title: Effect of oral oleoyl-estrone on the energy balance of diabetic rats.
abstract: We studied the effects of a 10-day oral 10 micromol/kg oleoyl-estrone (OE) treatment on streptozotocin-diabetic Wistar, Goto-Kakizaki and control Wistar rats. Streptozotocin rats lost more than half the energy ingested as urine glucose. Oleoyl-estrone induced the loss of body weight (mainly body fat) in all groups. Energy expenditure was similar in the three groups of rats studied. Water turnover was deranged in streptozotocin rats, which spent 14% of energy available heating the water drunk. Body lipids were highest in Goto-Kakizaki; lipid levels in streptozotocin rats were very low. Oleoyl-estrone decreased body lipid content in Wistar and Goto-Kakizaki; oleoyl-estrone decreased triacylglycerols (44% in Wistar and Goto-Kakizaki and 22% in streptozotocin rats) and phospholipids but did not affect body cholesterol. Oleoyl-estrone decreased insulin and leptin, did not affect blood glucose but decreased plasma glucose in all groups. There were no changes in plasma triacylglycerols or fatty acids, but HDL, LDL and cholesterol decreased in all groups. The same effects of OE on insulin, plasma (but not blood) glucose and leptin were observed in both models, but the presence of insulin seems to be needed for OE to normalise glycaemia and to facilitate the uptake and utilisation of glucose by tissues. This different handling of glucose and triacylglycerol energy accounts for the disparate effects of OE on energy balance. The main conclusion of this study is that OE function as a lipid-mobilising hormone is dependent on the mass of reserves available, which in turn is closely related to insulin status. Lack of insulin thus results in limited OE effects, and insulin resistance does not prevent or limit the effects of OE on energy homeostasis or the mobilisation of fat.
authors.affiliation: Centre Especial de Recerca en Nutrició i Ciència dels Aliments, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain.
authors.forename: M
authors.initials: M
authors.lastname: Díaz-Silva
authors.forename: M M
authors.initials: MM
authors.lastname: Grasa
authors.forename: J
authors.initials: J
authors.lastname: López-Martí
authors.forename: J A
authors.initials: JA
authors.lastname: Fernández-López
authors.forename: X
authors.initials: X
authors.lastname: Remesar
authors.forename: M
authors.initials: M
authors.lastname: Alemany
mesh_terms: D000284:Administration, Oral; D000818:Animals; D019440:Anti-Obesity Agents / Q000008:administration & dosage*; D001786:Blood Glucose / Q000187:drug effects; D001834:Body Water / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D008076:Cholesterol, HDL / Q000037:antagonists & inhibitors; D008078:Cholesterol, LDL / Q000037:antagonists & inhibitors; D004326:Drinking; D004734:Energy Metabolism / Q000187:drug effects*; D004970:Estrone / Q000008:administration & dosage* / Q000031:analogs & derivatives*; D005947:Glucose / Q000031:analogs & derivatives*; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000037:antagonists & inhibitors; D050356:Lipid Metabolism; D008055:Lipids / Q000037:antagonists & inhibitors; D009829:Oleic Acids / Q000008:administration & dosage*; D051381:Rats; D011919:Rats, Inbred Strains; D017208:Rats, Wistar; D013311:Streptozocin / Q000378:metabolism* / Q000652:urine; D014508:Urea / Q000031:analogs & derivatives*
chemical_list: D019440:Anti-Obesity Agents; D001786:Blood Glucose; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D007328:Insulin; D020738:Leptin; D008055:Lipids; D009829:Oleic Acids; D004970:Estrone; D013311:Streptozocin; C108709:oleoyl-estrone; C036060:glucosylurea; D014508:Urea; D005947:Glucose