Fatty Acid and Ketone Body Metabolism in the Rat: Response to Diet and Exercise

Askew, E. W.; Dohm, G. Lynis; Huston, R. L.

doi:10.1093/jn/105.11.1422

Cited by 47 publications

(30 citation statements)

References 27 publications

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“…1C). The result is consistent with the observation in rats that the concentration of plasma P-hydroxybutyric acid elevates after exhaustive exercise accompanying a doubling of the activity of skeletal muscle 3-oxid acid CoA transferase, a key enzyme in extrahepatic ketone body utilization [26]. Carlson et al [27] and Scheele et al [28] also observed a higher plasma concentration of P-hydroxybutyric acid and acetoacetate in response to exercise in humans.…”

Section: Discussionsupporting

confidence: 86%

Reciprocal Responses to Exercise in Hepatic Ketogenesis and Lipid Secretion in the Rat

et al. 1991

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The effects of 4 weeks of voluntary exercise (rotating wheel) on serum and liver lipid levels were studied in 6-week-old male Wistar rats. The hypotriglyceridemic effect of exercise was not influenced by the dietary fat levels (4.5 and 14.5%), whereas the hypocholesterolemic effect was higher in a low-fat diet than in a high-fat diet. Although the serum cholesterol-lowering effect of exercise was marginal, the beneficial effect on hepatic lipids was observed only in rats fed a high-cholesterol diet. The hepatic contribution to the serum lipid-lowering action of exercise was examined in the isolated perfused livers of rats fed a low fat diet. The reduction (34%) of serum triglyceride by exercise corresponded to the decrease (32%) in the hepatic triglyceride secretion rate, indicating a significant role of the liver in the hypotriglyceridemic effect of exercise. In contrast, the decrease (31 %) in serum total cholesterol was considerably greater than that (23%) in the hepatic secretion, suggesting an extra-hepatic contribution. On the other hand, the hepatic production of ketone body was increased by exercise. These results indicate that the altered hepatic partition of long-chain free fatty acids between esterification and oxidation is one of the causative factors for the serum lipid-lowering effect of exercise.

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Section: Discussionsupporting

confidence: 86%

Reciprocal Responses to Exercise in Hepatic Ketogenesis and Lipid Secretion in the Rat

et al. 1991

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“…Mitochon drial protein yield, cytochrome c, pyruvate and palmitylcarnitine oxidation were all significantly (p < 0.05) increased per gram of muscle. These adaptations are most apparent when expressed per gram of tissue, as noted previously (4,29). If these enzyme activities are expressed relative to mitochondrial protein, the differences are not apparent because of the increased mitochondrial protein in the trained rat muscle.…”

Section: Resultssupporting

confidence: 69%

Supplemental Dietary Carnitine and Lipid Metabolism in Exercising Rats

Askew¹,

Dohm²,

Weiser³

et al. 1980

Ann Nutr Metab

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Rats were physically trained by treadmill running and fed normal, high fat, or identical diets supplemented with 1.0% DL-carnitine. Fatty acid oxidation, stimulated by exercise and/or by a high fat diet was studied to determine if it might be further augmented by supplemental dietary carnitine. Fatty acid oxidation in vitro or in vivo was unaffected by carnitine feeding. Carnitine feeding was associated with an increase in heart and muscle palmitylcarnitine acyltransferase activity and reduced serum cholesterol in trained rats fed the high fat diet. Under the conditions of this study, supplemental dietary carnitine did not greatly alter glyceride synthesis, lipolysis, or fatty acid oxidation, which indirectly indicates that the increased demands for fatty acid oxidation resulting from exercise or from fat feeding are adequately supported by endogenous levels of carnitine.

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“…The illustrations are based on data in several different studies, including those in REFS 184–187. Although plasma β-hydroxybutyrate levels are rarely measured in exercise studies, there are data showing that bouts of vigorous exercise (running or swimming) do elevate circulating ketone levels in rodents 188,189 .…”

mentioning

confidence: 99%

Intermittent metabolic switching, neuroplasticity and brain health

et al. 2018

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During evolution, individuals whose brains and bodies functioned well in a fasted state were successful in acquiring food, enabling their survival and reproduction. With fasting and extended exercise, liver glycogen stores are depleted and ketones are produced from adipose-cell-derived fatty acids. This metabolic switch in cellular fuel source is accompanied by cellular and molecular adaptations of neural networks in the brain that enhance their functionality and bolster their resistance to stress, injury and disease. Here, we consider how intermittent metabolic switching, repeating cycles of a metabolic challenge that induces ketosis (fasting and/or exercise) followed by a recovery period (eating, resting and sleeping), may optimize brain function and resilience throughout the lifespan, with a focus on the neuronal circuits involved in cognition and mood. Such metabolic switching impacts multiple signalling pathways that promote neuroplasticity and resistance of the brain to injury and disease.

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Fatty Acid and Ketone Body Metabolism in the Rat: Response to Diet and Exercise

Cited by 47 publications

References 27 publications

Reciprocal Responses to Exercise in Hepatic Ketogenesis and Lipid Secretion in the Rat

Reciprocal Responses to Exercise in Hepatic Ketogenesis and Lipid Secretion in the Rat

Supplemental Dietary Carnitine and Lipid Metabolism in Exercising Rats

Intermittent metabolic switching, neuroplasticity and brain health

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