triolein and Starvation

The pyruvate dehydrogenase complex (PDC) has a pivotal role in islet metabolism. The pyruvate dehydrogenase kinases (PDK1-4) regulate glucose oxidation through inhibitory phosphorylation of PDC. Starvation increases islet PDK activity (Am J Physiol Endocrinol Metab 270:E988-E994, 1996). In this study, using antibodies against PDK1, PDK2, and PDK4 (no sufficiently specific antibodies are as yet available for PDK3), we identified the PDK isoform profile of the pancreatic islet and delineated the effects of starvation (48 h) on protein expression of individual PDK isoforms. Rat islets were demonstrated to contain all three PDK isoforms, PDK1, PDK2, and PDK4. Using immunoblot analysis with antibodies raised against the individual recombinant PDK isoforms, we demonstrated increased islet protein expression of PDK4 in response to starvation (2.3-fold; P < 0.01). Protein expression of PDK1 and PDK2 was suppressed in response to starvation (by 27% [P < 0.01] and 10% [NS], respectively). We demonstrated that activation of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) by the selective agonist WY14,643 for 24 h in vivo leads to specific upregulation of islet PDK4 protein expression by 1.8-fold (P < 0.01), in the absence of change in islet PDK1 and PDK2 protein expression but in conjunction with a 2.2-fold increase (P < 0.01) in islet PPAR-alpha protein expression. Thus, although no changes in islet PPAR-alpha expression were observed after the starvation protocol, activation of PPAR-alpha in vivo may be a potential mechanism underlying upregulation of islet PDK4 protein expression in starvation. We evaluated the effects of antecedent changes in PDK profile and/or PPAR-alpha activation induced by starvation or PPAR-alpha activation in vivo on glucose-stimulated insulin secretion (GSIS) in isolated islets. GSIS at 20 mmol/l glucose was modestly impaired on incubation with exogenous triglyceride (1 mmol/l triolein) ( approximately 20% inhibition; P < 0.05) in islets from fed rats. Starvation (48 h) impaired GSIS in the absence of triolein (by 57%; P < 0.001), but GSIS after the further addition of triolein did not differ significantly between islets from fed or starved rats. GSIS by islets prepared from WY14,643-treated fed rats did not differ significantly from that seen with islets from control fed rats, and the response to triolein addition resembled that of islets prepared from fed rather than starved rats. PPAR-alpha activation in vivo led to incre

Topics: Animals; Blood Glucose; Blotting, Western; Fatty Acids, Nonesterified; Female; Gene Expression; Gene Expression Regulation, Enzymologic; Glucose; Insulin; Insulin Secretion; Islets of Langerhans; Isoenzymes; Protein Kinases; Protein Serine-Threonine Kinases; Pyrimidines; Pyruvate Dehydrogenase Acetyl-Transferring Kinase; Rats; Rats, Wistar; Receptors, Cytoplasmic and Nuclear; RNA, Messenger; Starvation; Transcription Factors; Triolein

This study tried to find what fat level of diets would have a good effect on recovery of the ultrastructure and the digestion-absorption function of jejunal absorptive cells in rats which had been subjected to starvation. Fat-free, 5% fat, 10% fat, or 20% fat diet was given for 3 days to the starved rats, and changes in the ultrastructure of the jejunal absorptive cells were observed by transmission electron microscopy. Also, glucose and triolein absorption were studied using an in situ perfusion system. Good recovery of the ultrastructure of jejunal absorptive cells was observed in rats re-fed the 5% fat diet. Glucose absorption did not differ among the groups except in rats given the 20% fat diet. However, triolein absorption in this group was lower than that of the other groups in both the upper and lower jejunum. The best fat level for recovery of the ultrastructure and absorption of glucose and triolein in the jejunal absorptive cells was concluded to be the 5% fat diet.

Topics: Animals; Endoplasmic Reticulum; Food; Glucose; Intestinal Absorption; Jejunum; Kinetics; Male; Microscopy, Electron; Mitochondria; Rats; Rats, Sprague-Dawley; Ribosomes; Starvation; Triolein; Vacuoles

1. The effects of starvation and refeeding on the disposal of oral [14C]triolein between 14CO2 production and 14C-lipid accumulation in tissues of virgin rats, lactating rats and lactating rats with pups removed were studied. 2. Starvation (24 h) increased 14CO2 production in lactating rats and lactating rats with pups removed to values found in virgin rats. This increase was accompanied by decreases in 14C-lipid accumulation in mammary gland and pups of lactating rats and in white and brown adipose tissue of lactating rats with pups removed. 3. Short-term (2 h) refeeding ad libitum decreased 14CO2 production in lactating rats and lactating rats with pups removed, and restored the 14C-lipid accumulation in mammary glands plus pups and in white and brown adipose tissue respectively 4. Insulin deficiency induced with mannoheptulose inhibited the restoration of 14C-lipid accumulation in white adipose tissue on refeeding of lactating rats with pups removed, but did not prevent the restoration of 14C-lipid accumulation in mammary gland. 5. Changes in the activity of lipoprotein lipase in mammary gland and white adipose tissue paralleled the changes in 14C-lipid accumulation in these tissues. 6. It is concluded that 14C-lipid accumulation in mammary gland may not be affected by changes in plasma insulin concentration and that it is less sensitive to starvation than is lipogenesis or lactose synthesis. This has the advantage that the milk lipid content can still be maintained from hepatic very-low-density lipoprotein for a period after withdrawal of food. The major determinant of the disposal of oral 14C-triolein appears to be the total tissue activity of lipoprotein lipase. When this is high in mammary gland (fed lactating rats) or white adipose tissue (fed lactating rats with pups removed), less triacylglycerol is available for the muscle mass and consequently less is oxidized.

Topics: Adipose Tissue; Animals; Blood Glucose; Carbon Radioisotopes; Dietary Fats, Unsaturated; Female; Food; Insulin; Lactation; Lipid Metabolism; Mammary Glands, Animal; Pregnancy; Rats; Rats, Inbred Strains; Starvation; Tissue Distribution; Triolein

1. Oral administration of triacylglycerol (triolein) to starved/chow-refed lactating rats suppressed the lipogenic switch-on in the mammary gland in vivo. 2. A time-course study revealed that triolein, administered at 30 min after the onset of refeeding, had no influence on lipogenic rate in the mammary gland between 30 and 60 min, but markedly decreased it between 60 and 90 min. Glucose uptake by the mammary gland (arteriovenous difference) increased by 30 min of refeeding, as did lactate production. Between 30 and 90 min glucose uptake remained high in the control animals, but glucose uptake and net C3-unit uptake were decreased in the triolein-loaded animals by 90 min. 3. Triolein increased [glucose 6-phosphate] in the gland and simultaneously decreased [fructose 1,6-bisphosphate], indicative of a decrease in phosphofructokinase activity. This cross-over occurred at 60 min, i.e. immediately before the inhibition of lipogenesis, and by 90 min had reached 'starved' values. 4. Triolein had no effect on plasma [insulin] nor on whole-blood [glucose], [lactate] or [3-hydroxybutyrate]; a small increase in [acetoacetate] was observed. 5. Infusion of the lipoprotein lipase inhibitor, Triton WR1339, abolished the suppression of mammary-gland lipogenesis by triolein and the increase in the [glucose 6-phosphate]/[fructose 1,6-bisphosphate] ratio, suggesting a direct influence of dietary lipid on mammary-gland glucose utilization and phosphofructokinase activity.

Topics: Animals; Dietary Fats; Female; Food; Gastrointestinal Contents; Glucose; Insulin; Lactates; Lactation; Lactic Acid; Lipids; Mammary Glands, Animal; Pregnancy; Rats; Rats, Inbred Strains; Starvation; Triolein

A fed and a starved group of mice were injected with a 14C-labelled triolein emulsion, similar to Intralipid, in a dose corresponding to 0.1 mg triglyceride per gram body weight. The animals were sacrificed from 30 sec to 24 h after injection. The tissue distribution of the fat emulsion depended on the nutritional state of the animals. A marked concentration of radioactivity was found in the gastric mucosa of all animals as soon as 30 sec after injection which declined with time but was still clearly discernible in the autoradiograms 24 h after injection. Although the radioactivity only demonstrates the presence of the labelled oleic acid without indication of the degree of triglyceride lipolysis, the autoradiograms showed marked differences in the concentration of radioactivity between the various groups of skeletal muscles and between the different parts of the reticulo-endothelial system.

Topics: Animals; Autoradiography; Fat Emulsions, Intravenous; Gastric Mucosa; Kidney; Liver; Lung; Male; Mice; Myocardium; Rats; Starvation; Tissue Distribution; Triolein

Topics: Adenosine Monophosphate; Adipose Tissue; Animals; Carbon Isotopes; Centrifugation, Density Gradient; Epididymis; Epinephrine; Glucose; Glycerol; In Vitro Techniques; Insulin; Lipase; Lipoprotein Lipase; Male; Phosphorylases; Rats; Starvation; Triolein