title: Lack of the effect of mycotoxins-aflatoxin B1 and ochratoxin A on some functions of rat adipocytes.
abstract: Mycotoxins-aflatoxin B1 (AFB1) and ochratoxin A (OTA)-compounds which are strong carcinogenic, mutagenic and cytotoxic factors-are also known to evoke a decrease of food intake and body weight gains. The purpose of our study was to determine the direct influence of AFB1 and OTA incubated with isolated rat fat cells on the lipogenesis, lipolysis and leptin secretion. Adipocytes were isolated from the epididymal fat tissue by the collagenase digestion. Toxins used at concentrations 1, 10 and 100 microM were incubated for 90 min with adipocytes. Basal and insulin-stimulated lipogenesis-determined by the measure of [U-14C]glucose conversion to total lipids-was abated by AFB1 only at the highest concentration. At two lower ones, AFB1 did not affect the process. OTA at all used concentrations decreased insulin-stimulated lipogenesis but the effect was not dose-dependent. The lipolysis was determined by the measure of glycerol release from adipocytes. The basal lipolysis was unchanged by both toxins. The epinephrine-stimulated lipolysis was intensified by AFB1 only at the highest concentration, however, the process was not altered by OTA. The antilipolytic action of insulin was unaffected by both compounds (10 microM). To determine the influence of the tested toxins on leptin secretion, adipocytes were incubated for 120 min in the presence of glucose and insulin as stimulators of hormone secretion. AFB1 and OTA added to the incubation medium (1, 10 and 100 microM) had no significant influence on the leptin release. The results obtained in this experiment demonstrate that adipocytes are susceptible to the direct action of AFB1 and OTA. This susceptibility is, however, rather weak and is exhibited by a slight restriction of the lipogenesis (in the case of both toxins) and by a slight increase of the lipolysis (in the case of AFB1).
authors.affiliation: Department of Animal Physiology and Biochemistry, August Cieszkowski University of Agriculture, 60-637 Wołyńska 35, Poznań, Poland. tszkudel@jay.au.pozman.pl
authors.forename: K
authors.initials: K
authors.lastname: Szkudelska
authors.forename: H
authors.initials: H
authors.lastname: Drzymała
authors.forename: T
authors.initials: T
authors.lastname: Szkudelski
authors.forename: K
authors.initials: K
authors.lastname: Bukowska
authors.forename: L
authors.initials: L
authors.lastname: Nogowski
mesh_terms: D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D016604:Aflatoxin B1 / Q000633:toxicity*; D000818:Animals; D004435:Eating / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects; D004837:Epinephrine / Q000494:pharmacology; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology; D020738:Leptin / Q000096:biosynthesis; D008055:Lipids / Q000096:biosynthesis; D008066:Lipolysis / Q000187:drug effects; D008297:Male; D009793:Ochratoxins / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000318:Adrenergic beta-Agonists; D007004:Hypoglycemic Agents; D007328:Insulin; D020738:Leptin; D008055:Lipids; D009793:Ochratoxins; C025589:ochratoxin A; D016604:Aflatoxin B1; D004837:Epinephrine