Search Results
Search for other papers by Alia H Sukkar in
Google Scholar
PubMed
Search for other papers by Aaron M Lett in
Google Scholar
PubMed
Search for other papers by Gary Frost in
Google Scholar
PubMed
Search for other papers by Edward S Chambers in
Google Scholar
PubMed
expression of peroxisome-proliferator-activated receptor alpha ( Ppara ) via activation of AMP-activated, alpha 2 catalytic subunit ( Prkaa2 ) in hepatocytes. This metabolic response increased fatty acid oxidation enzymes such as acyl-CoA oxidase (ACO) and
Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
Movement Sciences, Maastricht University, Maastricht, 6200 The Netherlands
Search for other papers by Sabina Paglialunga in
Google Scholar
PubMed
Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
Movement Sciences, Maastricht University, Maastricht, 6200 The Netherlands
Search for other papers by Patrick Schrauwen in
Google Scholar
PubMed
Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
Movement Sciences, Maastricht University, Maastricht, 6200 The Netherlands
Search for other papers by Christian Roy in
Google Scholar
PubMed
Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
Movement Sciences, Maastricht University, Maastricht, 6200 The Netherlands
Search for other papers by Esther Moonen-Kornips in
Google Scholar
PubMed
Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
Movement Sciences, Maastricht University, Maastricht, 6200 The Netherlands
Search for other papers by Huiling Lu in
Google Scholar
PubMed
Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
Movement Sciences, Maastricht University, Maastricht, 6200 The Netherlands
Search for other papers by Matthijs K C Hesselink in
Google Scholar
PubMed
Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
Movement Sciences, Maastricht University, Maastricht, 6200 The Netherlands
Search for other papers by Yves Deshaies in
Google Scholar
PubMed
Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
Movement Sciences, Maastricht University, Maastricht, 6200 The Netherlands
Search for other papers by Denis Richard in
Google Scholar
PubMed
Centre de Recherche de l’Hôpital Laval, Université Laval, Y2186, 2725 Chemin Ste-Foy, Québec, Canada G1V 4G5
Department of Human Biology, Nutrition and Toxicology Research Institute Maastricht,
Movement Sciences, Maastricht University, Maastricht, 6200 The Netherlands
Search for other papers by Katherine Cianflone in
Google Scholar
PubMed
) with no change in skeletal muscle GLUT-4 protein levels as assessed by western analysis (data not shown). Evaluation of fatty acid oxidation The increased food intake despite similar weight gain in C5L2KO-LF mice
Search for other papers by Karen R Kelly in
Google Scholar
PubMed
Search for other papers by Chin K Sung in
Google Scholar
PubMed
Search for other papers by Marcia J Abbott in
Google Scholar
PubMed
Departments of Kinesiology and Biological Sciences, Biological Sciences, Physiology and Biophysics, College of Letters, Arts, and Sciences, University of Southern California, 3560 Watt Way, PED 107, Los Angeles, California 90089-0652, USA Departments of
Search for other papers by Lorraine P Turcotte in
Google Scholar
PubMed
( Salteil & Kahn 2001 ). More recently, in muscle perfused or incubated with glucose, insulin has also been shown to decrease long-chain fatty acid (LCFA) oxidation, increase triacylglycerol (TG) synthesis, and increase LCFA uptake via translocation of the
Search for other papers by MC Sugden in
Google Scholar
PubMed
Search for other papers by HS Lall in
Google Scholar
PubMed
Search for other papers by RA Harris in
Google Scholar
PubMed
Search for other papers by MJ Holness in
Google Scholar
PubMed
The pyruvate dehydrogenase kinases (PDK1-4) regulate glucose oxidation through inhibitory phosphorylation of the pyruvate dehydrogenase complex (PDC). Immunoblot analysis with antibodies raised against recombinant PDK isoforms demonstrated changes in PDK isoform expression in response to experimental hyperthyroidism (100 microg/100 g body weight; 3 days) that was selective for fast-twitch vs slow-twitch skeletal muscle in that PDK2 expression was increased in the fast-twitch skeletal muscle (the anterior tibialis) (by 1. 6-fold; P<0.05) but not in the slow-twitch muscle (the soleus). PDK4 protein expression was increased by experimental hyperthyroidism in both muscle types, there being a greater response in the anterior tibialis (4.2-fold increase; P<0.05) than in the soleus (3.2-fold increase; P<0.05). The hyperthyroidism-associated up-regulation of PDK4 expression was observed in conjunction with suppression of skeletal-muscle PDC activity, but not suppression of glucose uptake/phosphorylation, as measured in vivo in conscious unrestrained rats (using the 2-[(3)H]deoxyglucose technique). We propose that increased PDK isoform expression contributes to the pathology of hyperthyroidism and to PDC inactivation by facilitating the operation of the glucose --> lactate --> glucose (Cori) and glucose --> alanine --> glucose cycles. We also propose that enhanced relative expression of the pyruvate-insensitive PDK isoform (PDK4) in skeletal muscle in hyperthyroidism uncouples glycolytic flux from pyruvate oxidation, sparing pyruvate for non-oxidative entry into the tricarboxylic acid (TCA) cycle, and thereby supporting entry of acetyl-CoA (derived from fatty acid oxidation) into the TCA cycle.
Search for other papers by M Furuhashi in
Google Scholar
PubMed
Search for other papers by N Ura in
Google Scholar
PubMed
Search for other papers by H Murakami in
Google Scholar
PubMed
Search for other papers by M Hyakukoku in
Google Scholar
PubMed
Search for other papers by K Yamaguchi in
Google Scholar
PubMed
Search for other papers by K Higashiura in
Google Scholar
PubMed
Search for other papers by K Shimamoto in
Google Scholar
PubMed
We investigated the effect of fenofibrate, a peroxisome proliferator-activated receptor-alpha agonist, on insulin sensitivity including lipid metabolism in skeletal muscle. Six-week-old male Sprague-Dawley rats were divided into two groups: those fed a standard chow (control) or a fructose-rich chow (fructose-fed rats (FFRs)) for 6 weeks. FFRs were treated either with a vehicle or with 30 mg/kg per day of fenofibrate for the last 2 weeks. Insulin sensitivity (M-value) was estimated by the euglycemic hyperinsulinemic glucose clamp method. Fatty acid-binding protein (FABP) in skeletal muscle was measured by ELISA, and the expression of FABP mRNA was analyzed by semi-quantitative RT-PCR. The serum and muscle triglyceride (sTG and mTG) levels and the activity of 3-hydroxyacyl-CoA dehydrogenase (HADH), a beta-oxidation enzyme, in muscle were also determined. FFRs showed a lower M-value and higher blood pressure, sTG and mTG than did the control group. The mTG was correlated positively with sTG and negatively with the M-value. Fenofibrate treatment for 2 weeks did not change blood pressure but significantly improved the M-value, sTG and mTG. FABP content and mRNA in the soleus muscle were significantly elevated in FFRs compared with those in the control group. Fenofibrate treatment further increased FABP. The HADH activity was comparable between the control group and FFRs, but significantly increased by fenofibrate treatment. These results suggest that fenofibrate improves insulin sensitivity not only by lowering serum lipids and subsequent influx of fatty acids into muscles but also by reducing intramuscular lipid content via further induction of FABP and stimulation of beta-oxidation in muscles.
Search for other papers by Caroline E Geisler in
Google Scholar
PubMed
Search for other papers by Benjamin J Renquist in
Google Scholar
PubMed
hepatic de novo lipogenesis (DNL), (3) decreased hepatic beta-oxidation and ketogenesis, or (4) decreased export of lipids from the liver in very low density lipoproteins (VLDL). Hepatic lipids as signaling molecules Hepatic fatty acids act as
Search for other papers by J. PEARCE in
Google Scholar
PubMed
Search for other papers by D. BALNAVE in
Google Scholar
PubMed
The increases in liver and blood lipid contents which occur at the onset of lay in the fowl can be simulated in the immature pullet by oestrogen administration (Lorenz, 1954). The liver is the major site of lipogenesis (Goodridge, 1968) and also of oestrogen-induced lipaemia (Ranney & Chaikoff, 1951). Androgens and progestagens are also involved in the physiological changes encountered at point-of-lay (see Balnave & Pearce, 1974) but neither affects the total blood or liver lipid content. Balnave (1968, 1969) suggested that testosterone and progesterone can influence hepatic lipid metabolism and gonadal hormones other than oestrogens can affect hepatic lipogenic enzyme activities (Pearce & Balnave, 1973; Balnave & Pearce, 1974). The present experiments investigated the hypothesis (Balnave, 1968) that gonadal hormones may also affect lipid degradation.
Four-week-old pullets, given food and water ad libitum, received i.m. injections, in 0·2 ml corn oil, of either 2 mg oestradiol dipropionate, 2 mg
Search for other papers by Rosemari Otton in
Google Scholar
PubMed
Search for other papers by Danielly Oliveira da Silva in
Google Scholar
PubMed
Search for other papers by Thais Regina Campoio in
Google Scholar
PubMed
Search for other papers by Leonardo R Silveira in
Google Scholar
PubMed
Search for other papers by Maria Oliveira de Souza in
Google Scholar
PubMed
Search for other papers by Elaine Hatanaka in
Google Scholar
PubMed
Search for other papers by Rui Curi in
Google Scholar
PubMed
Search for other papers by Rosemari Otton in
Google Scholar
PubMed
Search for other papers by Danielly Oliveira da Silva in
Google Scholar
PubMed
Search for other papers by Thais Regina Campoio in
Google Scholar
PubMed
Search for other papers by Leonardo R Silveira in
Google Scholar
PubMed
Search for other papers by Maria Oliveira de Souza in
Google Scholar
PubMed
Search for other papers by Elaine Hatanaka in
Google Scholar
PubMed
Search for other papers by Rui Curi in
Google Scholar
PubMed
Search for other papers by Rosemari Otton in
Google Scholar
PubMed
Search for other papers by Danielly Oliveira da Silva in
Google Scholar
PubMed
Search for other papers by Thais Regina Campoio in
Google Scholar
PubMed
Search for other papers by Leonardo R Silveira in
Google Scholar
PubMed
Search for other papers by Maria Oliveira de Souza in
Google Scholar
PubMed
Search for other papers by Elaine Hatanaka in
Google Scholar
PubMed
Search for other papers by Rui Curi in
Google Scholar
PubMed
