Postprandial effects of long-term niacin/laropiprant use on glucose and lipid metabolism and on cardiovascular risk in patients with polycystic ovary syndrome

Myint M. Aye, E. S. Kilpatrick, P. Afolabi, S. A. Wootton, A. S. Rigby, A. M. Coady, D. D. Sandeman, Stephen Atkin

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Aim: This study investigated the effect of long-term niacin/laropiprant therapy on CV risk and IR in obese women with PCOS. Methods: In this double-blind randomized placebo-controlled trial, 13 and 12 PCOS women completed a 12week course of niacin/laropiprant or placebo, respectively. Fasted subjects had an endothelial function test (EndoPat2000) and then consumed a mixed meal with blood sampled postprandially for 6h before and after intervention. Results: By 12weeks, niacin/laropiprant lowered low-density lipoprotein cholesterol (LDL-c) (13%) and increased HDL-c (17%). Despite a reduction in fasting triglycerides (21%), the drug had no effect on their postprandial rise (2.69±1.44 vs. 2.49±1.14mmol/l, p=0.72). However, following the mixed meal, plasma glucose area under the response curve increased from 13.1±2.9 to 14.0±2.8mmol/l, p=0.05, as a consequence of both increased insulin resistance [HOMA-IR: 2.2 (1.2, 4.2) vs. 3.8(1.3, 5.5), p=0.02] and a reduced acute insulin response to glucose [424 (211, 975) vs. 257(122, 418) pmol/mmol, p=0.04]. Niacin/laropiprant did not improve RHI (1.97±0.40 vs. 2.05±0.58, p=0.33) or hsCRP. Conclusions: In PCOS, niacin/laropiprant had a significant negative impact on postprandial glucose and no improvement in postprandial hypertriglyceridaemia, with at least the former mediated through increased IR and reduced β-cell function. This data may help explain why the improvement in fasting lipids has not translated into improved CV risk markers in PCOS.

Original languageEnglish
Pages (from-to)545-552
Number of pages8
JournalDiabetes, Obesity and Metabolism
Volume16
Issue number6
DOIs
Publication statusPublished - 2014
Externally publishedYes

Fingerprint

Polycystic Ovary Syndrome
Niacin
Lipid Metabolism
Glucose
Meals
Fasting
Placebos
Hypertriglyceridemia
Double-Blind Method
LDL Cholesterol
Area Under Curve
Insulin Resistance
Triglycerides
Randomized Controlled Trials
MK-0524
Insulin
Lipids
Pharmaceutical Preparations

Keywords

  • Endothelial dysfunction
  • Insulin resistance
  • Niacin/laropiprant
  • Polycystic ovary syndrome
  • Triglycerides

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Postprandial effects of long-term niacin/laropiprant use on glucose and lipid metabolism and on cardiovascular risk in patients with polycystic ovary syndrome. / Aye, Myint M.; Kilpatrick, E. S.; Afolabi, P.; Wootton, S. A.; Rigby, A. S.; Coady, A. M.; Sandeman, D. D.; Atkin, Stephen.

In: Diabetes, Obesity and Metabolism, Vol. 16, No. 6, 2014, p. 545-552.

Research output: Contribution to journalArticle

Aye, Myint M. ; Kilpatrick, E. S. ; Afolabi, P. ; Wootton, S. A. ; Rigby, A. S. ; Coady, A. M. ; Sandeman, D. D. ; Atkin, Stephen. / Postprandial effects of long-term niacin/laropiprant use on glucose and lipid metabolism and on cardiovascular risk in patients with polycystic ovary syndrome. In: Diabetes, Obesity and Metabolism. 2014 ; Vol. 16, No. 6. pp. 545-552.
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abstract = "Aim: This study investigated the effect of long-term niacin/laropiprant therapy on CV risk and IR in obese women with PCOS. Methods: In this double-blind randomized placebo-controlled trial, 13 and 12 PCOS women completed a 12week course of niacin/laropiprant or placebo, respectively. Fasted subjects had an endothelial function test (EndoPat2000) and then consumed a mixed meal with blood sampled postprandially for 6h before and after intervention. Results: By 12weeks, niacin/laropiprant lowered low-density lipoprotein cholesterol (LDL-c) (13{\%}) and increased HDL-c (17{\%}). Despite a reduction in fasting triglycerides (21{\%}), the drug had no effect on their postprandial rise (2.69±1.44 vs. 2.49±1.14mmol/l, p=0.72). However, following the mixed meal, plasma glucose area under the response curve increased from 13.1±2.9 to 14.0±2.8mmol/l, p=0.05, as a consequence of both increased insulin resistance [HOMA-IR: 2.2 (1.2, 4.2) vs. 3.8(1.3, 5.5), p=0.02] and a reduced acute insulin response to glucose [424 (211, 975) vs. 257(122, 418) pmol/mmol, p=0.04]. Niacin/laropiprant did not improve RHI (1.97±0.40 vs. 2.05±0.58, p=0.33) or hsCRP. Conclusions: In PCOS, niacin/laropiprant had a significant negative impact on postprandial glucose and no improvement in postprandial hypertriglyceridaemia, with at least the former mediated through increased IR and reduced β-cell function. This data may help explain why the improvement in fasting lipids has not translated into improved CV risk markers in PCOS.",
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T1 - Postprandial effects of long-term niacin/laropiprant use on glucose and lipid metabolism and on cardiovascular risk in patients with polycystic ovary syndrome

AU - Aye, Myint M.

AU - Kilpatrick, E. S.

AU - Afolabi, P.

AU - Wootton, S. A.

AU - Rigby, A. S.

AU - Coady, A. M.

AU - Sandeman, D. D.

AU - Atkin, Stephen

PY - 2014

Y1 - 2014

N2 - Aim: This study investigated the effect of long-term niacin/laropiprant therapy on CV risk and IR in obese women with PCOS. Methods: In this double-blind randomized placebo-controlled trial, 13 and 12 PCOS women completed a 12week course of niacin/laropiprant or placebo, respectively. Fasted subjects had an endothelial function test (EndoPat2000) and then consumed a mixed meal with blood sampled postprandially for 6h before and after intervention. Results: By 12weeks, niacin/laropiprant lowered low-density lipoprotein cholesterol (LDL-c) (13%) and increased HDL-c (17%). Despite a reduction in fasting triglycerides (21%), the drug had no effect on their postprandial rise (2.69±1.44 vs. 2.49±1.14mmol/l, p=0.72). However, following the mixed meal, plasma glucose area under the response curve increased from 13.1±2.9 to 14.0±2.8mmol/l, p=0.05, as a consequence of both increased insulin resistance [HOMA-IR: 2.2 (1.2, 4.2) vs. 3.8(1.3, 5.5), p=0.02] and a reduced acute insulin response to glucose [424 (211, 975) vs. 257(122, 418) pmol/mmol, p=0.04]. Niacin/laropiprant did not improve RHI (1.97±0.40 vs. 2.05±0.58, p=0.33) or hsCRP. Conclusions: In PCOS, niacin/laropiprant had a significant negative impact on postprandial glucose and no improvement in postprandial hypertriglyceridaemia, with at least the former mediated through increased IR and reduced β-cell function. This data may help explain why the improvement in fasting lipids has not translated into improved CV risk markers in PCOS.

AB - Aim: This study investigated the effect of long-term niacin/laropiprant therapy on CV risk and IR in obese women with PCOS. Methods: In this double-blind randomized placebo-controlled trial, 13 and 12 PCOS women completed a 12week course of niacin/laropiprant or placebo, respectively. Fasted subjects had an endothelial function test (EndoPat2000) and then consumed a mixed meal with blood sampled postprandially for 6h before and after intervention. Results: By 12weeks, niacin/laropiprant lowered low-density lipoprotein cholesterol (LDL-c) (13%) and increased HDL-c (17%). Despite a reduction in fasting triglycerides (21%), the drug had no effect on their postprandial rise (2.69±1.44 vs. 2.49±1.14mmol/l, p=0.72). However, following the mixed meal, plasma glucose area under the response curve increased from 13.1±2.9 to 14.0±2.8mmol/l, p=0.05, as a consequence of both increased insulin resistance [HOMA-IR: 2.2 (1.2, 4.2) vs. 3.8(1.3, 5.5), p=0.02] and a reduced acute insulin response to glucose [424 (211, 975) vs. 257(122, 418) pmol/mmol, p=0.04]. Niacin/laropiprant did not improve RHI (1.97±0.40 vs. 2.05±0.58, p=0.33) or hsCRP. Conclusions: In PCOS, niacin/laropiprant had a significant negative impact on postprandial glucose and no improvement in postprandial hypertriglyceridaemia, with at least the former mediated through increased IR and reduced β-cell function. This data may help explain why the improvement in fasting lipids has not translated into improved CV risk markers in PCOS.

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KW - Niacin/laropiprant

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KW - Triglycerides

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