Lower brain-derived neurotrophic factor in patients with Prader-Willi syndrome compared to obese and lean control subjects

Joan Han, Michael J. Muehlbauer, Huaxia N. Cui, Christopher B. Newgard, Andrea M. Haqq

Research output: Contribution to journalArticle

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Abstract

Context: Brain-derived neurotrophic factor (BDNF) haploinsufficiency is associated with hyperphagia and obesity in both animals and humans. BDNF appears to function downstream of the leptinmelanocortin signaling pathway to control energy balance. The potential role of BDNF in the etiology of the severe hyperphagia associated with PWS has not been previously explored. Objective: The aim was to compare BDNF concentrations in subjects with PWS and obese controls (OC) and lean controls (LC). Design and Setting: We conducted a cross-sectional study at an outpatient clinical research center. Participants: We studied 13 subjects with PWS [five females and eight males; mean±SD: age, 11.0±4.1 yr; body mass index (BMI)-Z, 2.05 ± 0.78], 13 OC (eight females, five males; age, 12.3 ± 2.7 yr; BMI-Z, 2.18 ± 0.61), and 13 LC (six females, seven males; age, 12.4 ± 2.6 yr; BMI-Z, -0.57 ± 0.73). Main Outcome Measure: BDNF was measured in serum and plasma by ELISA. Analysis of covariance adjusted for age, sex, and BMI-Z. Results: All groups were comparable for age (P = 0.50) and sex distribution (P = 0.49). BMI-Z was comparable between PWS and OC (P = 0.89) and lower in LC (P < 0.001). Adjusted serum BDNF was comparable (P=0.35) in OC (mean±SEM: 13.5±1.2 ng/ml) and LC (19.2±1.3 ng/ml), but lower inPWS (8.3 ± 1.2 ng/ml; P = 0.01 vs. OC; P = 0.03 vs. LC). Adjusted plasma BDNF in PWS (217±130 pg/ml) was lower than OC (422±126 pg/ml;P=0.02), but statistically comparable with LC (540±143 pg/ml;P=0.10). Conclusions: Lower BDNF in PWS suggests insufficient central BDNF production because BDNF in peripheral circulation is believed to reflect cerebral BDNF output. Decreased BDNF may be a potential cause for the disordered satiety and morbid obesity associated with PWS. Further studies are needed to confirm this preliminary pilot study in a larger cohort of patients with PWS.

Original languageEnglish (US)
Pages (from-to)3532-3536
Number of pages5
JournalJournal of Clinical Endocrinology and Metabolism
Volume95
Issue number7
DOIs
StatePublished - Jan 1 2010

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Prader-Willi Syndrome
Brain-Derived Neurotrophic Factor
Body Mass Index
Hyperphagia
Plasmas
Haploinsufficiency
Sex Distribution
Morbid Obesity
Energy balance
Serum
Animals

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

Lower brain-derived neurotrophic factor in patients with Prader-Willi syndrome compared to obese and lean control subjects. / Han, Joan; Muehlbauer, Michael J.; Cui, Huaxia N.; Newgard, Christopher B.; Haqq, Andrea M.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 95, No. 7, 01.01.2010, p. 3532-3536.

Research output: Contribution to journalArticle

Han, Joan ; Muehlbauer, Michael J. ; Cui, Huaxia N. ; Newgard, Christopher B. ; Haqq, Andrea M. / Lower brain-derived neurotrophic factor in patients with Prader-Willi syndrome compared to obese and lean control subjects. In: Journal of Clinical Endocrinology and Metabolism. 2010 ; Vol. 95, No. 7. pp. 3532-3536.
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abstract = "Context: Brain-derived neurotrophic factor (BDNF) haploinsufficiency is associated with hyperphagia and obesity in both animals and humans. BDNF appears to function downstream of the leptinmelanocortin signaling pathway to control energy balance. The potential role of BDNF in the etiology of the severe hyperphagia associated with PWS has not been previously explored. Objective: The aim was to compare BDNF concentrations in subjects with PWS and obese controls (OC) and lean controls (LC). Design and Setting: We conducted a cross-sectional study at an outpatient clinical research center. Participants: We studied 13 subjects with PWS [five females and eight males; mean±SD: age, 11.0±4.1 yr; body mass index (BMI)-Z, 2.05 ± 0.78], 13 OC (eight females, five males; age, 12.3 ± 2.7 yr; BMI-Z, 2.18 ± 0.61), and 13 LC (six females, seven males; age, 12.4 ± 2.6 yr; BMI-Z, -0.57 ± 0.73). Main Outcome Measure: BDNF was measured in serum and plasma by ELISA. Analysis of covariance adjusted for age, sex, and BMI-Z. Results: All groups were comparable for age (P = 0.50) and sex distribution (P = 0.49). BMI-Z was comparable between PWS and OC (P = 0.89) and lower in LC (P < 0.001). Adjusted serum BDNF was comparable (P=0.35) in OC (mean±SEM: 13.5±1.2 ng/ml) and LC (19.2±1.3 ng/ml), but lower inPWS (8.3 ± 1.2 ng/ml; P = 0.01 vs. OC; P = 0.03 vs. LC). Adjusted plasma BDNF in PWS (217±130 pg/ml) was lower than OC (422±126 pg/ml;P=0.02), but statistically comparable with LC (540±143 pg/ml;P=0.10). Conclusions: Lower BDNF in PWS suggests insufficient central BDNF production because BDNF in peripheral circulation is believed to reflect cerebral BDNF output. Decreased BDNF may be a potential cause for the disordered satiety and morbid obesity associated with PWS. Further studies are needed to confirm this preliminary pilot study in a larger cohort of patients with PWS.",
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AU - Han, Joan

AU - Muehlbauer, Michael J.

AU - Cui, Huaxia N.

AU - Newgard, Christopher B.

AU - Haqq, Andrea M.

PY - 2010/1/1

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N2 - Context: Brain-derived neurotrophic factor (BDNF) haploinsufficiency is associated with hyperphagia and obesity in both animals and humans. BDNF appears to function downstream of the leptinmelanocortin signaling pathway to control energy balance. The potential role of BDNF in the etiology of the severe hyperphagia associated with PWS has not been previously explored. Objective: The aim was to compare BDNF concentrations in subjects with PWS and obese controls (OC) and lean controls (LC). Design and Setting: We conducted a cross-sectional study at an outpatient clinical research center. Participants: We studied 13 subjects with PWS [five females and eight males; mean±SD: age, 11.0±4.1 yr; body mass index (BMI)-Z, 2.05 ± 0.78], 13 OC (eight females, five males; age, 12.3 ± 2.7 yr; BMI-Z, 2.18 ± 0.61), and 13 LC (six females, seven males; age, 12.4 ± 2.6 yr; BMI-Z, -0.57 ± 0.73). Main Outcome Measure: BDNF was measured in serum and plasma by ELISA. Analysis of covariance adjusted for age, sex, and BMI-Z. Results: All groups were comparable for age (P = 0.50) and sex distribution (P = 0.49). BMI-Z was comparable between PWS and OC (P = 0.89) and lower in LC (P < 0.001). Adjusted serum BDNF was comparable (P=0.35) in OC (mean±SEM: 13.5±1.2 ng/ml) and LC (19.2±1.3 ng/ml), but lower inPWS (8.3 ± 1.2 ng/ml; P = 0.01 vs. OC; P = 0.03 vs. LC). Adjusted plasma BDNF in PWS (217±130 pg/ml) was lower than OC (422±126 pg/ml;P=0.02), but statistically comparable with LC (540±143 pg/ml;P=0.10). Conclusions: Lower BDNF in PWS suggests insufficient central BDNF production because BDNF in peripheral circulation is believed to reflect cerebral BDNF output. Decreased BDNF may be a potential cause for the disordered satiety and morbid obesity associated with PWS. Further studies are needed to confirm this preliminary pilot study in a larger cohort of patients with PWS.

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