Effect of niacin on triglyceride‐rich lipoprotein apolipoprotein B‐48 kinetics in statin‐treated patients with type 2 diabetes. Issue 4 (28th January 2016)

• Record Type: Journal Article
• Authors: Pang, J.; Chan, D. C.; Hamilton, S. J.; Tenneti, V. S.; Watts, G. F.; Barrett, P. H. R.
• Is Part Of: Diabetes, obesity & metabolism. Volume 18:Issue 4(2016)
• Page Start: 384
• Page End: 391
• Publication Date: 2016-01-28
• Subjects: apolipoprotein B‐48 -- chylomicron -- niacin -- statins -- type 2 diabetes; Diabetes -- Periodicals; Obesity -- Periodicals; Metabolism -- Disorders -- Periodicals; Clinical pharmacology -- Periodicals; 616.462
• DOI: 10.1111/dom.12622
• Languages: English
• ISSNs: 1462-8902

Abstract

Abstract : Aim: To investigate the effects of extended‐release (ER) niacin on apolipoprotein B‐48 (apoB‐48) kinetics in statin‐treated patients with type 2 diabetes (T2DM). Methods: A total of 12 men with T2DM were randomized to rosuvastatin or rosuvastatin plus ER niacin for 12 weeks and then crossed to the alternate therapy. Postprandial metabolic studies were performed at the end of each treatment period. D3‐leucine tracer was administered as subjects consumed a high‐fat liquid meal. ApoB‐48 kinetics were determined using stable isotope tracer kinetics with fractional catabolic rates (FCRs) and secretion rates derived using a non‐steady‐state compartmental model. Area‐under‐the‐curve (AUC) and incremental AUC (iAUC) for plasma triglyceride and apoB‐48 were also calculated over the 10‐h period after ingestion of the fat meal. Results: In statin‐treated patients with T2DM, apoB‐48 concentration was lower with ER niacin (8.24 ± 1.98 vs 5.48 ± 1.14 mg/l, p = 0.03) compared with statin alone. Postprandial triglyceride and apoB‐48 AUC were also significantly lower on ER niacin treatment (‐15 and ‐26%, respectively; p < 0.05), without any change to triglyceride and apoB‐48 iAUC. ApoB‐48 secretion rate in the basal state (3.21 ± 0.34 vs 2.50 ± 0.31 mg/kg/day; p = 0.04) and number of apoB‐48‐containing particles secreted in response to the fat load (1.35 ± 0.19 vs 0.84 ± 0.12 mg/kg; p = 0.02) were lower on ER niacin. ApoB‐48 FCR was not altered with ER niacin (8.78 ± 1.04 vs 9.17 ± 1.26 pools/day; p = 0.79). Conclusions: ER niacin reduces apoB‐48 concentration by lowering fasting and postprandial apoB‐48 secretion rate. This effect may be beneficial for lowering atherogenic postprandial lipoproteins and may provide cardiovascular disease risk benefit in patients with T2DM.