Short- and medium-chain fatty acids in energy metabolism: the cellular perspective

Schönfeld, Peter; Wojtczak, Lech

doi:10.1194/jlr.r067629

Cited by 720 publications

(610 citation statements)

References 160 publications

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“…This enhances their availability to various organs including the CNS and muscles. In contrast, long chain fatty acids are bound to plasma proteins and require transporter proteins for uptake into cells and mitochondria (Schönfeld and Wojtczak, 2016). When heptanoate is metabolized by β-oxidation, it generates two molecules of acetyl-CoA and one molecule of propionyl-CoA.…”

Section: Metabolic Treatments In Alsmentioning

confidence: 99%

“…After hydrolysis of the ester bonds, octanoic (caprylic) acid can be metabolized quickly by β-oxidation to acetyl CoA and C4 ketone bodies to supply the TCA cycle. As mentioned above, one advantage of medium chain fatty acids is that they are able to easily diffuse through plasma as well as mitochondrial membranes and do not require transport proteins (Schönfeld and Wojtczak, 2016). Thus, MCTs can serve as a fast fuel especially in conditions with decreased uptake of glucose.…”

Section: Metabolic Treatments In Alsmentioning

confidence: 99%

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Metabolic Dysfunctions in Amyotrophic Lateral Sclerosis Pathogenesis and Potential Metabolic Treatments

Tefera

Borges

2017

Front. Neurosci.

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease primarily characterized by loss of motor neurons in brain and spinal cord. The death of motor neurons leads to denervation of muscle which in turn causes muscle weakness and paralysis, decreased respiratory function and eventually death. Growing evidence indicates disturbances in energy metabolism in patients with ALS and animal models of ALS, which are likely to contribute to disease progression. Particularly, defects in glucose metabolism and mitochondrial dysfunction limit the availability of ATP to CNS tissues and muscle. Several metabolic approaches improving mitochondrial function have been investigated in vitro and in vivo and showed varying effects in ALS. The effects of metabolic approaches in ALS models encompass delays in onset of motor symptoms, protection of motor neurons and extension of survival, which signifies an important role of metabolism in the pathogenesis of the disease. There is now an urgent need to test metabolic approaches in controlled clinical trials. In addition, more detailed studies to better characterize the abnormalities in energy metabolism in patients with ALS and ALS models are necessary to develop metabolically targeted effective therapies that can slow the progression of the disease and prolong life for patients with ALS.

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Section: Metabolic Treatments In Alsmentioning

confidence: 99%

Section: Metabolic Treatments In Alsmentioning

confidence: 99%

Metabolic Dysfunctions in Amyotrophic Lateral Sclerosis Pathogenesis and Potential Metabolic Treatments

Tefera

Borges

2017

Front. Neurosci.

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“…HCO contains large amounts of medium-chain FA (> 70% in total FA). Since medium-chain FA are quickly metabolized in cells compared with long-chain FA (Schönfeld and Wojtczak 2016), the effect of this HCO-based high-fat diet on hepatic and whole-body fat accumulation is probably less than that of typical high-fat diets composed of longchain FA-based oils. However, we cannot deny the possibility that feeding of HCO-based high-fat diets affects hepatic expression of several genes involved in lipid metabolism (Lin et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Decreased Fatty Acid <i>β</i>-Oxidation Is the Main Cause of Fatty Liver Induced by Polyunsaturated Fatty Acid Deficiency in Mice

Nakajima

Yang

et al. 2017

Tohoku J. Exp. Med.

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Insufficient intake of polyunsaturated fatty acids (PUFA) causes fatty liver. The mechanism responsible is primarily related to increased lipogenesis and decreased FA degradation based on rodent studies. However, these studies were limited by the fact that the typical PUFA-deficient diets contained insufficient amounts of long-chain FA, the PUFA-containing diets were primarily composed of n-3 PUFA-enriched oil, and the intake of PUFA was excessive compared with the physiological requirement. To address these issues, mice were fed a PUFA-deficient diet containing long-chain FA at a standard fed level and then were orally fed a n-3/n-6-balanced PUFA-containing oil [PUFA (+)] or a PUFA-deficient oil [PUFA (−)] at physiological relevant levels (0.1 mL/mouse/2d). We compared these groups and examined whether fatty liver in PUFA deficiency was attributable to both the effects of increased lipogenesis and decreased FA catabolism. Compared with the PUFA (+) group, the PUFA (−) group showed increases in liver triglyceride and serum FA content. Hepatic gene expression of several mitochondrial β-oxidation enzymes, the serum 3-hydroxybutyrate level, and DNA-binding ability of peroxisome proliferator-activated receptor α (PPARα) were increased in the PUFA (+) group, whereas these adaptive responses were significantly attenuated in the PUFA (−) group. The hepatic expression of typical lipogenesis genes did not differ between the groups. Therefore, fatty liver in PUFA deficiency is attributable to suppression of the FA-degrading system probably from decreased PPARα adaptive responsiveness, and PUFA may be an essential factor for PPARα functioning. This finding is helpful for managing clinical situations having a risk of PUFA deficiency.

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“…Onge & Jones, 2002;McCarty & DiNicolantonio, 2016;Schonfeld & Wojtczak, 2016;TMIC, 2017). MCFAs possess special properties that differentiate them from LCFAs.…”

Section: **It Is Relevant To Mention Here That Commercial Products Wimentioning

confidence: 99%

“…However, a concentrated injection of C12 has been shown to distribute about half to the portal vein and half to the lymphatic system (Sigalet et al, 1997). Ingestion of C12 together with proteins may direct more C12 to the lymphatic system (Schonfeld & Wojtczak, 2016) (Figure 3). This special behavior of C12 was foretold as early as the 1950s, when some researchers suggested the additional categories of "intermediatechain fatty acids" (Schon et al, 1955;Goransson, 1965;Knox et al, 2000), and "transition fatty acid" (You et al, 2008).…”

Section: Distribution In Intestinementioning

confidence: 99%

A Half-Truth is Not the Whole Truth: The AHA Position on Saturated Fat

Dayrit

2017

KIMIKA

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This second in this series of papers will present the biases in the American Heart Association's 2017 Presidential Advisory with respect to saturated fat. Although important differences in the metabolic properties of specific SFA have been known since the 1960s, the AHA still considers all SFA as one group having the same properties. There is abundant research available that supports the designation of C6 to C12 fatty acids as medium-chain fatty acids (MCFA). This is particularly relevant to coconut oil, which is made up of about 65% MCFA. Ignoring the evidence, AHA simply labels coconut oil as SFA. The AHA promotes half-truths, not the whole truth.

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Short- and medium-chain fatty acids in energy metabolism: the cellular perspective

Cited by 720 publications

References 160 publications

Metabolic Dysfunctions in Amyotrophic Lateral Sclerosis Pathogenesis and Potential Metabolic Treatments

Metabolic Dysfunctions in Amyotrophic Lateral Sclerosis Pathogenesis and Potential Metabolic Treatments

Decreased Fatty Acid <i>β</i>-Oxidation Is the Main Cause of Fatty Liver Induced by Polyunsaturated Fatty Acid Deficiency in Mice

A Half-Truth is Not the Whole Truth: The AHA Position on Saturated Fat

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