Prenatal androgen excess negatively impacts body fat distribution in a nonhuman primate model of polycystic ovary syndrome

C. M. Bruns, S. T. Baum, R. J. Colman, D. A. Dumesic, J. R. Eisner, Michael Dennis Jensen, L. D. Whigham, D. H. Abbott

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Introduction: Prenatally androgenized (PA) female rhesus monkeys share metabolic abnormalities in common with polycystic ovary syndrome (PCOS) women. Early gestation exposure (E) results in insulin resistance, impaired pancreatic β-cell function and type 2 diabetes, while late gestation exposure (L) results in supranormal insulin sensitivity that declines with increasing body mass index (BMI). Objective: To determine whether PA females have altered body fat distribution. Design: Five early-treated PA (EPA), five late-treated PA (LPA) and five control adult female monkeys underwent somatometrics, dual-X-ray absorptiometry (DXA) and abdominal computed tomography (CT). Five control and five EPA females underwent an intravenous glucose tolerance test to assess the relationship between body composition and glucoregulation. Results: There were no differences in age, weight, BMI or somatometrics. LPA females had ∼20% greater DXA-determined total fat and percent body fat, as well as total and percent abdominal fat than EPA or control females (P≤0.05). LPA females also had ∼40% more CT-determined non-visceral abdominal fat than EPA or control females (P≤0.05). The volume of visceral fat was similar among the three groups. EPA (R2=0.94, P≤0.01) and LPA (R2=0.53, P=0.16) females had a positive relationship between visceral fat and BMI, although not significant for LPA females. Conversely, control females had a positive relationship between non-visceral fat and BMI (R2=0.98, P≤0.001). There was a positive relationship between basal insulin and total body (R 2=0.95, P≤0.007), total abdominal (R2=0.81, P≤0.04) and visceral (R2=0.82, P≤0.03) fat quantities in EPA, but not control females. Conclusions: Prenatal androgenization in female rhesus monkeys induces adiposity-dependent visceral fat accumulation, and late gestation androgenization causes increased total body and non-visceral fat mass. Early gestation androgenization induces visceral fat-dependent hyperinsulinemia. The relationship between the timing of prenatal androgen exposure and body composition phenotypes in this nonhuman primate model for PCOS may provide insight into the heterogeneity of metabolic defects found in PCOS women.

Original languageEnglish (US)
Pages (from-to)1579-1585
Number of pages7
JournalInternational Journal of Obesity
Volume31
Issue number10
DOIs
StatePublished - Oct 2007

Fingerprint

polycystic ovary syndrome
Body Fat Distribution
body fat distribution
Polycystic Ovary Syndrome
androgens
Primates
Androgens
animal models
visceral fat
Intra-Abdominal Fat
masculinization
Virilism
body mass index
Body Mass Index
pregnancy
Pregnancy
Abdominal Fat
Fat Body
Photon Absorptiometry
abdominal fat

Keywords

  • Body composition
  • Insulin resistance
  • Polycystic ovary syndrome
  • Testosterone
  • Type 2 diabetes

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Public Health, Environmental and Occupational Health
  • Endocrinology
  • Food Science
  • Endocrinology, Diabetes and Metabolism

Cite this

Prenatal androgen excess negatively impacts body fat distribution in a nonhuman primate model of polycystic ovary syndrome. / Bruns, C. M.; Baum, S. T.; Colman, R. J.; Dumesic, D. A.; Eisner, J. R.; Jensen, Michael Dennis; Whigham, L. D.; Abbott, D. H.

In: International Journal of Obesity, Vol. 31, No. 10, 10.2007, p. 1579-1585.

Research output: Contribution to journalArticle

Bruns, C. M. ; Baum, S. T. ; Colman, R. J. ; Dumesic, D. A. ; Eisner, J. R. ; Jensen, Michael Dennis ; Whigham, L. D. ; Abbott, D. H. / Prenatal androgen excess negatively impacts body fat distribution in a nonhuman primate model of polycystic ovary syndrome. In: International Journal of Obesity. 2007 ; Vol. 31, No. 10. pp. 1579-1585.
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abstract = "Introduction: Prenatally androgenized (PA) female rhesus monkeys share metabolic abnormalities in common with polycystic ovary syndrome (PCOS) women. Early gestation exposure (E) results in insulin resistance, impaired pancreatic β-cell function and type 2 diabetes, while late gestation exposure (L) results in supranormal insulin sensitivity that declines with increasing body mass index (BMI). Objective: To determine whether PA females have altered body fat distribution. Design: Five early-treated PA (EPA), five late-treated PA (LPA) and five control adult female monkeys underwent somatometrics, dual-X-ray absorptiometry (DXA) and abdominal computed tomography (CT). Five control and five EPA females underwent an intravenous glucose tolerance test to assess the relationship between body composition and glucoregulation. Results: There were no differences in age, weight, BMI or somatometrics. LPA females had ∼20{\%} greater DXA-determined total fat and percent body fat, as well as total and percent abdominal fat than EPA or control females (P≤0.05). LPA females also had ∼40{\%} more CT-determined non-visceral abdominal fat than EPA or control females (P≤0.05). The volume of visceral fat was similar among the three groups. EPA (R2=0.94, P≤0.01) and LPA (R2=0.53, P=0.16) females had a positive relationship between visceral fat and BMI, although not significant for LPA females. Conversely, control females had a positive relationship between non-visceral fat and BMI (R2=0.98, P≤0.001). There was a positive relationship between basal insulin and total body (R 2=0.95, P≤0.007), total abdominal (R2=0.81, P≤0.04) and visceral (R2=0.82, P≤0.03) fat quantities in EPA, but not control females. Conclusions: Prenatal androgenization in female rhesus monkeys induces adiposity-dependent visceral fat accumulation, and late gestation androgenization causes increased total body and non-visceral fat mass. Early gestation androgenization induces visceral fat-dependent hyperinsulinemia. The relationship between the timing of prenatal androgen exposure and body composition phenotypes in this nonhuman primate model for PCOS may provide insight into the heterogeneity of metabolic defects found in PCOS women.",
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AU - Bruns, C. M.

AU - Baum, S. T.

AU - Colman, R. J.

AU - Dumesic, D. A.

AU - Eisner, J. R.

AU - Jensen, Michael Dennis

AU - Whigham, L. D.

AU - Abbott, D. H.

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N2 - Introduction: Prenatally androgenized (PA) female rhesus monkeys share metabolic abnormalities in common with polycystic ovary syndrome (PCOS) women. Early gestation exposure (E) results in insulin resistance, impaired pancreatic β-cell function and type 2 diabetes, while late gestation exposure (L) results in supranormal insulin sensitivity that declines with increasing body mass index (BMI). Objective: To determine whether PA females have altered body fat distribution. Design: Five early-treated PA (EPA), five late-treated PA (LPA) and five control adult female monkeys underwent somatometrics, dual-X-ray absorptiometry (DXA) and abdominal computed tomography (CT). Five control and five EPA females underwent an intravenous glucose tolerance test to assess the relationship between body composition and glucoregulation. Results: There were no differences in age, weight, BMI or somatometrics. LPA females had ∼20% greater DXA-determined total fat and percent body fat, as well as total and percent abdominal fat than EPA or control females (P≤0.05). LPA females also had ∼40% more CT-determined non-visceral abdominal fat than EPA or control females (P≤0.05). The volume of visceral fat was similar among the three groups. EPA (R2=0.94, P≤0.01) and LPA (R2=0.53, P=0.16) females had a positive relationship between visceral fat and BMI, although not significant for LPA females. Conversely, control females had a positive relationship between non-visceral fat and BMI (R2=0.98, P≤0.001). There was a positive relationship between basal insulin and total body (R 2=0.95, P≤0.007), total abdominal (R2=0.81, P≤0.04) and visceral (R2=0.82, P≤0.03) fat quantities in EPA, but not control females. Conclusions: Prenatal androgenization in female rhesus monkeys induces adiposity-dependent visceral fat accumulation, and late gestation androgenization causes increased total body and non-visceral fat mass. Early gestation androgenization induces visceral fat-dependent hyperinsulinemia. The relationship between the timing of prenatal androgen exposure and body composition phenotypes in this nonhuman primate model for PCOS may provide insight into the heterogeneity of metabolic defects found in PCOS women.

AB - Introduction: Prenatally androgenized (PA) female rhesus monkeys share metabolic abnormalities in common with polycystic ovary syndrome (PCOS) women. Early gestation exposure (E) results in insulin resistance, impaired pancreatic β-cell function and type 2 diabetes, while late gestation exposure (L) results in supranormal insulin sensitivity that declines with increasing body mass index (BMI). Objective: To determine whether PA females have altered body fat distribution. Design: Five early-treated PA (EPA), five late-treated PA (LPA) and five control adult female monkeys underwent somatometrics, dual-X-ray absorptiometry (DXA) and abdominal computed tomography (CT). Five control and five EPA females underwent an intravenous glucose tolerance test to assess the relationship between body composition and glucoregulation. Results: There were no differences in age, weight, BMI or somatometrics. LPA females had ∼20% greater DXA-determined total fat and percent body fat, as well as total and percent abdominal fat than EPA or control females (P≤0.05). LPA females also had ∼40% more CT-determined non-visceral abdominal fat than EPA or control females (P≤0.05). The volume of visceral fat was similar among the three groups. EPA (R2=0.94, P≤0.01) and LPA (R2=0.53, P=0.16) females had a positive relationship between visceral fat and BMI, although not significant for LPA females. Conversely, control females had a positive relationship between non-visceral fat and BMI (R2=0.98, P≤0.001). There was a positive relationship between basal insulin and total body (R 2=0.95, P≤0.007), total abdominal (R2=0.81, P≤0.04) and visceral (R2=0.82, P≤0.03) fat quantities in EPA, but not control females. Conclusions: Prenatal androgenization in female rhesus monkeys induces adiposity-dependent visceral fat accumulation, and late gestation androgenization causes increased total body and non-visceral fat mass. Early gestation androgenization induces visceral fat-dependent hyperinsulinemia. The relationship between the timing of prenatal androgen exposure and body composition phenotypes in this nonhuman primate model for PCOS may provide insight into the heterogeneity of metabolic defects found in PCOS women.

KW - Body composition

KW - Insulin resistance

KW - Polycystic ovary syndrome

KW - Testosterone

KW - Type 2 diabetes

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