Effects of Niacin Therapy That Simulate Neoplasia: Hepatic Steatosis with Concurrent Hepatic Dysfunction

Kristensen, Torben; Olcott, Eric W.

doi:10.1097/00004728-199903000-00026

Cited by 10 publications

(3 citation statements)

References 21 publications

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“…46,[49][50][51][52][53][54][55] Our recent studies have shown that there is a strong lag-correlation between the prevalence of obesity and diabetes in the US population and the increased per capita consumption of niacin, which was attributed primarily to the consumption of fortified grains. 34,35 The toxic effects of niacin may involve a variety of mechanisms, including methyl depletion, changes in NAD-dependent reactions and excessive ROS generation.…”

Section: Arsenicmentioning

confidence: 99%

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Dietary methyl-consuming compounds and metabolic syndrome

Zhou

et al. 2011

Hypertens Res

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The metabolic syndrome, a major risk factor for type 2 diabetes and cardiovascular disease, is a cluster of metabolic abnormalities including obesity, insulin resistance, hypertension and dyslipidemia. Although systemic oxidative stress and aberrant methylation status are known to have important roles in the development of metabolic syndrome, how they occur remains unclear. The metabolism of methyl-consuming compounds generates reactive oxygen species and consumes labile methyl groups; therefore, a chronic increase in the levels of methyl-consuming compounds in the body can induce not only oxidative stress and subsequent tissue injury, but also methyl-group pool depletion and subsequent aberrant methylation status. In the past few decades, the intake amount of methyl-consuming compounds has substantially increased primarily due to pollution, food additives, niacin fortification and high meat consumption. Thus, increased methyl consumers might have a causal role in the development and prevalence of metabolic syndrome and its related diseases. Moreover, factors that decrease the elimination/ metabolism of methyl-consuming compounds and other xenobiotics (for example, sweat gland inactivity and decreased liver function) or increase the generation of endogenous methyl-consuming compounds (for example, mental stress-induced increase in catecholamine release) may accelerate the progression of metabolic syndrome. Based on current nutrition knowledge and the available evidence from epidemiological, ecological, clinical and laboratory studies on metabolic syndrome and its related diseases, this review outlines the relationship between methyl supply-consumption imbalance and metabolic syndrome, and proposes a novel mechanism for the pathogenesis and prevalence of metabolic syndrome and its related diseases.

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Section: Arsenicmentioning

confidence: 99%

“…56 Interestingly, niacin has been found to induce both lipid-lowering effect 52 and adverse hepatic outcomes. 46,52,54,55 Thus, it seems that the lipidlowering effect of niacin may be mediated by methyl depletion, which, although improving cardiovascular outcomes, may increase the risk of adverse hepatic outcomes.…”

Section: Arsenicmentioning

confidence: 99%

Dietary methyl-consuming compounds and metabolic syndrome

Zhou

et al. 2011

Hypertens Res

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“…There are additional reports of both niacin-induced lactic acidosis, especially associated with coingestion of alcohol and abnormal computed tomography scan images simulating hepatobiliary neoplasia. 3 Niacin can influence vascular function directly by modulating the activity of immune cells and endothelial cells. The mechanisms underlying the proangiogenic response remain to be determined.…”

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confidence: 99%