The Causes And Consequences Of Metabolic Inflexibility

1272 words - 5 pages

Metabolic flexibility is the ability to adjust and modify fuel oxidation depending on the fuel that is currently available. This capacity to adapt requires an ability to use lipid and carbohydrate fuels properly and the ability to efficiently switch between them, depending on fuel availability (Kelley et al., 2002). On the other hand, metabolic inflexibility is defined as the inability to change fuel oxidation in response to variations in macronutrient availability (Koves et al., 2008). There are opposing views among researchers on which types of diets and other nutritional factors can affect the onset of metabolic inflexibility and its results, such as insulin resistance. Some studies have supported the hypothesis that insulin resistance develops from metabolic inflexibility due to decreased fat oxidation and accumulation of cytosolic lipid molecules (Koves et al., 2008). However, increasing amounts of recent studies have presented observations that point to excessive, not diminished, incomplete beta-oxidation is the true cause of obesity-related insulin resistance in skeletal muscle (Koves et al., 2008). In addition, Koves et al. (2008) also revealed that insulin resistance is related to metabolic inflexibility during the fasted-to-fed transition as well as the depletion of organic acid intermediates from the citric acid cycle (Koves et al., 2008). Despite disagreeing on the precise cause of insulin resistance, all of the published research agrees on one central theme: it is imperative to remain metabolically flexible in order to avoid the numerous, and potentially disastrous, consequences associated with metabolic inflexibility.
As previously described, metabolic inflexibility is the inability to appropriately switch back and forth between fuels depending on their availability in the fed and fasted states. This inflexibility can result in weight gain, which in turn will eventually lead to obesity and other weight-related health issues. Furthermore, insulin resistance can develop and ultimately advance into type II diabetes. Another adverse effect of metabolic inflexibility is decreased expression of OXPHOS genes (Sparks et al., 2005). As a result, the occurrence of fat oxidation will increase while the rate of carbohydrate oxidation will decrease. The mitochondrial overload that is produced from a high-fat diet will result in incomplete beta-oxidation of fatty acids. The organism’s mitochondria might even double in size in an effort to try to compensate for this overload (Sparks et al., 2007). Obesity-related glucose intolerance might also arise from metabolic overload of the mitochondria in skeletal muscle due to a high-fat diet (Koves et al., 2005).
Similarly, Fex et al. (2007) found that a high fat diet resulted in insulin resistance as well as glucose intolerance, two hallmark issues associated with metabolic inflexibility. Further analysis of the high-fat diet mice revealed an accumulation of lipid droplets in beta cells in addition to...

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