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Fat Oxidation (fat + oxidation)
Selected AbstractsQuality and Microbial Population of Cornish Game Hen Carcasses as Affected by Electron Beam IrradiationJOURNAL OF FOOD SCIENCE, Issue 7 2006C. Gomes ABSTRACT:, We evaluated the chemical and microbiological quality of Cornish game hen carcasses irradiated up to 7 kGy with a 10 MeV linear accelerator (dual beam configuration). Eighty frozen and vacuum packaged (approximately 0.45 kg) Cornish game hens (Gallus domesticus) were irradiated and stored in low-density polyethylene bags at 4 ± 1 °C for 21 d; nonirradiated chickens served as controls. Fat oxidation (in terms of malonaldehyde content) increased with storage time and dose for all chicken parts analyzed (breast, thigh, and skin). As expected, the skin had the highest level of fat oxidation while the breast samples had the lowest. Oxidation level in all samples exposed to 2 kGy reached a maximum on day 14. Sensory evaluation showed that irradiation caused significant textural toughening, and increased the redness of raw chicken meat. In terms of overall quality and aroma, lipid oxidation was not a major problem since it was not detected by the panelists. Irradiation significantly reduced the total viable microbial counts (TVC) in the breast and thigh samples. Exposure to 3-kGy dose decreased the TVC by 0.3-log cycles on the surface of the skin. In less than 14 d, the nonirradiated chicken carcasses had counts greater than 6 log CFU/50 cm2, while the 2 and 3 kGy irradiated samples reached these numbers only after 21 d of storage. Samples irradiated at 7 kGy had consistently the lowest counts (2.5 log CFU/50 cm2) throughout storage time. This study shows that irradiation up to 7 kGy and refrigerated storage (4 °C) inhibits microbial growth and extends shelf life of Cornish game hens without affecting consumers' acceptability. [source] Substrate oxidation and retention in pigs and poultryANIMAL SCIENCE JOURNAL, Issue 2 2002André CHWALIBOG ABSTRACT A model combining data from gas exchange measurements with nutrient balances, demonstrating energy transfer between the pools of protein, carbohydrate and fat and their partition in the body, is described. Data from energy metabolism experiments with growing pigs and laying hens is incorporated into the model in order to illustrate methods of calculations and interpretations of the model. The experiments with pigs were carried out with growing pigs (20,100 kg) measured alternately on high (ad libitum) and low (near maintenance) feed levels on diets with low or high fat concentration. When energy intake from digested carbohydrate covered the requirements for growth, heat from oxidation of carbohydrate contributed 85,90% to the total heat production, while there was no net oxidation of fat. When the intake of digested carbohydrate was not sufficient to cover requirements, fat was mobilized from the body and oxidized. Energy from oxidation of carbohydrate was in all measurements below the energy in the carbohydrate pool, indicating transfer of energy from carbohydrate to fat metabolism in the process of de novo lipogeneis. The experiments with hens were carried out with 62 hens during the laying period from 26 to 47 weeks of age. The hens originated from two strains (A and B); they were kept in battery cages either individually or 3 hens/cage and fed ad libitum with an identical commercial diet. The partition of the protein pool between oxidation and retention was not influenced by the housing system. However, the genetic origin of hens effected protein utilization with relatively lower oxidation and higher retention in Strain B. The main part of the carbohydrate pool was oxidized (45,60%), but the hens kept individually oxidized more carbohydrate than those kept 3 hens/cage. Further, there were significant differences between the strains. Generally, about half of the fat pool originated from de novo lipogenesis from carbohydrate, indicating the importance of this process for fat retention in eggs. Fat oxidation depended on the energy supply from carbohydrate, hence with higher use of carbohydrate for oxidation in Strain B less fat was oxidized and more was used for fat synthesis. The presented results indicate that by combining results from gas exchange measurements with nitrogen and energy balances it is possible to evaluate the contribution of nutrients to the oxidative processes and the energy transfer between substrate pools. [source] OCTN2 is associated with carnitine transport capacity of rat skeletal musclesACTA PHYSIOLOGICA, Issue 1 2010Y. Furuichi Abstract Aim:, Carnitine plays an essential role in fat oxidation in skeletal muscles; therefore carnitine influx could be crucial for muscle metabolism. OCTN2, a sodium-dependent solute carrier, is assumed to transport carnitine into various organs. However, OCTN2 protein expression and the functional importance of carnitine transport for muscle metabolism have not been studied. We tested the hypothesis that OCTN2 is expressed at higher levels in oxidative muscles than in other muscles, and that the carnitine uptake capacity of skeletal muscles depends on the amount of OCTN2. Methods:, Rat hindlimb muscles (soleus, plantaris, and the surface and deep portions of gastrocnemius) were used for Western blotting to detect OCTN2. Tissue carnitine uptake was examined by an integration plot analysis using l -[3H]carnitine as a tracer. Tissue carnitine content was determined by enzymatic cycling methods. The percentage of type I fibres was determined by histochemical analysis. Results:, OCTN2 was detected in all skeletal muscles although the amount was lower than that in the kidney. OCTN2 expression was significantly higher in soleus than in the other skeletal muscles. The amount of OCTN2 was positively correlated with the percentage of type I fibres in hindlimb muscles. The integration plot analysis revealed a positive correlation between the uptake clearance of l -[3H]carnitine and the amount of OCTN2 in skeletal muscles. However, the carnitine content in soleus was lower than that in other skeletal muscles. Conclusion:, OCTN2 is functionally expressed in skeletal muscles and is involved in the import of carnitine for fatty acid oxidation, especially in highly oxidative muscles. [source] AMPK activators , potential therapeutics for metabolic and other diseasesACTA PHYSIOLOGICA, Issue 1 2009G. Zhou Abstract AMP-activated protein kinase (AMPK)-mediated cellular metabolic responses to tissue-specific and whole-body stimuli play a vital role in the control of energy homeostasis. As a cellular energy-sensing mechanism, AMPK activation stimulates glucose uptake and fat oxidation, while it suppresses lipogenesis and gluconeogenesis. The cumulative effects of AMPK activation lead to beneficial metabolic states in liver, muscle and other peripheral tissues that are critical in the pathogenesis of obesity, type 2 diabetes and related metabolic disorders. Activators of AMPK that target selected tissues hold potential as novel therapeutics for diseases in which altered energy metabolism contributes to aetiology. [source] Increased fat oxidation and regulation of metabolic genes with ultraendurance exerciseACTA PHYSIOLOGICA, Issue 1 2007J. W. Helge Abstract Aim:, Regular endurance exercise stimulates muscle metabolic capacity, but effects of very prolonged endurance exercise are largely unknown. This study examined muscle substrate availability and utilization during prolonged endurance exercise, and associated metabolic genes. Methods:, Data were obtained from 11 competitors of a 4- to 5-day, almost continuous ultraendurance race (seven males, four females; age: 36 ± 11 years; cycling o2peak: males 57.4 ± 5.9, females 48.1 ± 4.0 mL kg,1 min,1). Before and after the race muscle biopsies were obtained from vastus lateralis, respiratory gases were sampled during cycling at 25 and 50% peak aerobic power output, venous samples were obtained, and fat mass was estimated by bioimpedance under standardized conditions. Results:, After the race fat mass was decreased by 1.6 ± 0.4 kg (11%; P < 0.01). Respiratory exchange ratio at the 25 and 50% workloads decreased (P < 0.01) from 0.83 ± 0.06 and 0.93 ± 0.03 before, to 0.71 ± 0.01 and 0.85 ± 0.02, respectively, after the race. Plasma fatty acids were 3.5 times higher (from 298 ± 74 to 1407 ± 118 ,mol L,1; P < 0.01). Muscle glycogen content fell 50% (from 554 ± 28 to 270 ± 25 nmol kg,1 d.w.; n = 7, P < 0.01), whereas the decline in muscle triacylglycerol (from 32 ± 5 to 22 ± 3 mmol kg,1 d.w.; P = 0.14) was not statistically significant. After the race, muscle mRNA content of lipoprotein lipase and glycogen synthase increased (P < 0.05) 3.9- and 1.7-fold, respectively, while forkhead homolog in rhabdomyosarcoma, pyruvate dehydrogenase kinase 4 and vascular endothelial growth factor mRNA tended (P < 0.10) to be higher, whereas muscle peroxisome proliferator-activated receptor , co-activator-1, mRNA tended to be lower (P = 0.06). Conclusion:, Very prolonged exercise markedly increases plasma fatty acid availability and fat utilization during exercise. Exercise-induced regulation of genes encoding proteins involved in fatty acid recruitment and oxidation may contribute to these changes. [source] Quality and Microbial Population of Cornish Game Hen Carcasses as Affected by Electron Beam IrradiationJOURNAL OF FOOD SCIENCE, Issue 7 2006C. Gomes ABSTRACT:, We evaluated the chemical and microbiological quality of Cornish game hen carcasses irradiated up to 7 kGy with a 10 MeV linear accelerator (dual beam configuration). Eighty frozen and vacuum packaged (approximately 0.45 kg) Cornish game hens (Gallus domesticus) were irradiated and stored in low-density polyethylene bags at 4 ± 1 °C for 21 d; nonirradiated chickens served as controls. Fat oxidation (in terms of malonaldehyde content) increased with storage time and dose for all chicken parts analyzed (breast, thigh, and skin). As expected, the skin had the highest level of fat oxidation while the breast samples had the lowest. Oxidation level in all samples exposed to 2 kGy reached a maximum on day 14. Sensory evaluation showed that irradiation caused significant textural toughening, and increased the redness of raw chicken meat. In terms of overall quality and aroma, lipid oxidation was not a major problem since it was not detected by the panelists. Irradiation significantly reduced the total viable microbial counts (TVC) in the breast and thigh samples. Exposure to 3-kGy dose decreased the TVC by 0.3-log cycles on the surface of the skin. In less than 14 d, the nonirradiated chicken carcasses had counts greater than 6 log CFU/50 cm2, while the 2 and 3 kGy irradiated samples reached these numbers only after 21 d of storage. Samples irradiated at 7 kGy had consistently the lowest counts (2.5 log CFU/50 cm2) throughout storage time. This study shows that irradiation up to 7 kGy and refrigerated storage (4 °C) inhibits microbial growth and extends shelf life of Cornish game hens without affecting consumers' acceptability. [source] Abnormalities of whole body protein turnover, muscle metabolism and levels of metabolic hormones in patients with chronic heart failureJOURNAL OF INTERNAL MEDICINE, Issue 1 2006H. NØRRELUND Abstract. Objective., It is well known that chronic heart failure (CHF) is associated with insulin resistance and cachexia, but little is known about the underlying substrate metabolism. The present study was undertaken to identify disturbances of basal glucose, lipid and protein metabolism. Design., We studied eight nondiabetic patients with CHF (ejection fraction 30 ± 4%) and eight healthy controls. Protein metabolism (whole body and regional muscle fluxes) and total glucose turnover were isotopically assayed. Substrate oxidation were obtained by indirect calorimetry. The metabolic response to exercise was studied by bicycle ergometry exercise. Results., Our data confirm that CHF patients have a decreased lean body mass. CHF patients are characterised by (i) decreased glucose oxidation [glucose oxidation (mg kg,1 min,1): 1.25 ± 0.09 (patients) vs. 1.55 ± 0.09 (controls), P < 0.01] and muscle glucose uptake [a , v diffglucose (,mol L,1): ,10 ± 25 (patients) vs. 70 ± 22 (controls), P < 0.01], (ii) elevated levels of free fatty acids (FFA) [FFA (mmol L,1): 0.72 ± 0.05 (patients) vs. 0.48 ± 0.03 (controls), P < 0.01] and 3-hydroxybutyrate and signs of elevated fat oxidation and muscle fat utilization [a , v diffFFA (mmol L,1): 0.12 ± 0.02 (patients) vs. 0.05 ± 0.01 (controls), P < 0.05] and (iii) elevated protein turnover and protein breakdown [phenylalanine flux (,mol kg,1 h,1): 36.4 ± 1.5 (patients) vs. 29.6 ± 1.3 (controls), P < 0.01]. Patients had high circulating levels of noradrenaline, glucagon, and adiponectin, and low levels of ghrelin. We failed to observe any differences in metabolic responses between controls and patients during short-term exercise. Conclusions., In the basal fasting state patients with CHF are characterized by several metabolic abnormalities which may contribute to CHF pathophysiology and may provide a basis for targeted intervention. [source] Are Hormonal Responses to Exercise in Young Men with Down's Syndrome Related to Reduced Endurance Performance?JOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2008V-A. Bricout The aim of the present study was to analyse whether hormonal responses could explain an exercise limitation in Down's syndrome (DS). Fourteen young men with DS (mean age 22.5 ± 0.7 years) and 15 controls (CONT, mean age 22.5 ± 0.3 years) participated in the study. During a treadmill submaximal incremental test, blood samples were collected for determination of hormonal and metabolic variables. Compared to CONT, DS individuals showed lower VO2max (P < 0.05), and lower duration of submaximal incremental exercise (P < 0.001). At rest, DS individuals showed greater catecholamines, insulin and leptin values (P < 0.05), but lower testosteronemia and cortisolemia (P < 0.05), compared to CONT. During submaximal incremental tests, catecholamines and cortisol were not increased, whereas the insulin concentration of DS individuals was significantly higher (P < 0.01) compared to CONT. Glycaemia increased significantly at the end of submaximal incremental test for CONT but not for DS individuals (P < 0.01). Maximal fat oxidation was lower (P < 0.01), whereas non-esterified fatty acids concentrations rose significantly during submaximal exercise in DS individuals. These results indicate an altered hormonal response to exercise in DS individuals. This endocrine profile at rest and during exercise may limit endurance performance in DS individuals. [source] Ketones: Metabolism's Ugly DucklingNUTRITION REVIEWS, Issue 10 2003Theodore B. Vanitallie MD Ketones were first discovered in the urine of diabetic patients in the mid-19th century; for almost 50 years thereafter, they were thought to be abnormal and undesirable by-products of incomplete fat oxidation. In the early 20th century, however, they were recognized as normal circulating metabolites produced by liver and readily utilized by extrahepatic tissues. In the 1920s, a drastic "hyperketogenic" diet was found remarkably effective for treatment of drug-resistant epilepsy in children. In 1967, circulating ketones were discovered to replace glucose as the brain's major fuel during the marked hyperketonemia of prolonged fasting. Until then, the adult human brain was thought to be entirely dependent upon glucose. During the 1990s, dietinduced hyperketonemia was found therapeutically effective for treatment of several rare genetic disorders involving impaired neuronal utilization of glucose or its metabolic products. Finally, growing evidence suggests that mitochondrial dysfunction and reduced bioenergetic efficiency occur in brains of patients with Parkinson's disease (PD) and Alzheimer's disease (AD). Because ketones are efficiently used by mitochondria for ATP generation and may also help protect vulnerable neurons from free radical damage, hyperketogenic diets should be evaluated for ability to benefit patients with PD, AD, and certain other neurodegenerative disorders. [source] The Link Between Childhood Undernutrition and Risk of Chronic Diseases in Adulthood: A Case Study of BrazilNUTRITION REVIEWS, Issue 5 2003Ana L. Sawaya PhD Obesity, cardiovascular disease, and type 2 diabetes mellitus are now prevalent among adults living in developing countries; these chronic diseases affect socioeconomically disadvantaged adults living in impoverished families with under-nourished children. This review summarizes data from Brazil - a developing country undergoing the nutrition transition - suggesting an association between childhood undernutrition and obesity and chronic degenerative disease. Potential mechanisms for the association include longterm effects of childhood undernutrition on energy expenditure, fat oxidation, regulation of food intake, susceptibility to the effects of high-fat diets, and altered insulin sensitivity. The combination of childhood undernutrition and adult chronic degenerative disease results in enormous social and economic burdens for developing countries. Further research is urgently needed to examine the effect of childhood undernutrition on risk of obesity and chronic degenerative diseases; one goal of such research would be to determine and provide low-cost methods for prevention and treatment. [source] Reduced fat oxidation and obesity risks among the Buryat of Southern Siberia,AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 5 2009William R. Leonard Over the last 20 years, obesity and associated metabolic diseases have emerged as major global health problems. Among urbanizing populations of developing regions of the world, childhood undernutrition often coexists with adult overnutrition, a phenomenon known as the "dual nutritional burden". A recent work (Frisancho 2003: Am J Hum Biol 15:522,532) suggests that linear growth stunting in early childhood may contribute to adult obesity by reducing the body's ability to oxidize fat. We test central aspects of this model drawing on data from 112 adult Buryat herders (53 males; 59 females) from Southern Siberia. The results are consistent with the predictions of the model, but only for women. Shorter Buryat women (height-for-age Z -scores , ,1) have significantly lower fasting fat oxidation levels compared to their taller counterparts. Shorter women are also significantly heavier and fatter, and have higher serum lipid levels. Among all Buryat women, reduced fat oxidation is significantly correlated with percent body fatness, serum triglyceride levels, and serum leptin levels, after controlling for relevant covariates. Additionally, Buryat women with high dietary fat intakes and low fat oxidation are significantly fatter and have higher lipid and leptin levels than those with low fat intakes and high fat oxidation. These results suggest that developmental changes in fat oxidation may play a role in the origins of obesity among populations with high rates of linear growth stunting. Further longitudinal research is necessary to elucidate the pathways through which early-life undernutrition may increase risks for adulthood obesity and cardiovascular disease. Am. J. Hum. Biol. 2009. © 2009 Wiley-Liss, Inc. [source] Lower ability to oxidize lipids in adult patients with growth hormone (GH) deficiency: reversal under GH treatmentCLINICAL ENDOCRINOLOGY, Issue 4 2006F. Brandou Summary Background, The aim of the study was to characterize lipid oxidation at exercise in adults with growth hormone deficiency (GHD) and to evaluate the effect of 6 and 12 months of GH replacement therapy on substrate carbohydrate (CHO) and lipid utilization at exercise. Patients and measurements, Twenty-five patients with GHD and 40 matched controls participated in the study. Ten of the 25 GH-deficient patients were treated with recombinant GH for 12 months. Anthropometric measurements and exercise calorimetry were performed before and after treatment. Maximal fat oxidation and the crossover point [that is the percentage of the theoretical maximal power (Wmax th) where CHO become the predominant fuel used for oxidation] were determined. Results and conclusion, The GH-deficient patients exhibited a highly significant shift in the balance of substrate oxidation during exercise, towards a decrease in fat oxidation, and a shift towards lower intensities of the crossover (52 ± 5·5%vs. 72·6 ± 6·6% of Wmax th, P < 0·03) and maximal fat oxidation (131·04 ± 14 vs. 234·4 ± 30·1 mg/min, P < 0·03) in the GHD and control groups, respectively. However, GH treatment at 6 and 12 months partially reversed this defect, resulting in an increase (+83%, P < 0·001) in the maximal ability to oxidize fat during exercise. These findings are consistent with the hypothesis that a lack of GH reduces the ability to oxidize lipids during exercise and that GH treatment restores this muscular metabolic property. [source] | |||||||||||||