Acetic Acid Upregulates the Expression of Genes for Fatty Acid Oxidation Enzymes in Liver To Suppress Body Fat Accumulation

2009 ◽  
Vol 57 (13) ◽  
pp. 5982-5986 ◽  
Author(s):  
Tomoo Kondo ◽  
Mikiya Kishi ◽  
Takashi Fushimi ◽  
Takayuki Kaga
Keyword(s):  
Acetic Acid ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Body Fat ◽  
Acid Oxidation ◽  
Fat Accumulation ◽  
Expression Of Genes

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.

Excess body fat in men decreases plasma fatty acid availability and oxidation during endurance exercise

2004 ◽  
Vol 286 (3) ◽  
pp. E354-E362 ◽  
Author(s):  
Bettina Mittendorfer ◽  
David A. Fields ◽  
Samuel Klein
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Body Fat ◽  
Fat Mass ◽  
Total Fatty Acid ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Plasma Fatty Acids ◽  
Exercise Induced

The effect of relative body fat mass on exercise-induced stimulation of lipolysis and fatty acid oxidation was evaluated in 15 untrained men (5 lean, 5 overweight, and 5 obese with body mass indexes of 21 ± 1, 27 ± 1, and 34 ± 1 kg/m2, respectively, and %body fat ranging from 12 to 32%). Palmitate and glycerol kinetics and substrate oxidation were assessed during 90 min of cycling at 50% peak aerobic capacity (V̇o2 peak) by use of stable isotope-labeled tracer infusion and indirect calorimetry. An inverse relationship was found between %body fat and exercise-induced increase in glycerol appearance rate relative to fat mass ( r2 = 0.74; P < 0.01). The increase in total fatty acid uptake during exercise [(μmol/kg fat-free mass) × 90 min] was ∼50% smaller in obese (181 ± 70; P < 0.05) and ∼35% smaller in overweight (230 ± 71; P < 0.05) than in lean (354 ± 34) men. The percentage of total fatty acid oxidation derived from systemic plasma fatty acids decreased with increasing body fat, from 49 ± 3% in lean to 39 ± 4% in obese men ( P < 0.05); conversely, the percentage of nonsystemic fatty acids, presumably derived from intramuscular and possibly plasma triglycerides, increased with increasing body fat ( P < 0.05). We conclude that the lipolytic response to exercise decreases with increasing adiposity. The blunted increase in lipolytic rate in overweight and obese men compared with lean men limits the availability of plasma fatty acids as a fuel during exercise. However, the rate of total fat oxidation was similar in all groups because of a compensatory increase in the oxidation of nonsystemic fatty acids.

A Case of Mistaken Identity

2005 ◽  
Vol 288 (1) ◽  
pp. H448-H448 ◽  
Author(s):  
Andreas Stahl
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Early Development ◽  
Mammalian Species ◽  
Expression Patterns ◽  
Acid Oxidation ◽  
Published Data ◽  
Acid Uptake ◽  
Expression Of Genes ◽  
Cpt I

The heart is a unique organ that can use several fuels for energy production. During development, the heart undergoes changes in fuel supply, and it must be able to respond to these changes. We have examined changes in the expression of several genes that regulate fuel transport and metabolism in rat hearts during early development. At birth, there was increased expression of fatty acid transporters and enzymes of fatty acid metabolism that allow fatty acids to become the major source of energy for cardiac muscle during the first 2 wk of life. At the same time, expression of genes that control glucose transport and oxidation was downregulated. After 2 wk, expression of genes for glucose uptake and oxidation was increased, and expression of genes for fatty acid uptake and utilization was decreased. Expression of carnitine palmitoyltransferase I (CPT I) isoforms during development was different from published data obtained from rabbit hearts. CPT Iα and Iβ isoforms were both highly expressed in hearts before birth, and both increased further at birth. Only after the second week did CPT Iα expression decrease appreciably below the level of CPT Iβ expression. These results represent another example of different expression patterns of CPT I isoforms among various mammalian species. In rats, changes in gene expression followed nutrient availability during development and may render cardiac fatty acid oxidation less sensitive to factors that influence malonyl-CoA content (e.g., fluctuations in glucose concentration) and thereby favor fatty acid oxidation as an energy source for cardiomyocytes in early development.

scholarly journals Leptin Regulates Peripheral Lipid Metabolism Primarily through Central Effects on Food Intake

Endocrinology ◽  
2008 ◽  
Vol 149 (11) ◽  
pp. 5432-5439 ◽  
Author(s):  
Xavier Prieur ◽  
Y. C. Loraine Tung ◽  
Julian L. Griffin ◽  
I. Sadaf Farooqi ◽  
Stephen O'Rahilly ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Food Intake ◽  
Fatty Acid Oxidation ◽  
Liver Weight ◽  
Metabolic Effects ◽  
Acid Oxidation ◽  
Mediated Effects ◽  
Expression Of Genes ◽  
Acyl Coenzyme A

The metabolic effects of leptin may involve both centrally and peripherally mediated actions with a component of the central actions potentially independent of alterations in food intake. Ob/ob mice have significant abnormalities in lipid metabolism, correctable by leptin administration. We used ob/ob mice to study the relative importance of the subtypes of actions of leptin (central vs. peripheral; food intake dependent vs. independent) on lipid metabolism. Mice were treated for 3 d with leptin, either centrally [intracerebroventricular (icv)] or peripherally (ip), and compared with mice pair-fed to the leptin-treated mice (PF) and with ad libitum-fed controls (C). All treatment groups (icv, ip, PF) showed indistinguishable changes in liver weight; hepatic steatosis; hepatic lipidemic profile; and circulating free fatty acids, triglycerides, and cholesterol lipoprotein profile. Changes in the expression of genes involved in lipogenesis and fatty acid oxidation in liver, muscle, and white fat were broadly similar in ip, icv, and PF groups. Leptin (both icv and ip) stimulated expression of both mitochondrial and peroxisomal acyl-coenzyme A oxidase (liver) and peroxisomal proliferator-activated receptor-α (skeletal muscle) to an extent not replicated by pair feeding. Leptin had profound effects on peripheral lipid metabolism, but the majority were explained by its effects on food intake. Leptin had additional centrally mediated effects to increase the expression of a limited number of genes concerned with fatty acid oxidation. Whereas we cannot exclude direct peripheral effects of leptin on certain aspects of lipid metabolism, we were unable to detect any such effects on the parameters measured in this study.

Molecular and metabolic profiles suggest that increased lipid catabolism in adipose tissue contributes to leanness in domestic chickens

2014 ◽  
Vol 46 (9) ◽  
pp. 315-327 ◽  
Author(s):  
Bo Ji ◽  
Jesse L. Middleton ◽  
Ben Ernest ◽  
Arnold M. Saxton ◽  
Susan J. Lamont ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
White Adipose Tissue ◽  
Broiler Chickens ◽  
Acid Oxidation ◽  
Human Obesity ◽  
Insulin Resistant ◽  
Expression Of Genes ◽  
Commercial Broiler

Domestic broiler chickens rapidly accumulate fat and are naturally hyperglycemic and insulin resistant, making them an attractive model for studies of human obesity. We previously demonstrated that short-term (5 h) fasting rapidly upregulates pathways of fatty acid oxidation in broiler chickens and proposed that activation of these pathways may promote leanness. The objective of the current study was to characterize adipose tissue from relatively lean and fatty lines of chickens and determine if heritable leanness in chickens is associated with activation of some of the same pathways induced by fasting. We compared adipose gene expression and metabolite profiles in white adipose tissue of lean Leghorn and Fayoumi breeds to those of fattier commercial broiler chickens. Both lipolysis and expression of genes involved in fatty acid oxidation were upregulated in lean chickens compared with broilers. Although there were strong similarities between the lean lines compared with broilers, distinct expression signatures were also found between Fayoumi and Leghorn, including differences in adipogenic genes. Similarities between genetically lean and fasted chickens suggest that fatty acid oxidation in white adipose tissue is adaptively coupled to lipolysis and plays a role in heritable differences in fatness. Unique signatures of leanness in Fayoumi and Leghorn lines highlight distinct pathways that may provide insight into the basis for leanness in humans. Collectively, our results provide a number of future directions through which to fully exploit chickens as unique models for the study of human obesity and adipose metabolism.

scholarly journals Increased muscle fatty acid oxidation in dairy cows with intensive body fat mobilization during early lactation

2013 ◽  
Vol 96 (10) ◽  
pp. 6449-6460 ◽  
Author(s):  
C. Schäff ◽  
S. Börner ◽  
S. Hacke ◽  
U. Kautzsch ◽  
H. Sauerwein ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Dairy Cows ◽  
Fatty Acid Oxidation ◽  
Body Fat ◽  
Acid Oxidation ◽  
Early Lactation ◽  
Fat Mobilization

Changes in environmental temperature influence leptin responsiveness in low- and high-fat-fed mice

2007 ◽  
Vol 293 (1) ◽  
pp. R106-R115 ◽  
Author(s):  
Ruth B. S. Harris ◽  
Tiffany D. Mitchell ◽  
Emily W. Kelso ◽  
W. P. Flatt
Keyword(s):  
Fatty Acid ◽  
Food Intake ◽  
Energy Expenditure ◽  
Fatty Acid Oxidation ◽  
Body Fat ◽  
Leptin Resistance ◽  
Positive Energy ◽  
Acid Oxidation ◽  
High Fat ◽  
Hot Environment

Loss of body fat in leptin-treated animals has been attributed to reduced energy intake, increased thermogenesis, and preferential fatty acid oxidation. Leptin does not decrease food intake or body fat in leptin-resistant high-fat (HF)-fed mice, possibly due to a failure of leptin to activate hypothalamic receptors. We measured energy expenditure of male C57BL/6 mice adapted to low-fat (LF) or HF diet and infused them for 13 days with PBS or 10 μg leptin/day from an intraperitoneal miniosmotic pump to test whether leptin resistance prevented leptin-induced increases in energy expenditure and fatty acid oxidation. There was no effect of low-dose leptin infusions on either of these measures in LF-fed or HF-fed mice, even though LF-fed mice lost body fat. Experiment 2 tested leptin responsiveness in LF-fed and HF-fed mice housed at different temperatures (18°C, 23°C, 27°C), assuming that the cold would increase and the hot environment would inhibit food intake and thermogenesis, which could potentially interfere with leptin action. LF-fed mice housed at 23°C were the only mice that lost body fat during leptin infusion, suggesting that an ability to modify energy expenditure is essential to the maintenance of leptin responsiveness. HF-fed mice in cold or warm environments did not respond to leptin. HF-fed mice in the hot environment were fatter than other HF-fed mice, and, surprisingly, leptin caused a further increase in body fat, demonstrating that the mice were not totally leptin resistant and that partial leptin resistance in a hot environment favors positive energy balance and fat deposition.

SGLT2 selective inhibitor ipragliflozin reduces body fat mass by increasing fatty acid oxidation in high-fat diet-induced obese rats

2014 ◽  
Vol 727 ◽  
pp. 66-74 ◽  
Author(s):  
Masanori Yokono ◽  
Toshiyuki Takasu ◽  
Yuka Hayashizaki ◽  
Keisuke Mitsuoka ◽  
Rumi Kihara ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Body Fat ◽  
Fat Mass ◽  
High Fat Diet ◽  
Selective Inhibitor ◽  
Acid Oxidation ◽  
Body Fat Mass ◽  
High Fat ◽  
Obese Rats

scholarly journals Interplay between Thyroid Hormones and Stearoyl-CoA Desaturase 1 in the Regulation of Lipid Metabolism in the Heart

2020 ◽  
Vol 22 (1) ◽  
pp. 109
Author(s):  
Adam Olichwier ◽  
Volodymyr V. Balatskyi ◽  
Marcin Wolosiewicz ◽  
James M. Ntambi ◽  
Pawel Dobrzyn
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Thyroid Hormones ◽  
Fatty Acid Oxidation ◽  
Monounsaturated Fatty Acids ◽  
Thyroid Stimulating Hormone ◽  
Acid Oxidation ◽  
Expression Of Genes ◽  
Triglyceride Content ◽  
Stearoyl Coa Desaturase

Stearoyl-CoA desaturase 1 (SCD1), an enzyme that is involved in the biosynthesis of monounsaturated fatty acids, induces the reprogramming of cardiomyocyte metabolism. Thyroid hormones (THs) activate both lipolysis and lipogenesis. Many genes that are involved in lipid metabolism, including Scd1, are regulated by THs. The present study used SCD1 knockout (SCD1−/−) mice to test the hypothesis that THs are important factors that mediate the anti-steatotic effect of SCD1 downregulation in the heart. SCD1 deficiency decreased plasma levels of thyroid-stimulating hormone and thyroxine and the expression of genes that regulate intracellular TH levels (i.e., Slc16a2 and Dio1-3) in cardiomyocytes. Both hypothyroidism and SCD1 deficiency affected genomic and non-genomic TH pathways in the heart. SCD1 deficiency is known to protect mice from genetic- or diet-induced obesity and decrease lipid content in the heart. Interestingly, hypothyroidism increased body adiposity and triglyceride and diacylglycerol levels in the heart in SCD1−/− mice. The accumulation of triglycerides in cardiomyocytes in SCD1−/− hypothyroid mice was caused by the activation of lipogenesis, which likely exceeded the upregulation of lipolysis and fatty acid oxidation. Lipid accumulation was also observed in the heart in wildtype hypothyroid mice compared with wildtype control mice, but this process was related to a reduction of triglyceride lipolysis and fatty acid oxidation. We also found that simultaneous SCD1 and deiodinase inhibition increased triglyceride content in HL-1 cardiomyocytes, and this process was related to the downregulation of lipolysis. Altogether, the present results suggest that THs are an important part of the mechanism of SCD1 in cardiac lipid utilization and may be involved in the upregulation of energetic metabolism that is associated with SCD1 deficiency.

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