title: Immobilization stress alters intermediate metabolism and circulating lipoproteins in the rat.
abstract: In humans, stress can increase the risk of cardiovascular disease by altering lipoprotein metabolism. Scarce experimental and clinical data are available on this effect. Therefore, we studied the metabolic response to acute and chronic stress following a model of immobilization (IMO) in rats and we evaluated the resulting circulating lipoprotein levels. Repeated IMO treatment (2 hours daily, always between 9:00 AM and 11:00 AM, for 2 periods of 5 and 4 consecutive days, separated by 2 days of rest) daily decreased body weight gain and food intake, increased adrenal weight, and slightly reduced liver glycogen and plasma insulin (without considerable variations of blood glucose), which is characteristic of chronic stress. A single IMO application (30 minutes of an unexpected IMO starting at 2:00 PM immediately before the animals were killed) significantly increased the circulating levels of corticosterone, glucose, insulin, glycerol, and ketone bodies, which is the typical response to acute stress. Both acute and chronic stress decreased the plasmatic triacylglycerol (TAG) concentration, as reflected by the reduction in the number of very-low-density lipoprotein (VLDL) particles. This may be due to an increase in the metabolization of TAG, as suggested by the slightly higher amounts of circulating LDLs. Chronic stress, but not acute stress, significantly increased both the number and the estimated size of circulating high-density lipoprotein (HDLs), as shown by the plasma cholesterol concentration. Acute stress did not have an additive effect over chronic stress on the lipoprotein parameters studied. The metabolic effects of these IMO-induced alterations on lipoprotein profiles are discussed, and future studies in lipidic metabolism are suggested.
authors.affiliation: Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain.
authors.forename: David
authors.initials: D
authors.lastname: Ricart-Jané
authors.forename: Victor
authors.initials: V
authors.lastname: Rodríguez-Sureda
authors.forename: Alex
authors.initials: A
authors.lastname: Benavides
authors.forename: Julia
authors.initials: J
authors.lastname: Peinado-Onsurbe
authors.forename: M Dolores
authors.initials: MD
authors.lastname: López-Tejero
authors.forename: Miquel
authors.initials: M
authors.lastname: Llobera
mesh_terms: D000311:Adrenal Glands / Q000033:anatomy & histology / Q000502:physiology; D000818:Animals; D001786:Blood Glucose / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D002784:Cholesterol / Q000097:blood; D003345:Corticosterone / Q000097:blood; D004435:Eating / Q000502:physiology; D005990:Glycerol / Q000097:blood; D006003:Glycogen / Q000378:metabolism; D007328:Insulin / Q000097:blood; D007657:Ketone Bodies / Q000097:blood; D008074:Lipoproteins / Q000097:blood*; D008079:Lipoproteins, VLDL / Q000097:blood; D008099:Liver / Q000378:metabolism; D008297:Male; D023421:Models, Animal; D009929:Organ Size / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000378:metabolism*; D013995:Time; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D007328:Insulin; D007657:Ketone Bodies; D008074:Lipoproteins; D008079:Lipoproteins, VLDL; D014280:Triglycerides; D006003:Glycogen; D002784:Cholesterol; D005990:Glycerol; D003345:Corticosterone