Lipoprotein(a) and apolipoprotein(a) in polycystic ovary syndrome

Enkhmaa Byambaa, Anuurad Erdembileg, Wei Zhang, Adnan Abbuthalha, Parneet Kaur, Jasmeen Visla, Siddika E Karakas, Lars Berglund

Research output: Contribution to journalArticle

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Abstract

Objective Levels of lipoprotein(a), Lp(a), an independent risk factor for cardiovascular disease (CVD), are affected by sex hormones. Women with polycystic ovary syndrome (PCOS) have elevated androgen levels and are at increased CVD risk. We investigated the impact of PCOS-related hormonal imbalance on Lp(a) levels in relation to apo(a) gene size polymorphism, a major regulator of Lp(a) level. Design Cross-sectional. Patients Forty-one Caucasian women with PCOS based on the NIH criteria. Measurements (1) Apo(a) gene size polymorphism measured as Kringle (K) 4 repeat number; (2) total plasma Lp(a) level; (3) allele-specific apo(a) level assessing the amount of Lp(a) carried by an individual apo(a) allele/isoform; and (4) sex hormone levels. Results The mean age was 32 ± 6 years, and the mean BMI was 35 ± 8 with 66% of women classified as obese (BMI >30 kg/m2). LDL cholesterol was borderline high (3·37 mmol/l), and HDL cholesterol was low (1·06 mmol/l). The distribution of Lp(a) level was skewed towards lower levels with a median level of 22·1 nmol/l (IQR: 6·2-66·5 nmol/l). Lp(a) levels were not correlated with age, body weight or BMI. The median allele-specific apo(a) level was 10·6 nmol/l (IQR: 3·1-31·2 nmol/l), and the median apo(a) size was 27 (IQR: 23-30) K4 repeats. Allele-specific apo(a) levels were significantly and inversely correlated with K4 repeats (r = -0·298, P = 0·007). Neither Lp(a) nor allele-specific apo(a) levels were significantly associated with testosterone or dehydroepiandrosterone sulphate levels. Conclusions The apo(a) genetic variability remains the major regulator of plasma Lp(a) levels in women with PCOS.

Original languageEnglish (US)
Pages (from-to)229-235
Number of pages7
JournalClinical Endocrinology
Volume84
Issue number2
DOIs
StatePublished - Feb 1 2016

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Apoprotein(a)
Lipoprotein(a)
Polycystic Ovary Syndrome
Alleles
Gonadal Steroid Hormones
Cardiovascular Diseases
Kringles
Dehydroepiandrosterone Sulfate
LDL Cholesterol
HDL Cholesterol
Androgens
Genes
Testosterone
Protein Isoforms
Body Weight

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism

Cite this

Lipoprotein(a) and apolipoprotein(a) in polycystic ovary syndrome. / Byambaa, Enkhmaa; Erdembileg, Anuurad; Zhang, Wei; Abbuthalha, Adnan; Kaur, Parneet; Visla, Jasmeen; Karakas, Siddika E; Berglund, Lars.

In: Clinical Endocrinology, Vol. 84, No. 2, 01.02.2016, p. 229-235.

Research output: Contribution to journalArticle

Byambaa, Enkhmaa ; Erdembileg, Anuurad ; Zhang, Wei ; Abbuthalha, Adnan ; Kaur, Parneet ; Visla, Jasmeen ; Karakas, Siddika E ; Berglund, Lars. / Lipoprotein(a) and apolipoprotein(a) in polycystic ovary syndrome. In: Clinical Endocrinology. 2016 ; Vol. 84, No. 2. pp. 229-235.
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abstract = "Objective Levels of lipoprotein(a), Lp(a), an independent risk factor for cardiovascular disease (CVD), are affected by sex hormones. Women with polycystic ovary syndrome (PCOS) have elevated androgen levels and are at increased CVD risk. We investigated the impact of PCOS-related hormonal imbalance on Lp(a) levels in relation to apo(a) gene size polymorphism, a major regulator of Lp(a) level. Design Cross-sectional. Patients Forty-one Caucasian women with PCOS based on the NIH criteria. Measurements (1) Apo(a) gene size polymorphism measured as Kringle (K) 4 repeat number; (2) total plasma Lp(a) level; (3) allele-specific apo(a) level assessing the amount of Lp(a) carried by an individual apo(a) allele/isoform; and (4) sex hormone levels. Results The mean age was 32 ± 6 years, and the mean BMI was 35 ± 8 with 66{\%} of women classified as obese (BMI >30 kg/m2). LDL cholesterol was borderline high (3·37 mmol/l), and HDL cholesterol was low (1·06 mmol/l). The distribution of Lp(a) level was skewed towards lower levels with a median level of 22·1 nmol/l (IQR: 6·2-66·5 nmol/l). Lp(a) levels were not correlated with age, body weight or BMI. The median allele-specific apo(a) level was 10·6 nmol/l (IQR: 3·1-31·2 nmol/l), and the median apo(a) size was 27 (IQR: 23-30) K4 repeats. Allele-specific apo(a) levels were significantly and inversely correlated with K4 repeats (r = -0·298, P = 0·007). Neither Lp(a) nor allele-specific apo(a) levels were significantly associated with testosterone or dehydroepiandrosterone sulphate levels. Conclusions The apo(a) genetic variability remains the major regulator of plasma Lp(a) levels in women with PCOS.",
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AU - Byambaa, Enkhmaa

AU - Erdembileg, Anuurad

AU - Zhang, Wei

AU - Abbuthalha, Adnan

AU - Kaur, Parneet

AU - Visla, Jasmeen

AU - Karakas, Siddika E

AU - Berglund, Lars

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N2 - Objective Levels of lipoprotein(a), Lp(a), an independent risk factor for cardiovascular disease (CVD), are affected by sex hormones. Women with polycystic ovary syndrome (PCOS) have elevated androgen levels and are at increased CVD risk. We investigated the impact of PCOS-related hormonal imbalance on Lp(a) levels in relation to apo(a) gene size polymorphism, a major regulator of Lp(a) level. Design Cross-sectional. Patients Forty-one Caucasian women with PCOS based on the NIH criteria. Measurements (1) Apo(a) gene size polymorphism measured as Kringle (K) 4 repeat number; (2) total plasma Lp(a) level; (3) allele-specific apo(a) level assessing the amount of Lp(a) carried by an individual apo(a) allele/isoform; and (4) sex hormone levels. Results The mean age was 32 ± 6 years, and the mean BMI was 35 ± 8 with 66% of women classified as obese (BMI >30 kg/m2). LDL cholesterol was borderline high (3·37 mmol/l), and HDL cholesterol was low (1·06 mmol/l). The distribution of Lp(a) level was skewed towards lower levels with a median level of 22·1 nmol/l (IQR: 6·2-66·5 nmol/l). Lp(a) levels were not correlated with age, body weight or BMI. The median allele-specific apo(a) level was 10·6 nmol/l (IQR: 3·1-31·2 nmol/l), and the median apo(a) size was 27 (IQR: 23-30) K4 repeats. Allele-specific apo(a) levels were significantly and inversely correlated with K4 repeats (r = -0·298, P = 0·007). Neither Lp(a) nor allele-specific apo(a) levels were significantly associated with testosterone or dehydroepiandrosterone sulphate levels. Conclusions The apo(a) genetic variability remains the major regulator of plasma Lp(a) levels in women with PCOS.

AB - Objective Levels of lipoprotein(a), Lp(a), an independent risk factor for cardiovascular disease (CVD), are affected by sex hormones. Women with polycystic ovary syndrome (PCOS) have elevated androgen levels and are at increased CVD risk. We investigated the impact of PCOS-related hormonal imbalance on Lp(a) levels in relation to apo(a) gene size polymorphism, a major regulator of Lp(a) level. Design Cross-sectional. Patients Forty-one Caucasian women with PCOS based on the NIH criteria. Measurements (1) Apo(a) gene size polymorphism measured as Kringle (K) 4 repeat number; (2) total plasma Lp(a) level; (3) allele-specific apo(a) level assessing the amount of Lp(a) carried by an individual apo(a) allele/isoform; and (4) sex hormone levels. Results The mean age was 32 ± 6 years, and the mean BMI was 35 ± 8 with 66% of women classified as obese (BMI >30 kg/m2). LDL cholesterol was borderline high (3·37 mmol/l), and HDL cholesterol was low (1·06 mmol/l). The distribution of Lp(a) level was skewed towards lower levels with a median level of 22·1 nmol/l (IQR: 6·2-66·5 nmol/l). Lp(a) levels were not correlated with age, body weight or BMI. The median allele-specific apo(a) level was 10·6 nmol/l (IQR: 3·1-31·2 nmol/l), and the median apo(a) size was 27 (IQR: 23-30) K4 repeats. Allele-specific apo(a) levels were significantly and inversely correlated with K4 repeats (r = -0·298, P = 0·007). Neither Lp(a) nor allele-specific apo(a) levels were significantly associated with testosterone or dehydroepiandrosterone sulphate levels. Conclusions The apo(a) genetic variability remains the major regulator of plasma Lp(a) levels in women with PCOS.

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