obesity- decreased fatty acid oxidation

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  • 8/13/2019 Obesity- Decreased Fatty Acid Oxidation

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    Victoria Coglianese

    Obesity

    2/27/13

    Impaired plasma fatty acid oxidation in extremely obese women (Thyfaultet al.)

    Reduced fatty acid oxidation in the skeletal muscle has been observed in both obese people and

    weight-reduced (but still 1stclass obese) people. This could lead to excess free fatty acids in circulation

    and therefore more fat storage. The purpose of this study was to determine whether this defect in lipid

    oxidation in muscle was due to phenotype that inclines toward obesity and remains even after weight

    loss. In this experiment, free fatty acid oxidation was studied at rest and during exercise in women who

    were either lean, obese, or weight-reduced due to gastric bypass surgery. It was hypothesized that the

    lean women would have the highest rates of fatty acid oxidation while those who had undergone gastric

    bypass would have similar levels of free fatty acid oxidation as the obese women. This suggests to me

    that the researchers hypothesized that impaired fatty acid oxidation in obese women was due to

    phenotype.

    The most important finding was about the amount of lipid oxidation. The result that stated:

    The extremely obese and weight-reduced groups oxidized 78 and 58% of the plasma FFA oxidized by

    the lean group at rest, respectively does not seem to comply with their other results. Although total

    lipid oxidation was about the same between each group, the percent of FFA oxidation in the blood

    correlated with BMI- the obese with the lowest percent oxidation and the lean with the highest. Obesepeople have more free fatty acids in their blood as a result of higher rates of appearance of FFA in the

    blood. Yet they still oxidize the same amount as people with lower body masses. This is one of the most

    detrimental factors in causing conditions like those of metabolic syndrome observed in many obese

    people.

    The results of this study and across similar studies are contradictory. More research is needed as

    well as better operational definitions, for example, of the types of participants in terms of differences in

    body types. However, the finding that I believe is most significant to the purpose of this study is that

    previously extremely obese women have reduced lipid utilization during exercise compared with

    healthy women of the same BMI. This suggests that it is the exposing of the body to extreme excess

    weight that can cause impaired plasma fatty acid oxidation rather than a phenotype inducing the

    impairment and causes obesity. It also suggests that this impairment is a consequence that may not bealleviated by simply reversing the process.

    Intramuscular lipid oxidation and obesity (Houmard)

    Across studies, it has been found that weight gain is related to a decrease in the ability to oxidize

    fatty acids. These studies used methods involving respiratory quotient. In this article, it is said that the

    finding that relative percentage of fat oxidation was similar in both the extremely obese and extremely

    obese women after weight loss and significantly reduced compared with the lean subjects suggests

    that a reduced capacity for lipid oxidation is linked with a propensity toward extreme obesity.

    However, I see this result as suggesting the decrement in fatty acid oxidation is due to the conditions

    that accumulate over time with increasing weight gain rather than a predisposition to obesity. It is

    interesting that the decreased lipid oxidation is followed by an increase in allocation of the lipids toward

    storage.Data suggests the mechanisms for impaired fatty acid oxidation involve decreased enzyme

    activity at important regulatory steps in the cellular respiratory pathway. Anomalies of mitochondria in

    obese individuals may also play a role in the faulty oxidative processes. CPT1 is one of the enzymes

    involved in fatty acid oxidation through transferring lipids across the mitochondrial membrane and is

    depressed in obese individuals. CPT1 expression has been shown to improve insulin action, therefore

    linking fatty acid oxidation as a role in insulin action.

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    In addition to the decrease fatty acid oxidation, an increased ability to carry out lipogenesis is

    seen in obese people. Together, these conditions promote fatty acid esterification and storage in

    skeletal muscle.

    Weight-reduced individuals do not show improvement in fatty acid oxidation in skeletal muscle,

    and therefore weight loss does fix the defected fatty acid oxidation. However, studies show that

    contractile activity increases fatty acid oxidation in skeletal muscle of obese individuals. Because the

    exact mechanisms by which defects in fatty acid oxidation are involved in obesity are still unclear,

    weight loss treatments should put the most emphasis on physical activity to promote more effective

    weight loss as well as improved functioning.