Glucose-induced effects and joker function of glucose: endocrine or genotoxic prevalence?

Horm Metab Res. 2006 Oct;38(10):650-5. doi: 10.1055/s-2006-954589.

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.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Blood Glucose / metabolism*
  • Blood Proteins / metabolism
  • Endocrine System / metabolism*
  • Female
  • Glucose / adverse effects*
  • Glucose / pharmacokinetics
  • Glucose Tolerance Test
  • Humans
  • Hyperglycemia / epidemiology
  • Hyperglycemia / metabolism*
  • Hyperglycemia / physiopathology*
  • Insulin / blood
  • Insulin / metabolism
  • Insulin Secretion
  • Leptin / blood
  • Lipids / blood
  • Male
  • Malondialdehyde / blood
  • Middle Aged
  • Postprandial Period / physiology
  • Prevalence
  • Reactive Oxygen Species / metabolism
  • Tumor Necrosis Factor-alpha / blood

Substances

  • Blood Glucose
  • Blood Proteins
  • Insulin
  • Leptin
  • Lipids
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • Malondialdehyde
  • Glucose