Tissue culture studies. V. Analogues for nicotinic acid

The use of acetyl-3-pyridine and pyridine-3-sulfonic acid as analogues for nicotinic acid has been tested with tissue cultures of embryonic chick heart. Both roller tube and Carrel flask cultures were employed. Cell migration, appearance of the cells, and the uptake of tracer P³² were used as criteria for the action of the analogues. Migration of the cells could be inhibited by both compounds, but at different levels. Both produced abnormal types of cells, but not the same type of abnormality. Uptake of P³² was inhibited by both compounds. Addition of nicotinic acid failed to reverse the effects of the analogues at the concentrations used.     

Maculopathy induced by nicotinic acid

Nicotinic acid is a commonly used oral medication for the treatment of hyperlipidemia. Numerous systemic and ocular adverse effects have been reported. Cystoid macular edema, although uncommon, has been reported and resolves upon cessation of the medication. What makes this maculopathy unusual is the absence of leakage on fluorescein angiography. A 47-year-old white male presented with the complaint of blurred vision OU for several months. The patient had an extensive medical history, including hyperlipidemia, for which he was taking nicotinic acid. Bilateral cystoid macular edema was diagnosed. Nicotinic acid was discontinued and the patient's vision returned to 20/20 after 2 months.     

The bacterial oxidation of nicotinic acid

N-Formylmaleamic acid, a probable intermediate in the bacterial metabolism of nicotinic acid, has been synthesized by photoisomerization of its transisomer, N-formylfumaramic acid. The compound previously reported to be N-formylmaleamic acid has been shown to be N-formylfumaramic acid.This paper is dedicated to Prof. R. Y. Stanier, who served as a model of elegant erudition to me during my graduate work with him.I thank the NIH and NSF for support     

Molecular identification of nicotinic acid receptor

Nicotinic acid and its derivative, Acipimox, have been widely used in the treatment of hyperlipidemia. Pharmacological studies have demonstrated that they exert the beneficial effect through the activation of a Gi-protein-coupled receptor on adipocyte, which has remained elusive to date. Here we show that a novel GPCR, designated HM74b because of its high similarity to HM74, is a receptor for nicotinic acid. HM74b mRNA is found in human, murine, and rat adipose tissues. Nicotinic acid and Acipimox inhibit forskolin-stimulated intracellular cAMP accumulation in human HM74b-expressing cells and activate GTP gamma S binding in a dose-dependent manner. [3H]Nicotinic acid specifically binds to HM74b-expressing membrane and its binding is replaced by Acipimox. This finding will open a new phase of research on the physiological role of nicotinic acid and will be a clue to develop novel antihyperlipidemic drugs.