title: Glucose-induced effects and joker function of glucose: endocrine or genotoxic prevalence?
abstract: The steady increase in chronic "glycemic load" is characteristic for modern times. Among myriad of glucose functions, two principals can be emphasized: first, endocrine (in particular, ability to induce insulin secretion) and second, DNA-damaging related to formation of reactive oxygen species (ROS). It was suggested by us earlier that a shift in the ratio of mentioned functions reflects a possible "joker" role of glucose as an important modifier of human pathology. Therefore, we embarked on a study to investigate an individual effect of peroral glucose challenge on serum insulin level and ROS generation by mononuclears (luminol-dependent/latex-induced chemiluminescence) in 20 healthy people aged between 28-75. Concentrations of glucose, blood lipids, carbonylated proteins, malondialdehyde, leptin and TNF-alpha were determined as well. On the basis of received data two separate groups could be distinguished: one (n=8), in which glucose stimulation of ROS generation by mononuclears was increased and relatively prevailed over induction of insulin secretion (state of the so called glucose-induced genotoxicity, GIGT), and another (n=12), in which signs of GIGT were not revealed. People who belonged to the first group were characterized with a tendency to lower body mass index, blood leptin and cholesterol and to higher TNF-alpha concentration. Thus, if joker function of glucose is realized in "genotoxic mode", the phenotype (and probably genotype) of subjects may be rather distinctive to the one discovered in glucose-induced "endocrine prevalence". Whether such changes may serve as a pro-mutagenic or pro-endocrine basis for the rise of different chronic diseases or, rather, different features/aggressiveness of the same disease warrants further study.
authors.affiliation: N. N. Petrov Research Institute of Oncology, Pesochny-2, Leningradskaja 68, St. Petersburg 197758, Russia. levmb@endocrin.spb.ru
authors.forename: L M
authors.initials: LM
authors.lastname: Berstein
authors.forename: D A
authors.initials: DA
authors.lastname: Vasilyev
authors.forename: T E
authors.initials: TE
authors.lastname: Poroshina
authors.forename: I G
authors.initials: IG
authors.lastname: Kovalenko
mesh_terms: D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism*; D001798:Blood Proteins / Q000378:metabolism; D004703:Endocrine System / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000009:adverse effects* / Q000493:pharmacokinetics; D005951:Glucose Tolerance Test; D006801:Humans; D006943:Hyperglycemia / Q000453:epidemiology / Q000378:metabolism* / Q000503:physiopathology*; D007328:Insulin / Q000097:blood / Q000378:metabolism; D000078790:Insulin Secretion; D020738:Leptin / Q000097:blood; D008055:Lipids / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D019518:Postprandial Period / Q000502:physiology; D015995:Prevalence; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D001786:Blood Glucose; D001798:Blood Proteins; D007328:Insulin; D020738:Leptin; D008055:Lipids; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D005947:Glucose