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- Sahlin, Kent
(författare)
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Control of lipid oxidation at the mitochondrial level.
- 2009
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Ingår i: Applied physiology, nutrition, and metabolism = Physiologie appliquée, nutrition et métabolisme. - : Canadian Science Publishing. - 1715-5312. ; 34:3, s. 382-8
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Tidskriftsartikel (refereegranskat)abstract
- The rate of lipid oxidation during exercise is controlled at several sites, and there is a reciprocal dependency between oxidation of lipids and carbohydrates (CHO). It is well known that the proportion of the 2 fuels oxidized is influenced by substrate availability and exercise intensity, but the mechanisms regulating fuel preferences remain unclear. During intense exercise, oxidation of long-chain fatty acids (LCFAs) decreases, and the major control is likely to be at the mitochondrial level. Potential mitochondrial sites for control of lipid oxidation include transport of LCFAs into mitochondrial matrix, beta-oxidation, the tricarboxylic acid cycle, and the electron transport chain (ETC). CHO catabolism may impair lipid oxidation by interfering with the transfer of LCFAs into mitochondria and by competing for mutual cofactors (i.e., nicotinamide adenine dinucleotide and (or) coenzyme A (CoA)). The different effect of energy state on the catabolism of CHO and lipids is likely to be of major importance in explaining the shift in fuel utilization during intensive exercise. Formation of acetyl-CoA from CHO is activated by a low energy state, and will lead to accumulation of products that are inhibitory to lipid oxidation. In contrast, beta-oxidation of LCFAs to acetyl-CoA is not stimulated by a low energy state. Further interaction between CHO and LCFAs may occur by substrate competition for electron carriers at ETC, due to provisions of electrons through different complexes. Feedback inhibition of beta-oxidation by redox state is thought to be an important mechanism for the slowing of lipid oxidation during intensive exercise.
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| 2. |
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| 3. |
- Hawke, Emma, et al.
(författare)
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Acidosis and cell signalling
- 2009
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Ingår i: Proceedings of 14th International Biochemistry of Exercise Conference, Muscles as Molecular and Metabolic Machines. Guelph, Canada. Appl Physiol Nutr Metab 2009 Jun 34(3):307-492. - Canadian Science Publishing (NRC Research Press) : Canadian Science Publishing. ; , s. 307-492-
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Konferensbidrag (refereegranskat)
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| 4. |
- Huang, Terry T-K, et al.
(författare)
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Metabolic syndrome in youth : current issues and challenges.
- 2007
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Ingår i: Appl Physiol Nutr Metab. - : Canadian Science Publishing. - 1715-5312. ; 32:1, s. 13-22
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Tidskriftsartikel (refereegranskat)abstract
- The current paper reviews the important issues and challenges facing children and adolescents with the metabolic syndrome (MetS). Studies suggest that the MetS and its risk components may be on the rise in children along with rising rates of obesity; however, further study remains warranted. The topics reviewed encompass the definition of the syndrome, its prevalence, clustering and tracking of metabolic risk factors, the role of physical activity and diet in the development of the MetS, criticisms and utility of the MetS definition, and special considerations needed in the pediatric population. Physical activity and diet may play important roles in the MetS; however, research with precise measurements of activity, diet, and metabolic outcomes is needed. The paper concludes by emphasizing that regardless of one’s position in the ongoing debate about the MetS, the long-term risks attributable to each individual risk component are real. The abnormality of one component should automatically prompt the screening of other components. Among children and adolescents, lifestyle modification should always serve as the frontline strategy. Prevention during childhood is key to the largest possible impact on adult health at the population level.
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| 5. |
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| 6. |
- Williams, Craig, et al.
(författare)
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Critical power in adolescent boys and girls – an exploratory study
- 2008
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Ingår i: Applied Physiology, Nutrition and Metabolism. - 1715-5312 .- 1715-5320. ; 33:6, s. 1105-1111
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Tidskriftsartikel (refereegranskat)abstract
- The purpose of the study was to identify critical power (CP) in boys and girls and to examine the physiological responses to exercise at and 10% above CP (CP+10%) in a sub-group of boys. Nine boys and 9 girls (mean age 12.3 (0.5) y performed 3 constant-load tests to derive CP. Eight of the boys then exercised, in random order, at CP and CP+10% until volitional exhaustion. CP was 123 (28) and 91 (26) W for boys and girls, respectively (p < 0.02), which was equivalent to 75 (6) and 72 (10) % of peak oxygen uptake, respectively (p > 0.47). Boys' time to exhaustion at CP was 18 min 37 s (4 min 13 s), which was significantly longer (p < 0.007) than that at CP+10% (9 min 42 s (2 min 31 s)). End-exercise values for blood lactate concentration (B[La]) and maximal oxygen uptake were higher in the CP+10% trial (5.0 (2.4) mmol·L-1 and 2.15 (0.4) L·min-1, respectively) than in the CP trial, (B[La], 4.7 (2.1) mmol·L-1; maximal oxygen uptake, 2.05 (0.35) L·min-1; p > 0.13). Peak oxygen uptake (expressed as a percentage of the peak value) was not attained at the end of the trials (94 (12) and 98 (14) % for CP and CP+10%, respectively). These results provide information about the boundary between the heavy and severe exercise intensity domains in children, and have demonstrated that CP in a group of boys does not represent a sustainable steady-state intensity of exercise.
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| 8. |
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| 9. |
- Vaag, Allan, et al.
(författare)
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Non-obese patients with type 2 diabetes and prediabetic subjects: distinct phenotypes requiring special diabetes treatment and (or) prevention?
- 2007
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Ingår i: Applied Physiology, Nutrition and Metabolism. - 1715-5320. ; 32:5, s. 912-920
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Tidskriftsartikel (refereegranskat)abstract
- A major reason for the increased incidence of type 2 diabetes mellitus (T2DM) across the world is the so-called obesity epidemic, which occurs both in developed and developing countries. However, a large proportion of patients with T2DM in European and, in particular, Asian countries are non-obese. The non-obese T2DM phenotype is characterized by disproportionally reduced insulin secretion and less insulin resistance, as compared with obese patients with T2DM. Importantly, non-obese patients with T2DM have a similar increased risk of cardiovascular disease as obese T2DM patients. The risk of T2DM in non-obese patients is influenced by genetics as well as factors operating in utero indicated by low birth weight. Furthermore, this phenotype is slightly more prevalent among patients with latent autoimmune diabetes in adults, characterized by positive anti-GAD antibodies. The recently identified TCF7L2 gene polymorphism resulting in low insulin secretion influences the risk of T2DM in both obese and non-obese subjects, but is relatively more prevalent among non-obese patients with T2DM. Furthermore, the Prol2Ala polymorphism of the PPAR-gamma gene influencing insulin action increases the risk of T2DM in non-obese subjects. Despite a "normal" body mass index, non-obese patients with T2DM are generally characterized by a higher degree of both abdominal and total fat masses (adiposity). Prevention of T2DM with lifestyle intervention is at least as effective in non-obese as in obese prediabetic subjects, and recent data suggest that metformin treatment targeting insulin resistance and non-glycemic cardiovascular disease risk factors is as beneficial in non-obese as in obese patients with T2DM. Nevertheless, non-obese patients with T2DM may progress to insulin treatment more rapidly as compared with obese patients with T2DM.
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