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204. Polymorphisms of cytochrome P4501A2 and N -acetyltransferase genes, smoking, and risk of pancreatic cancer

Author

Li, Donghui, primary, Jiao, Li, additional, Li, Yanan, additional, Doll, Mark A., additional, Hein, David W., additional, Bondy, Melissa L., additional, Evans, Douglas B., additional, Wolff, Robert A., additional, Lenzi, Renato, additional, Pisters, Peter W., additional, Abbruzzese, James L., additional, and Hassan, Manal M., additional

Published
2005
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210. Association of metabolic gene polymorphisms with tobacco consumption in healthy controls

Author

Smits, Kim M., primary, Benhamou, Simone, additional, Garte, Seymour, additional, Weijenberg, Matty P., additional, Alamanos, Yannis, additional, Ambrosone, Christine, additional, Autrup, Herman, additional, Autrup, Judith L., additional, Baranova, Helena, additional, Bathum, Lisa, additional, Boffetta, Paolo, additional, Bouchardy, C., additional, Brockmoller, Jurgen, additional, Butkiewicz, Dorota, additional, Cascorbi, Ingolf, additional, Clapper, Margie L., additional, Coutelle, Christiane, additional, Daly, Ann K., additional, Muzi, Giacomo, additional, Dolzan, Vita, additional, Duzhak, Tatyana G., additional, Farker, Katrin, additional, Golka, Klaus, additional, Haugen, Aage, additional, Hein, David W., additional, Hildesheim, Allan, additional, Hirvonen, Ari, additional, Hsieh, Ling L., additional, Ingelman-Sundberg, Magnus, additional, Kalina, Ivan, additional, Kang, Daehee, additional, Katoh, Takahiko, additional, Kihara, Masahiro, additional, Ono-Kihara, Masako, additional, Kim, Heon, additional, Kiyohara, Chikako, additional, Kremers, Pierre, additional, Lazarus, Philip, additional, Le Marchand, Loic, additional, Lechner, Maria C., additional, London, Stephanie, additional, Manni, Johannes J., additional, Maugard, Christine M., additional, Morgan, Gareth J., additional, Morita, Shunji, additional, Nazar-Stewart, Valle, additional, Kristensen, Vessela Nedelcheva, additional, Oda, Yoshio, additional, Parl, Fritz F., additional, Peters, Wilbert H.M., additional, Rannug, Agneta, additional, Rebbeck, Timothy, additional, Pinto, Luis F. Ribeiro, additional, Risch, Angela, additional, Romkes, Marjorie, additional, ?alagovic, Jan, additional, Schoket, Bernadette, additional, Seidegard, Janeric, additional, Shields, Peter G., additional, Sim, Edith, additional, Sinnett, Daniel, additional, Strange, Richard C., additional, Stucker, Isabelle, additional, Sugimura, Haruhiko, additional, To-Figueras, Jordi, additional, Vineis, Paolo, additional, Yu, Mimi C., additional, Zheng, Wei, additional, Pedotti, Paola, additional, and Taioli, Emanuela, additional

Published
2004
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211. Pharmacogenomics: Social, Ethical, and Clinical Dimensions

Author

Hein, David W.

Abstract

Edited by Mark A. Rothstein. Hoboken, NJ: John Wiley & Sons, 2003. 320 pp. ISBN: 0 471-22769-2, $59.95 cloth. This interesting and timely book presents a multidisciplinary analysis of the [...]

Published
2003

224. Phenotypic and Genotypic Characterization of N-Acetylation.

Author

Kang, Y. James, Las, Lawrence H., Svensson, Craig K., and Hein, David W.

Abstract

Variation among the human population in the ability to acetylate drugs has been known since the observations on individual variations in isoniazid toxicity in the 1950s. The genetic basis for this was soon appreciated and has come to be known as the N-acetylation polymorphism. This chapter provides as background a description of some key studies that showed that acetylation was variable in the human population, that it is inherited, and the molecular basis for this phenomenon. Since accurate determination of acetylator phenotype is critical to testing a number of important hypotheses, including the link between disease risk and acetylator phenotype, limitations and potential problems with various methods of phenotype determination are discussed. Similarly, procedures and approaches for determination of NAT1 and NAT2 genotype are described. The final section brings phenotype and genotype together by examining the relationship between variant alleles and disease incidence. Increasingly, these studies have relied solely on the measurement of genotype, with the assumption that phenotype may be accurately deduced from genotype. There is a fairly wide degree of variability in the frequency of discordance between genotype and phenotype, however, especially when caffeine is used as a probe for phenotype determination. The potential consequences of this discordance are discussed. [ABSTRACT FROM AUTHOR]

Published
2005
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230. Induction of glucose production by heterocyclic amines is dependent on N-acetyltransferase 2 genetic polymorphism in cryopreserved human hepatocytes.

Author

Walls, Kennedy M., Hong, Kyung U., and Hein, David W.

Subjects
*GENETIC polymorphisms, *TYPE 2 diabetes, *LIVER cells, *INSULIN, *GLUCOSE, *HYPERGLYCEMIA, *AMINES, *AROMATIC amines
Abstract

Heterocyclic amines (HCAs) are mutagenic compounds found in cooked meat. Recent epidemiological studies reported significant associations between dietary HCA exposure and insulin resistance and type II diabetes, and we recently reported that HCAs induce insulin resistance and glucose production in human hepatocytes. It is well known that HCAs require hepatic bioactivation by cytochrome P450 1A2 (CYP1A2) and N -acetyltransferase 2 (NAT2). NAT2 expresses a well-defined genetic polymorphism in humans that, depending on the combination of NAT2 alleles, correlates to rapid, intermediate, or slow acetylator phenotype that exhibits differential metabolism of aromatic amines and HCAs. No previous studies have examined the role of NAT2 genetic polymorphism in the context of HCA-mediated induction of glucose production. In the present study, we assessed the effect of three HCAs commonly found in cooked meat (2-amino-3,4-dimethylimidazo[4,5- f ]quinoline [MeIQ], 2-amino-3,8-dimethylimidazo[4,5- f ]quinoxaline [MeIQx], and 2-amino-1-methyl-6-phenylimidazo[4,5- b ]pyridine [PhIP]) on glucose production in cryopreserved human hepatocytes with slow, intermediate, or rapid NAT2 acetylator phenotype. HCA treatment did not affect glucose production in slow NAT2 acetylator hepatocytes, while a slight increase in glucose production was observed in intermediate NAT2 acetylators treated with MeIQ or MeIQx. However, significant increases in glucose production were observed in rapid NAT2 acetylators following each HCA. The current findings suggest that individuals who are rapid NAT2 acetylators may be at a greater risk of developing hyperglycemia and insulin resistance following dietary exposure to HCAs. [Display omitted] • HCAs promote insulin resistance and glucose production in human hepatocytes. • HCA-induced glucose production required N -acetyltransferase 2 (NAT2) metabolism. • Rapid NAT2 acetylators may be more susceptible to the metabolic effect of HCAs. [ABSTRACT FROM AUTHOR]

Published
2023
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231. Heterocyclic amines reduce insulin-induced AKT phosphorylation and induce gluconeogenic gene expression in human hepatocytes.

Author

Walls, Kennedy M., Hong, Kyung U., and Hein, David W.

Subjects
*INSULIN receptors, *LIVER cells, *TYPE 2 diabetes, *GENE expression, *HUMAN genes, *AMINES
Abstract

Heterocyclic amines (HCAs) are well-known for their mutagenic properties. One of the major routes of human exposure is through consumption of cooked meat, as certain cooking methods favor formation of HCAs. Recent epidemiological studies reported significant associations between dietary HCA exposure and insulin resistance and type II diabetes. However, no previous studies have examined if HCAs, independent of meat consumption, contributes to pathogenesis of insulin resistance or metabolic disease. In the present study, we have assessed the effect of three HCAs commonly found in cooked meat (2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline [MeIQ], 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline [MeIQx], and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine [PhIP]) on insulin signaling and glucose production. HepG2 or cryopreserved human hepatocytes were treated with 0–50 μM of MeIQ, MeIQx, or PhIP for 3 days. Treatment of HepG2 cells and hepatocytes with MeIQ and MeIQx resulted in a significant reduction in insulin-induced AKT phosphorylation, suggesting that HCA exposure decreases hepatic insulin signaling. HCA treatment also led to significant increases in expression of gluconeogenic genes, G6PC and PCK1, in both HepG2 and cryopreserved human hepatocytes. Additionally, the level of phosphorylated FOXO1, a transcriptional regulator of gluconeogenesis, was significantly reduced by HCA treatment in hepatocytes. Importantly, HCA treatment of human hepatocytes led to increases in extracellular glucose level in the presence of gluconeogenic substrates, suggesting that HCAs induce hepatic glucose production. The current findings suggest that HCAs induce insulin resistance and promote hepatic glucose production in human hepatocytes. This implicates that exposure to HCAs may lead to the development of type II diabetes or metabolic syndrome. [ABSTRACT FROM AUTHOR]

Published
2023
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232. DNA Adduct Levels and Intestinal Lesions in Congenic Rapid and Slow Acetylator Syrian Hamsters Administered the Food Mutagens 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) or 2-Amino-3-methylimidazo[4,5-f]quinoline (IQ

Author

Steffensen, Inger-Lise, primary, Fretland, Adrian J., additional, Paulsen, Jan Erik, additional, Feng, Yi, additional, Eide, Tor Jacob, additional, Devanaboyina, Udaya-Sankar, additional, Hein, David W., additional, and Alexander, Jan, additional

Published
2000
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