Open AccessInsulin stimulates triacylglycerol secretion by perfused livers from fed rats but inhibits it in livers from fasted or insulin‐deficient rats
Author(s) -
Zammit Victor A.,
Lankester David J.,
Brown Anna M.,
Park ByungSung
Publication year - 1999
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1046/j.1432-1327.1999.00568.x
Subject(s) - medicine , endocrinology , insulin , secretion , streptozotocin , triglyceride , insulin oscillation , in vivo , biology , diabetes mellitus , cholesterol , insulin resistance , microbiology and biotechnology
We determined whether the direction of the acute effect of insulin on hepatic triacylglycerol secretion is dependent on the prior physiological state or on the in vitro experimental system used. The effect of insulin on triacylglycerol secretion was studied using perfused livers isolated from rats under three metabolic conditions: fed normo‐insulinaemic, 24‐h fasted and fed, streptozotocin‐diabetic (insulin‐deficient). Insulin acutely activated triacylglycerol secretion (by 43%) in organs from fed, normo‐insulinaemic animals, whereas it inhibited triacylglycerol secretion in livers isolated from fasted or insulin‐deficient rats (by 30 and 33%, respectively). By contrast, in 24‐h‐cultured hepatocytes insulin invariably acutely inhibited triacylglycerol secretion irrespective of the metabolic state of the donor animals. It is concluded that the use of perfused livers enables the observation of a switch in the direction of insulin action on hepatic triacylglycerol secretion from stimulatory, in the normo‐insulinaemic state, to inhibitory in the fasting or insulin‐deficient state. The possible implications of this switch for the relationship between hyperinsulinaemia, increased hepatic very‐low‐density lipoprotein–triacylglycerol secretion and hypertriglyceridaemia observed in vivo are discussed.