Is HPS2-THRIVE the death knell for niacin?

Tóth, Peter P.; Murthy, Avinash; Sidhu, Mandeep S.; Boden, William E.

doi:10.1016/j.jacl.2015.01.008

Cited by 9 publications

(6 citation statements)

References 50 publications

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“…This is important because, due to the negative outcomes of two recent clinical trials (46)(47)(48), prescriptions have been declining (49), and there is now considerable uncertainty about the value of niacin therapy (50)(51)(52). Bedtime dosing has been standard since the late 1990s after the introduction of prescription…”

Section: Damage Control By Minimizing Ffa Reboundmentioning

confidence: 99%

Nicotinic acid timed to feeding reverses tissue lipid accumulation and improves glucose control in obese Zucker rats[S]

Kroon

Baccega

Olsen

et al. 2017

Journal of Lipid Research

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Section: Damage Control By Minimizing Ffa Reboundmentioning

confidence: 99%

Nicotinic acid timed to feeding reverses tissue lipid accumulation and improves glucose control in obese Zucker rats[S]

Kroon

Baccega

Olsen

et al. 2017

Journal of Lipid Research

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“…24 Whether lowering Lp(a) specifically confers CVD benefits can only be addressed by therapeutic interventions that selectively lower Lp(a). 10 Recent in vitro studies point to a role of the LDL receptor in the catabolism of Lp(a).…”

Section: Arterioscler Thromb Vasc Biol December 2015mentioning

confidence: 99%

Effects of Extended-Release Niacin on the Postprandial Metabolism of Lp(a) and ApoB-100–Containing Lipoproteins in Statin-Treated Men With Type 2 Diabetes Mellitus

Ooi

Watts

Chan

et al. 2015

ATVB

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Objective— The effects of extended-release niacin (ERN; 1–2 g/d) on the metabolism of lipoprotein(a) (Lp(a)) and apolipoprotein (apo) B-100–containing lipoproteins were investigated in 11 statin-treated white men with type 2 diabetes mellitus in a randomized, crossover trial of 12-weeks duration. Approach and Results— The kinetics of Lp(a) and very low–density lipoprotein (VLDL), intermediate-density lipoprotein, and low-density lipoprotein (LDL) apoB-100 were determined following a standardized oral fat load (87% fat) using intravenous administration of D 3 -leucine, gas chromatography–mass spectrometry, and compartmental modeling. ERN significantly decreased fasting plasma total cholesterol, LDL cholesterol, and triglyceride concentrations. These effects were achieved without significant changes in body weight or insulin resistance. ERN significantly decreased plasma Lp(a) concentration (−26.5%) and the production rates of apo(a) (−41.5%) and Lp(a)-apoB-100 (−32.1%); the effect was greater in individuals with elevated Lp(a) concentration. ERN significantly decreased VLDL (−58.7%), intermediate-density lipoprotein (−33.6%), and LDL (−18.3%) apoB-100 concentrations and the corresponding production rates (VLDL, −49.8%; intermediate-density lipoprotein, −44.7%; LDL, −46.1%). The number of VLDL apoB-100 particles secreted increased in response to the oral fat load. Despite this, total VLDL apoB-100 production over the 10-hour postprandial period was significantly decreased with ERN (−21.9%). Conclusions— In statin-treated men with type 2 diabetes mellitus, ERN decreased plasma Lp(a) concentrations by decreasing the production of apo(a) and Lp(a)-apoB-100. ERN also decreased the concentrations of apoB-100–containing lipoproteins by decreasing VLDL production and the transport of these particles down the VLDL to LDL cascade. Our study provides further mechanistic insights into the lipid-regulating effects of ERN.

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“…; Toth et al. ). Intriguingly, retrospective meta‐analyses (Lavigne and Karas ) and studies in cell culture, mouse models, healthy subjects, and patients with type 2 diabetes mellitus suggest that the vascular benefits of niacin may be driven by direct effects on endothelial and immune cells (Wu et al.…”

Section: Introductionmentioning

confidence: 98%

Niacin promotes revascularization and recovery of limb function in diet‐induced obese mice with peripheral ischemia

Pang

Zhang

Sutherland

et al. 2016

Pharmacology Res & Perspec

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Niacin can reduce vascular disease risk in individuals with metabolic syndrome, but in light of recent large randomized controlled trials outcomes, its biological actions and clinical utility remain controversial. Niacin can improve endothelial function, vascular inflammation, and vascular regeneration, independent of correcting dyslipidemia, in various lean rodent models of vascular injury. Here, we tested whether niacin could directly improve endothelial cell angiogenic function during combined exposure to excess fatty acids and hypoxia, and whether intervention with niacin during continued feeding of western diet could improve revascularization and functional recovery in obese, hyperlipidemic mice with peripheral ischemia. Treatment with niacin (10 μmol/L) increased human microvascular endothelial cell angiogenic function during exposure to high fatty acids and hypoxia (2% oxygen), as determined by tube formation on Matrigel. To assess revascularization in vivo, we used western diet‐induced obese mice with unilateral hind limb femoral artery ligation and excision. Treatment for 14 days postinjury with once daily i.p. injections of a low dose of niacin (50 mg/kg) improved recovery of hind limb use, in association with enhanced revascularization and decreased inflammation of the tibialis anterior muscle. These effects were concomitant with decreased plasma triglycerides, but not increased plasma apoAI. Thus, niacin improves endothelial tube formation under lipotoxic and hypoxic conditions, and moreover, promotes revascularization and functional hind limb recovery following ischemic injury in diet‐induced obese mice with hyperlipidemia. These data may have implications for niacin therapy in the treatment of peripheral ischemic vascular disease associated with metabolic syndrome.

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Is HPS2-THRIVE the death knell for niacin?

Cited by 9 publications

References 50 publications

Nicotinic acid timed to feeding reverses tissue lipid accumulation and improves glucose control in obese Zucker rats[S]

Nicotinic acid timed to feeding reverses tissue lipid accumulation and improves glucose control in obese Zucker rats[S]

Effects of Extended-Release Niacin on the Postprandial Metabolism of Lp(a) and ApoB-100–Containing Lipoproteins in Statin-Treated Men With Type 2 Diabetes Mellitus

Niacin promotes revascularization and recovery of limb function in diet‐induced obese mice with peripheral ischemia

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