 · 2021: 22 · 2020: 24 · 2019: 20 · 2018: 21 · 2017: 17 · 2016: 29 · 2015: 28 · 2014: 32 · 2013: 22 · 2012: 16
FWCI
2.34
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Trends in Endocrinology and Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK055243, R01DK055342)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords
beta-cell mass expansion, pregnancy, beta-cell proliferation, beta-cell apoptosis, insulin resistance, islet transplantation, insulin deficiency, diabetes mellitus
MeSH terms
Animals, Diabetes Mellitus, Female, Humans, Insulin Resistance, Models, Biological, Pregnancy, Apoptosis, Cell Size, Cell Proliferation, Insulin-Secreting Cells

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