scholarly journals The Expression of Uncoupling Protein 3 Coincides With the Fatty Acid Oxidation Type of Metabolism in Adult Murine Heart

2018 ◽  
Vol 9 ◽  
Author(s):  
Karolina E. Hilse ◽  
Anne Rupprecht ◽  
Monika Egerbacher ◽  
Sarah Bardakji ◽  
Lars Zimmermann ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Uncoupling Protein ◽  
Acid Oxidation ◽  
Uncoupling Protein 3

scholarly journals Pancreatic Islet Adaptation to Fasting Is Dependent on Peroxisome Proliferator-Activated Receptor α Transcriptional Up-Regulation of Fatty Acid Oxidation

Endocrinology ◽  
2005 ◽  
Vol 146 (1) ◽  
pp. 375-382 ◽  
Author(s):  
Sandrine Gremlich ◽  
Christopher Nolan ◽  
Raphaël Roduit ◽  
Rémy Burcelin ◽  
Marie-Line Peyot ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Pancreatic Islet ◽  
Cellular Response ◽  
Uncoupling Protein ◽  
Acid Oxidation ◽  
Hyperinsulinemic Hypoglycemia ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

The cellular response to fasting and starvation in tissues such as heart, skeletal muscle, and liver requires peroxisome proliferator-activated receptor-α (PPARα)-dependent up-regulation of energy metabolism toward fatty acid oxidation (FAO). PPARα null (PPARαKO) mice develop hyperinsulinemic hypoglycemia in the fasting state, and we previously showed that PPARα expression is increased in islets at low glucose. On this basis, we hypothesized that enhanced PPARα expression and FAO, via depletion of lipid-signaling molecule(s) for insulin exocytosis, are also involved in the normal adaptive response of the islet to fasting. Fasted PPARαKO mice compared with wild-type mice had supranormal ip glucose tolerance due to increased plasma insulin levels. Isolated islets from the PPARα null mice had a 44% reduction in FAO, normal glucose use and oxidation, and enhanced glucose-induced insulin secretion. In normal rats, fasting for 24 h increased islet PPARα, carnitine palmitoyltransferase 1, and uncoupling protein-2 mRNA expression by 60%, 62%, and 82%, respectively. The data are consistent with the view that PPARα, via transcriptionally up-regulating islet FAO, can reduce insulin secretion, and that this mechanism is involved in the normal physiological response of the pancreatic islet to fasting such that hypoglycemia is avoided.

Uncoupling protein‐2 controls proliferation by promoting fatty acid oxidation and limiting glycolysis‐derived pyruvate utilization

2007 ◽  
Vol 22 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Claire Pecqueur ◽  
Thi Bui ◽  
Chantal Gelly ◽  
Julie Hauchard ◽  
Céline Barbot ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Uncoupling Protein ◽  
Acid Oxidation ◽  
Uncoupling Protein 2

scholarly journals Induction by leptin of uncoupling protein-2 and enzymes of fatty acid oxidation

1997 ◽  
Vol 94 (12) ◽  
pp. 6386-6390 ◽  
Author(s):  
Y.-T. Zhou ◽  
M. Shimabukuro ◽  
K. Koyama ◽  
Y. Lee ◽  
M.-Y. Wang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Uncoupling Protein ◽  
Acid Oxidation ◽  
Uncoupling Protein 2

scholarly journals Role of ketone signaling in the hepatic response to fasting

2019 ◽  
Vol 316 (5) ◽  
pp. G623-G631 ◽  
Author(s):  
Caroline E. Geisler ◽  
Susma Ghimire ◽  
Randy L. Bogan ◽  
Benjamin J. Renquist
Keyword(s):  
Fatty Acid ◽  
Mrna Expression ◽  
Fatty Acid Oxidation ◽  
Uncoupling Protein ◽  
Whole Body ◽  
Metabolic Adaptation ◽  
Acid Oxidation ◽  
Transcriptional Level ◽  
Nonalcoholic Fatty Liver ◽  
Fasting Response

Ketosis is a metabolic adaptation to fasting, nonalcoholic fatty liver disease (NAFLD), and prolonged exercise. β-OH butyrate acts as a transcriptional regulator and at G protein-coupled receptors to modulate cellular signaling pathways in a hormone-like manner. While physiological ketosis is often adaptive, chronic hyperketonemia may contribute to the metabolic dysfunction of NAFLD. To understand how β-OH butyrate signaling affects hepatic metabolism, we compared the hepatic fasting response in control and 3-hydroxy-3-methylglutaryl-CoA synthase II (HMGCS2) knockdown mice that are unable to elevate β-OH butyrate production. To establish that rescue of ketone metabolic/endocrine signaling would restore the normal hepatic fasting response, we gave intraperitoneal injections of β-OH butyrate (5.7 mmol/kg) to HMGCS2 knockdown and control mice every 2 h for the final 9 h of a 16-h fast. In hypoketonemic, HMGCS2 knockdown mice, fasting more robustly increased mRNA expression of uncoupling protein 2 (UCP2), a protein critical for supporting fatty acid oxidation and ketogenesis. In turn, exogenous β-OH butyrate administration to HMGCS2 knockdown mice decreased fasting UCP2 mRNA expression to that observed in control mice. Also supporting feedback at the transcriptional level, β-OH butyrate lowered the fasting-induced expression of HMGCS2 mRNA in control mice. β-OH butyrate also regulates the glycemic response to fasting. The fast-induced fall in serum glucose was absent in HMGCS2 knockdown mice but was restored by β-OH butyrate administration. These data propose that endogenous β-OH butyrate signaling transcriptionally regulates hepatic fatty acid oxidation and ketogenesis, while modulating glucose tolerance. NEW & NOTEWORTHY Ketogenesis regulates whole body glucose metabolism and β-OH butyrate produced by the liver feeds back to inhibit hepatic β-oxidation and ketogenesis during fasting.

scholarly journals Effect of acute exercise on uncoupling protein 3 is a fat metabolism-mediated effect

2002 ◽  
Vol 282 (1) ◽  
pp. E11-E17 ◽  
Author(s):  
Patrick Schrauwen ◽  
Matthijs K. C. Hesselink ◽  
Ilonca Vaartjes ◽  
Esther Kornips ◽  
Wim H. M. Saris ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Mrna Expression ◽  
Fatty Acid Oxidation ◽  
Glucose Oxidation ◽  
Acute Exercise ◽  
Uncoupling Protein ◽  
Acid Oxidation ◽  
Fasted State ◽  
Glucose Ingestion ◽  
Plasma Ffa

Human and rodent uncoupling protein (UCP)3 mRNA is upregulated after acute exercise. Moreover, exercise increases plasma levels of free fatty acid (FFA), which are also known to upregulate UCP3. We investigated whether the upregulation of UCP3 after exercise is an effect of exercise per se or an effect of FFA levels or substrate oxidation. Seven healthy untrained men [age: 22.7 ± 0.6 yr; body mass index: 23.8 ± 1.0 kg/m2; maximal O2 uptake (V˙o 2 max): 3,852 ± 211 ml/min] exercised at 50% V˙o 2 max for 2 h and then rested for 4 h. Muscle biopsies and blood samples were taken before and immediately after 2 h of exercise and 1 and 4 h in the postexercise period. To modulate plasma FFA levels and fat/glucose oxidation, the experiment was performed two times, one time with glucose ingestion and one time while fasting. UCP3 mRNA and UCP3 protein were determined by RT-competitive PCR and Western blot. In the fasted state, plasma FFA levels significantly increased ( P < 0.0001) during exercise (293 ± 25 vs. 1,050 ± 127 μmol/l), whereas they were unchanged after glucose ingestion (335 ± 54 vs. 392 ± 74 μmol/l). Also, fat oxidation was higher after fasting ( P < 0.05), whereas glucose oxidation was higher after glucose ingestion ( P< 0.05). In the fasted state, UCP3L mRNA expression was increased significantly ( P < 0.05) 4 h after exercise (4.6 ± 1.2 vs. 9.6 ± 3.3 amol/μg RNA). This increase in UCP3L mRNA expression was prevented by glucose ingestion. Acute exercise had no effect on UCP3 protein levels. In conclusion, we found that acute exercise had no direct effect on UCP3 mRNA expression. Abolishing the commonly observed increase in plasma FFA levels and/or fatty acid oxidation during and after exercise prevents the upregulation of UCP3 after acute exercise. Therefore, the previously observed increase in UCP3 expression appears to be an effect of prolonged elevation of plasma FFA levels and/or increased fatty acid oxidation.

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