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Mol Genet Metab DOI:10.1016/j.ymgme.2014.11.010

Effects of sodium benzoate, a widely used food preservative, on glucose homeostasis and metabolic profiles in humans.

Publication TypeJournal Article
Year of Publication2015
AuthorsLennerz, BS, Vafai, SB, Delaney, NF, Clish, CB, Deik, AA, Pierce, KA, Ludwig, DS, Mootha, VK
JournalMol Genet Metab
Volume114
Issue1
Pages73-9
Date Published2015 Jan
ISSN1096-7206
KeywordsAdolescent, Adult, Anticonvulsants, Blood Glucose, Cross-Over Studies, Diet, Female, Food Preservatives, Glucagon, Glucose, Glycine, Hippurates, Homeostasis, Humans, Insulin, Male, Metabolome, ortho-Aminobenzoates, Overweight, Sodium Benzoate, Young Adult
Abstract

Sodium benzoate is a widely used preservative found in many foods and soft drinks. It is metabolized within mitochondria to produce hippurate, which is then cleared by the kidneys. We previously reported that ingestion of sodium benzoate at the generally regarded as safe (GRAS) dose leads to a robust excursion in the plasma hippurate level [1]. Since previous reports demonstrated adverse effects of benzoate and hippurate on glucose homeostasis in cells and in animal models, we hypothesized that benzoate might represent a widespread and underappreciated diabetogenic dietary exposure in humans. Here, we evaluated whether acute exposure to GRAS levels of sodium benzoate alters insulin and glucose homeostasis through a randomized, controlled, cross-over study of 14 overweight subjects. Serial blood samples were collected following an oral glucose challenge, in the presence or absence of sodium benzoate. Outcome measurements included glucose, insulin, glucagon, as well as temporal mass spectrometry-based metabolic profiles. We did not find a statistically significant effect of an acute oral exposure to sodium benzoate on glucose homeostasis. Of the 146 metabolites targeted, four changed significantly in response to benzoate, including the expected rise in benzoate and hippurate. In addition, anthranilic acid, a tryptophan metabolite, exhibited a robust rise, while acetylglycine dropped. Although our study shows that GRAS doses of benzoate do not have an acute, adverse effect on glucose homeostasis, future studies will be necessary to explore the metabolic impact of chronic benzoate exposure.

URLhttp://linkinghub.elsevier.com/retrieve/pii/S1096-7192(14)00355-2
DOI10.1016/j.ymgme.2014.11.010
Pubmed

http://www.ncbi.nlm.nih.gov/pubmed/25497115?dopt=Abstract

Alternate JournalMol. Genet. Metab.
PubMed ID25497115
PubMed Central IDPMC4289147
Grant ListP30 DK040561 / DK / NIDDK NIH HHS / United States
K24DK082730 / DK / NIDDK NIH HHS / United States
R01 DK081457 / DK / NIDDK NIH HHS / United States
K24 DK082730 / DK / NIDDK NIH HHS / United States
UL1 TR001102 / TR / NCATS NIH HHS / United States
UL1 RR025758 / RR / NCRR NIH HHS / United States
R01DK081457 / DK / NIDDK NIH HHS / United States