Expression of carnitine palmitoyl-CoA transferase-1B is influenced by a cis-acting eQTL in two chicken lines selected for high and low body weight

2013 ◽  
Vol 45 (9) ◽  
pp. 367-376 ◽  
Author(s):  
Sojeong Ka ◽  
Ellen Markljung ◽  
Henrik Ring ◽  
Frank W. Albert ◽  
Mohammad Harun-Or-Rashid ◽  
...  
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Differentially Expressed ◽  
Acid Oxidation ◽  
Altered Expression ◽  
Cis Acting ◽  
Chromosome 1P ◽  
Coa Transferase ◽  
Trait Locus

Carnitine palmitoyl-CoA transferase-1B is a mitochondrial enzyme in the fatty acid oxidation pathway. In a previous study, CPT1B was identified as differentially expressed in the hypothalamus of two lines of chickens established by long-term selection for high (HWS) or low (LWS) body weight. Mammals have three paralogs ( CPT1a, b and c) while nonmammalian vertebrates only have two ( CPT1A, B). CPT1A is expressed in liver and CPT1B in muscle. CPT1c is expressed in hypothalamus, where it regulates feeding and energy expenditure. We identified an intronic length polymorphism, fixed for different alleles in the two populations, and mapped the hitherto missing CPT1B locus in the chicken genome assembly, to the distal tip of chromosome 1p. Based on molecular phylogeny and gene synteny we suggest that chicken CPT1B is pro-orthologous of the mammalian CPT1c. Chicken CPT1B was differentially expressed in both muscle and hypothalamus but in opposite directions: higher levels in hypothalamus but lower levels in muscle in the HWS than in the LWS line. Using an advanced intercross population of the lines, we found CPT1B expression to be influenced by a cis-acting expression quantitative trait locus in muscle. The increased expression in hypothalamus and reduced expression in muscle is consistent with an increased food intake in the HWS line and at the same time reduced fatty acid oxidation in muscle yielding a net accumulation of energy intake and storage. The altered expression of CPT1B in hypothalamus and peripheral tissue is likely to be a mechanism contributing to the remarkable difference between lines.

Level of satiety: in vitro energy metabolism in brain during hypophagic and hyperphagic body weight recovery

1989 ◽  
Vol 257 (6) ◽  
pp. R1322-R1327 ◽  
Author(s):  
T. R. Kasser ◽  
R. B. Harris ◽  
R. J. Martin
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Fatty Acid ◽  
Food Intake ◽  
Fatty Acid Oxidation ◽  
Glucose Oxidation ◽  
Area Postrema ◽  
Tube Feeding ◽  
Acid Oxidation

Rates of in vitro glucose and fatty acid oxidation were examined in four brain sites during hypophagic and hyperphagic recovery of normal body weight. Rats were fed 40, 100, or 160% of normal intake, via gastric intubation, for 3 wk. Another group of rats was starved until body weight loss was equivalent to weight loss in 40%-fed rats. Groups of rats were killed at the conclusion of tube feeding or fasting and at specific periods during recovery of body weight. Brain sites examined were the ventrolateral hypothalamus (VLH), ventromedial hypothalamus (VMH), a caudal brain stem site encompassing the area postrema-nucleus of the solitary tract (AP-NTS), and cortex. During recovery, rats previously fed 160% of normal intake (anorectic) maintained low rates of VLH fatty acid oxidation and were hypophagic until most excess fat was depleted. Conversely, rats previously fed 40% of normal intake (hungry) maintained high rates of VLH fatty acid oxidation and were hyperphagic until most deficient fat was repleted. Rats previously starved maintained high rates of VLH fatty acid oxidation during hyperphagic recovery, although levels of VLH fatty acid oxidation and food intake were initially low on refeeding. Rates of glucose oxidation in the brain sites examined did not relate well to energy balance status and the needed adjustments in food intake. The results indicated that the level of glucose oxidation in the VLH and AP-NTS responded to the level of energy immediately coming into the system (food intake).(ABSTRACT TRUNCATED AT 250 WORDS)

Studies on Spermatogenesis in Rats. IV. Rates of Oxidation of Palmitate and Pyruvate by Various Testicular Cell Populations

1972 ◽  
Vol 50 (9) ◽  
pp. 963-968 ◽  
Author(s):  
C. H. Lin ◽  
I. B. Fritz
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Cell Suspensions ◽  
Acid Oxidation ◽  
Testicular Cell ◽  
Pyruvate Oxidation ◽  
Coa Transferase ◽  
Conversion Rates ◽  
Old Rats ◽  
Germinal Cells

Measurements are reported on the rates of oxidation of 14C-1-palmitate, 14C-1-pyruvate, and 14C-2-pyruvate by cell suspensions obtained from testes of normal rats of varying ages and from hypophysectomized regressed rats. Highest conversion rates of labeled pyruvate to CO2 were observed in testes from 24-day-old rats, in which all germinal cells except spermatids and spermatozoa were present. Cell suspensions from testes of adult rats, containing predominantly spermatids, had relatively low rates of palmitate and pyruvate oxidation. These rates were increased in cell suspensions from testes of regressed hypophysectomized rats towards those observed in testicular cell preparations from immature rats. The predominant cell types in testes from hypophysectomized, regressed rats are spermatogonia and early spermatocytes, although early stage spermatids are also present in lesser numbers. The ketogenic enzyme capacity was greatest in particulate preparations obtained from testes of normal 14-day-old rats, in which the predominant germinal cells present are spermatogonia. The activity of succinyl-CoA: 3-oxoacid CoA-transferase was also highest in these preparations. Cell suspensions from testes of 14-day-old rats incorporated significant amounts of labeled palmitate and pyruvate into acetoacetate, whereas cell suspensions from testes of other groups of animals examined did not. The data are discussed in relation to factors controlling rates of fatty acid oxidation in various germinal epithelial cells. It is concluded that spermatocytes have highest rates of pyruvate oxidation, but that both spermatogonia and spermatocytes have relatively high rates of palmitate oxidation. Since spermatogonia also were shown to contain the relatively highest ketogenic enzymic capacity, and since these cells had previously been observed to have lowest levels of carnitine acetyltransferase (CAT), it may be deduced that high CAT activity is not required for fatty acid oxidation or ketogenesis by testicular cells.

scholarly journals Dietary thylakoids reduce visceral fat mass and increase expression of genes involved in intestinal fatty acid oxidation in high-fat fed rats

2016 ◽  
Vol 311 (3) ◽  
pp. R618-R627 ◽  
Author(s):  
Eva-Lena Stenblom ◽  
Emil Egecioglu ◽  
Caroline Montelius ◽  
Deepti Ramachandran ◽  
Britta Bonn ◽  
...  
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Food Intake ◽  
Fatty Acid Oxidation ◽  
Body Fat ◽  
Dietary Fat ◽  
Visceral Fat ◽  
Acid Oxidation ◽  
High Fat ◽  
Fat Accumulation

Thylakoids reduce body weight gain and body fat accumulation in rodents. This study investigated whether an enhanced oxidation of dietary fat-derived fatty acids in the intestine contributes to the thylakoid effects. Male Sprague-Dawley rats were fed a high-fat diet with ( n = 8) or without thylakoids ( n = 8) for 2 wk. Body weight, food intake, and body fat were measured, and intestinal mucosa was collected and analyzed. Quantitative real-time PCR was used to measure gene expression levels of key enzymes involved in fatty acid transport, fatty acid oxidation, and ketogenesis. Another set of thylakoid-treated ( n = 10) and control rats ( n = 10) went through indirect calorimetry. In the first experiment, thylakoid-treated rats ( n = 8) accumulated 25% less visceral fat than controls. Furthermore, fatty acid translocase ( Fat/Cd36), carnitine palmitoyltransferase 1a ( Cpt1a), and mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase 2 ( Hmgcs2) genes were upregulated in the jejunum of the thylakoid-treated group. In the second experiment, thylakoid-treated rats ( n = 10) gained 17.5% less weight compared with controls and their respiratory quotient was lower, 0.86 compared with 0.91. Thylakoid-intake resulted in decreased food intake and did not cause steatorrhea. These results suggest that thylakoids stimulated intestinal fatty acid oxidation and ketogenesis, resulting in an increased ability of the intestine to handle dietary fat. The increased fatty acid oxidation and the resulting reduction in food intake may contribute to the reduced fat accumulation in thylakoid-treated animals.

Cold acclimation increases activities of mitochondrial long-chain acyl-CoA synthetase and carnitine acyl-CoA transferase I in heart of rainbow trout (Oncorhynchus mykiss)

1997 ◽  
Vol 75 (2) ◽  
pp. 324-331 ◽  
Author(s):  
Christopher P. Patey ◽  
William R. Driedzic
Keyword(s):  
Fatty Acid ◽  
Rainbow Trout ◽  
Low Temperature ◽  
Oncorhynchus Mykiss ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Coa Transferase ◽  
Chain Acyl ◽  
Long Chain

Rainbow trout (Oncorhynchus mykiss) were acclimated to 5 or 15 °C. Hearts were excised and assayed for the activity of enzymes essential for fatty acid metabolism. The activity of long-chain acyl-CoA synthetase, the first enzyme required in either fatty acid oxidation or complex fatty acid synthesis, was increased following acclimation to low temperature. Total crude homogenates exhibited an increase in activity with either palmitate (0.037–0.047 μmol/(min∙g)), stearate (0.037–0.055 μmol/(min∙g)), or oleate (0.041–0.064 μmol/(min∙g)) as substrate. Mitochondrial preparations showed the greatest increase in activity with palmitate (0.486–0.962 nmol/(min∙g)) as substrate, whereas microsomal preparations exhibited the greatest increase in activity with oleate (0.976–1.933 nmol/(min∙g)) as substrate. The activity of carnitine acyl-CoA transferase I, which is located on the outer mitochondrial membrane and is required for fatty acid oxidation, increased following acclimation to low temperature with palmitoyl CoA (0.137–0.352 μmol/(min∙g)), stearoyl CoA (0.066–0.152 μmol/(min∙g)), or oleoyl CoA (0.137–0.224 μmol/(min∙g)) as substrate. The parallel increase in mitochondrial long-chain acyl-CoA synthetase and carnitine acyl-CoA transferase I is consistent with previous observations of an elevated capacity of heart to oxidize fatty acids as exogenous fuels following acclimation to low temperature. The increase in microsome-based long-chain acyl-CoA synthetase may contribute to heart growth at low temperature.

scholarly journals Madecassoside Inhibits Body Weight Gain via Modulating SIRT1-AMPK Signaling Pathway and Activating Genes Related to Thermogenesis

2021 ◽  
Vol 12 ◽  
Author(s):  
Boju Sun ◽  
Misa Hayashi ◽  
Maya Kudo ◽  
Lili Wu ◽  
Lingling Qin ◽  
...  
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Weight Gain ◽  
Signaling Pathway ◽  
Fatty Acid Oxidation ◽  
The Body ◽  
Acid Oxidation ◽  
Ampk Signaling ◽  
Epididymal Fat ◽  
Mesenteric Fat

BackgroundPre-clinical research studies have shown that Madecassoside (MA) has favorable therapeutic effects on arthritis, acne, vitiligo and other diseases. However, the effects of MA on obesity have not yet been studied. This study mainly aimed to investigate the effects of MA in protecting against obesity and its underlying mechanism in reducing obesity.MethodsObese diabetic KKay/TaJcl mice model was adopted to the study. The body weight of all animals was recorded daily, and the blood glucose, blood lipid, and serum aminotransferase levels were examined, respectively. The expression of P-AMPK, SIRT1, P-LKB1, P-ACC, and P-HSL in abdominal fat, mesenteric fat, and epididymal fat was measured by western blotting, and the levels of PPARα, CPT1a, PGC-1α, UCP-1, Cidea, Cox7a1, and Cox8b were examined by real-time quantitative PCR (RT-qPCR).ResultsThe results revealed that the body weight of the mice in MA group was significantly reduced, and the body mass index (BMI) showed significant difference between the two groups after 8 weeks of MA treatment. Further research revealed that it affected the mesenteric fat and epididymis fat by activating SIRT1/AMPK signaling pathway, and then promoted fatty acid oxidation of epididymal fat (PPARα ↑, CPT1a↑, and PGC-1α↑). Last but not the least, it also promoted the expression of UCP-1 and stimulated thermoregulatory genes (Cidea, Cox7a1, and Cox8b) in brown fat and mesenteric fat.ConclusionsTaken together, these findings suggest that MA can inhibit the weight gain in obese diabetic mice, and reduce triglyceride levels, inhibit lipogenesis of mesenteric fat, promote epididymal fat lipolysis and fatty acid oxidation. Furthermore, MA treatment might promote mesenteric fat browning and activate mitochondrial function in brown fat as well as mesenteric fat.

scholarly journals The Influence of Shc Proteins on the Whole Body Energetic Response to Calorie Restriction Initiated in 3-Month-Old Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Jennifer H. Stern ◽  
Kyoungmi Kim ◽  
Jon J. Ramsey
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Calorie Restriction ◽  
Metabolic Response ◽  
Whole Body ◽  
Acid Oxidation ◽  
Wild Type ◽  
The Impact ◽  
Old Mice

There is increasing evidence that Shc proteins play a role in energy metabolism, and we have previously reported that knockdown of Shc proteins influences the energetic response to acute (3 days) calorie restriction (CR) in 18-month-old mice. Whether Shc proteins play a role in the metabolic response to CR in younger mice has yet to be elucidated. Hence, we sought to determine the impact of 3 days and longer term (2 months) CR on energy expenditure (EE) and respiratory quotient (RQ) in 3 month-old Shc knockout (ShcKO) and wild-type (WT) mice. ShcKO mice decreased (P < 0.001) EE normalized for body weight (EEBW) by 3 days of CR, while no such change was observed in WT animals. However, both ShcKO and WT mice decreased (P < 0.001) EEBW at 2 months of CR and there were no differences in body weight between the ShcKO and WT mice at either 3 days or 2 months of CR. Consistent with increased fatty acid oxidation, only ShcKO mice maintained decreased (P < 0.001) 24 h RQ through 2 months of CR, suggesting that they were able to maintain increased fatty acid oxidation for a longer period of time than WT mice. These results indicate that Shc proteins may contribute to some of the acute energetic responses to CR.

scholarly journals The effect of body weight and the fatty acid-oxidation inhibitor 2-tetradecylglycidic acid on pyruvate dehydrogenase complex activity in mouse heart

1984 ◽  
Vol 224 (3) ◽  
pp. 787-791 ◽  
Author(s):  
I D Caterson ◽  
P F Williams ◽  
A L Kerbey ◽  
L D Astbury ◽  
W E Plehwe ◽  
...  
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Pyruvate Dehydrogenase ◽  
Heart Muscle ◽  
Pyruvate Dehydrogenase Complex ◽  
Acid Oxidation ◽  
Mouse Heart ◽  
Complex Activity ◽  
Dehydrogenase Complex

The proportion of pyruvate dehydrogenase complex in the active, dephosphorylated form was decreased (compared with lean controls) in heart muscle in gold thioglucose-treated obese hyperinsulinaemic mice, and the extent of enzyme inactivation was significantly linearly correlated with both body weight and body fat content. A single oral dose (25 mg/kg body wt.) of the beta-oxidation inhibitor 2-tetradecylglycidic acid to obese animals restored pyruvate dehydrogenase complex activity to that of lean controls. It is suggested that increased fatty acid oxidation may be a major factor in mediating the phosphorylation and inactivation of pyruvate dehydrogenase complex in mouse heart muscle in obesity, and this may represent an important mechanism in the development and/or expression of insulin resistance in respect of abnormalities of cellular glucose homoeostasis in these animals.

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