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Cited by 137Genetic and Clinical Aspects of Sex Determination and Chromosomal AbnormalitiesPancreatic function and diabetesDiabetes, Cardiovascular Risks, and Lipoproteins

Impaired insulin secretion in the Turner metabolic syndrome

Bakalov, Vladimir K., Cooley, Margaret M., Quon, Michael J., Luo, Mei Lin, Yanovski, Jack A., Nelson, Lawrence M., Sullivan, Gail, Bondy, Carolyn A.·2004·The Journal of Clinical Endocrinology & Metabolism
DOI 10.1210/jc.2004-0122
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Abstract

An increased prevalence of impaired glucose homeostasis (IGH) and diabetes mellitus is reported in monosomy X, or Turner syndrome (TS). To determine whether IGH is an intrinsic feature of this syndrome, independent of obesity or hypogonadism, we compared results of a standard oral glucose challenge in age- and body mass index-matched women with TS and with karyotypically normal premature ovarian failure (POF). Fasting glucose levels were normal in both groups, but glucose values after oral glucose challenge were higher in TS [2-h glucose, 135 +/- 36 mg/dl (7.5 +/- 2.0 mmol/liter) in TS and 97 +/- 18 mg/dl (5.4 +/- 1.0 mmol/liter) in POF; P < 0.0001]. Glucose-stimulated insulin secretion was lower in TS; e.g. the initial insulin response (DeltaI/DeltaG(30)) was decreased by 60% compared with POF (P < 0.0001). We also compared responses to a standard iv glucose tolerance test in women with TS and in age- and body mass index-matched normal women and found that the insulin area under the curve was 50% lower in women with TS (P = 0.003). Insulin sensitivity measured by the quantitative insulin sensitivity check index was higher in women with TS compared with both control groups. Thus, IGH is not secondary to obesity or hypogonadism in TS, but it is a distinct entity characterized by decreased insulin secretion, suggesting that haploinsufficiency for X-chromosome gene(s) impairs beta-cell function and predisposes to diabetes mellitus in TS.

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  • Patients with TS are inherently at increased risk of disorders of carbohydrate metabolism and have a specific defect in glucose-stimulated insulin secretion.

    “Patients with TS are inherently at increased risk of disorders of carbohydrate metabolism226,227 and have a specific defect in glucose-stimulated insulin secretion.227,228”

    From Clinical practice guidelines for the care of girls and women with Turner syndrome. (2024) · cites this paper as [227]

  • Individuals with TS are at an increased risk for both type 1 and type 2 diabetes.

    “Individuals with TS are at an increased risk for both type 1 and type 2 diabetes.29,222,227,357,384,706”

    From Clinical practice guidelines for the care of girls and women with Turner syndrome. (2024) · cites this paper as [227]

  • Multiple studies demonstrate impaired beta cell function as well as reduced insulin sensitivity are involved in the development of diabetes in TS, while one study found glucose intolerance despite apparently normal beta cell function.

    “Furthermore, multiple studies demonstrate impaired beta cell function as well as reduced insulin sensitivity are involved in the development of diabetes in TS ,227,229,384,705,707,708 while one study found glucose intolerance despite apparently normal beta cell function.709”

    From Clinical practice guidelines for the care of girls and women with Turner syndrome. (2024) · cites this paper as [227]

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Authors
Bakalov, V. K., Cooley, M. M., Quon, M. J., Luo, M. L., Yanovski, J. A., Nelson, L. M., Sullivan, G., & Bondy, C. A.
Affiliations
  • Developmental Endocrinology Branch (V.K.B., M.M.C., M.L.L., J.A.Y., L.M.N., C.A.B.), Bethesda, Maryland 20892
  • National Institutes of Health (US)
Corresponding author
Bondy, Carolyn A.
ORCID
Venue
The Journal of Clinical Endocrinology & Metabolism
Publisher
The Endocrine Society
Published
2004-07-01
Volume
89
Issue
7
Pages
3516-3520
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
DOI
10.1210/jc.2004-0122
OpenAlex
W2149926350
Cited by
137
References
24
Citations by year
2025: 3 · 2024: 6 · 2023: 6 · 2022: 3 · 2021: 5 · 2020: 6 · 2019: 6 · 2018: 6 · 2017: 7 · 2016: 2 · 2015: 4 · 2014: 6 · 2013: 7 · 2012: 8
FWCI
5.18
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (Z99HD999999)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (Z01HD000641)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
Turner syndrome, monosomy X, impaired glucose homeostasis, impaired insulin secretion, beta-cell function, premature ovarian failure, insulin sensitivity, QUICKI, diabetes risk, oral glucose tolerance test
MeSH terms
Insulin Secretion, Adult, Blood Glucose, Female, Glucose, Glucose Tolerance Test, Humans, Insulin, Turner Syndrome, Case-Control Studies, Primary Ovarian Insufficiency, Area Under Curve

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