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

Fukuda, Nobuhiro; Tojho, Masakazu; Hidaka, T; Sho, Hiroko; Sugano, Michihiro

doi:10.1159/000177651

Cited by 27 publications

(24 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…One explanation may be that exercise decreased hepatic TG secretion, 31 partly by altering hepatic partitioning of fatty acids between esterification and oxidation. 32 In line with this thinking, the reduction in the postprandial 3-hydroxybutyrate response by the high-CHO intervention was somewhat attenuated by exercise (Table 4, Figure 3). Another explanation may be that exercise opposed the suppressive effects of a diet high in carbohydrates on LPL activity.…”

Section: Koutsari Et Alsupporting

confidence: 65%

Exercise Prevents the Accumulation of Triglyceride-Rich Lipoproteins and Their Remnants Seen When Changing to a High-Carbohydrate Diet

Koutsari

Karpe

Humphreys

et al. 2001

ATVB

View full text Add to dashboard Cite

Abstract-We tested the hypothesis that daily aerobic exercise opposes the fasting hypertriglyceridemia and exaggerated postprandial lipemia observed after substituting dietary fat with carbohydrate. Eight healthy postmenopausal women aged 51 to 66 years consumed the same high-fat mixed meal on 3 occasions: (1) after 3 days on a low-carbohydrate diet (35%, 50%, and 15% energy from carbohydrate, fat, and protein, respectively); (2) after 3 days on an isoenergetic high-carbohydrate diet (corresponding values 70%, 15%, and 15%); and (3) after 3 days on the same high-carbohydrate diet with 60 minutes of brisk walking daily. Plasma triglycerides were higher after the high-carbohydrate diet than after the low-carbohydrate diet: fasting, (TRLs) with coronary heart disease (CHD). 1 These lipoproteins are a heterogeneous group of particles, including chylomicrons (containing apoB-48), VLDLs (containing apoB-100), and their remnants. Remnants are formed from VLDLs and chylomicrons after partial removal of their TGs by the action of lipoprotein lipase (LPL). They have a reduced TG content but are enriched in cholesterol and have been implicated in atherosclerosis. 2 Determination of remnant-like lipoprotein particle (RLP) cholesterol 3 provides a measure of TRL particles with remnant characteristics 4,5 and can contribute to the assessment of CHD risk. 6,7 Current dietary guidelines for reducing the risk of CHD emphasize the replacement of saturated fat with complex carbohydrates so that total fat intake does not exceed 30% of energy intake. 8 Low-fat high-carbohydrate diets effectively reduce LDL cholesterol 8 but, in the absence of weight loss, can also increase fasting 9 and postprandial 10 plasma TG concentrations as well as RLP cholesterol. 11 As explained above, this effect on TRL metabolism may reduce the overall benefit expected from such diets. For these and related reasons, there is currently a debate concerning the effectiveness of high-carbohydrate diets as a means for reducing CHD risk.However, this debate has largely ignored the potential of exercise to offset these effects. Exercise conditioning is known to decrease fasting TG 12,13 and postprandial TRL concentrations 14 when subjects are on a Western diet. Therefore, the simultaneous adoption of a high-carbohydrate diet and a physically active lifestyle may optimize the lipoprotein profile, particularly in individuals who are susceptible to carbohydrate-induced hypertriglyceridemia.The purpose of the present study was to test the hypothesis that daily aerobic exercise of moderate intensity opposes the potentially detrimental effects on TRL metabolism of changing to a low-fat high-carbohydrate diet. We used a short-term intervention specifically to examine the influence of exercise on TRL metabolism during the initial period of dietary change, when lipoproteinemic changes are particularly marked. 15 Methods SubjectsThe study was approved by Loughborough University's Ethical Advisory Committee, and subjects gave their informed consent. Eight nonsmoking postme...

show abstract

Section: Koutsari Et Alsupporting

confidence: 65%

Exercise Prevents the Accumulation of Triglyceride-Rich Lipoproteins and Their Remnants Seen When Changing to a High-Carbohydrate Diet

Koutsari

Karpe

Humphreys

et al. 2001

ATVB

View full text Add to dashboard Cite

show abstract

“…The present studies showed similar results (Table 3). These observations therefore suggest that the hypocholesterolemic effect of dietary taurine results partly from a decreased rate of hepatic secretion of cholesteryl ester, since the influx of cholesterol entering the blood stream from the liver in the form of lipoprotein-cholesterol is a critical determinant of serum cholesterol concentration (22).…”

Section: Discussionmentioning

confidence: 90%

Dietary Taurine Reduces Hepatic Secretion of Cholesteryl Ester and Enhances Fatty Acid Oxidation in Rats Fed a High-Cholesterol Diet

Fukuda

Yoshitama

Sugita

et al. 2011

J Nutr Sci Vitaminol

Self Cite

View full text Add to dashboard Cite

SummaryWe investigated the fate of exogenous fatty acid in connection with decreased hepatic accumulation and secretion of cholesteryl esters in rats fed diets containing taurine. Providing taurine as 5% of the diet for 14 d significantly decreased concentrations of cholesterol, especially cholesteryl esters in both serum and liver. Ketone body production and incorporation of exogenous [1][2][3][4][5][6][7][8][9][10][11][12][13][14] C]oleate into ketone bodies in liver perfusate were consistently higher during a 4-h perfusion period in taurine-fed rats than in control rats. The elevation was accompanied by increased activity of liver mitochondrial carnitine palmitoyltransferase, a rate-limiting enzyme for fatty acid oxidation. Dietary taurine significantly reduced hepatic secretion of cholesteryl ester and decreased incorporation of exogenous oleic acid substrate into this lipid molecule. Further, the extent of reduction in hepatic secretion of cholesteryl ester was closely related to its diminished accumulation in the liver. The conversion pattern of exogenous [1-14 C]oleic acid substrate suggested a decreased esterification-to-oxidation ratio in the taurine group compared with the control. These results suggest that taurine-induced reduction in hepatic accumulation of cholesteryl ester was associated with reduced hepatic secretion of this lipid molecule, and was inversely related to enhanced ketone body production and fatty acid oxidation. Key Words taurine, cholesterol ester secretion, fatty acid oxidation, rat liver Taurine, a sulfur-containing amino acid present in high concentrations in animal tissues, is available from dietary sources and also can be synthesized in vivo from other amino acids. Dietary taurine exhibits various physiologic and pharmacological actions, including hypocholesterolemic and antiatherogenic effects, in experimental animals, especially rats, mice, and Japanese (LAP) quail fed high cholesterol diets ( 1-6 ). These beneficial effects of taurine have recently been reproduced in humans ( 7 , 8 ). Although these effects have attracted attention, the underlying mechanisms are not clearly understood. With regard to the hypocholesterolemic action of dietary taurine, we previously reported that in rats fed high-cholesterol diets, the lowering of serum cholesterol by taurine was partly attributable to a reduced secretion rate of cholesteryl ester by the liver, and that reductions in hepatic secretion rate and in hepatic accumulation of cholesteryl ester were inversely related to increased ketone body production, an index of fatty acid oxidation ( 9 ). This pattern of changes suggested that dietary taurine influences the metabolic fate of fatty acids, specifically whether they undergo esterification or oxidation. However, in that study, we did not assess the relative significance of these two pathways in the metabolism of exogenous fatty acids.We therefore undertook a more detailed examination of fatty acid metabolism using an exogenous [1-14 C]oleic acid, and found for the first time that th...

show abstract

“…Along with an increase in LPL activity, very low density lipoprotein (VLDL) secretion from the liver may be reduced by an acute exercise bout (41). In humans, reductions in postprandial plasma concentration of VLDL-TG has been shown to be reduced following exercise (39,59) and in mice, reduced postprandial secretion of VLDL from the liver has been observed after exercise (36,65). Resistance training and high-intensity interval training have also been shown to be effective for reducing PPL; however, energy expenditure does not seem to predict the attenuation as well as with aerobic exercise (5,22,93).…”

Section: Exercise and Lipid Metabolismmentioning

confidence: 99%

Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation

Johnson

Kurti

Smith

et al. 2016

Appl. Physiol. Nutr. Metab.

View full text Add to dashboard Cite

Obesity and asthma often coexist in the same people. Both are characterized by the presence of low-grade systemic inflammation. A high-fat diet may contribute to concurrent development of both conditions by promoting a pro-inflammatory postprandial environment leading to a transient accumulation of blood lipids (postprandial lipemia; PPL) and acute airway inflammation. Previous results from our lab have shown an ~20% increase in airway inflammation two hours after consuming a high-fat meal (HFM) that was significantly associated with increased plasma triglycerides. While acute exercise has been shown to attenuate PPL, it is unknown whether these protective effects will translate to reduced airway inflammation after a high-fat meal. PURPOSE: To determine the effects of an acute bout of exercise on airway inflammation after a HFM. We tested the hypothesis that an acute bout of exercise 12 hours before a high-fat meal would protect against subsequent airway inflammation in healthy men and would be related to the decreased PPL and systemic inflammatory markers. METHODS: In a randomized cross-over study, 12 healthy college-aged men consumed a HFM (1g fat/1kg body weight) 12 hours following exercise (EX; 60 min at 60% VO2max) or without exercise (CON).Exhaled nitric oxide (eNO; measure of airway inflammation), blood lipid profiles (venous sample; total cholesterol, HDL, LDL, triglycerides, glucose), inflammatory markers (hsCRP, TNF-α, IL-6) and pulmonary function tests (PFT) (forced expiratory volume in 1-s,forced vital capacity, forced expiratory flow at 25-75% of vital capacity) were measured pre-HFM, two hours, and four hours post-HFM. RESULTS: Baseline eNO was not different (p>0.05) between trials. eNO increased (p<0.05) post HFM at two hours in the both CON and EX conditions. eNO between trials was not different (p>0.05). Triglycerides were significantly increased two and four hours post HFM but were not different (p>0.05) between conditions. There was no relationship (p>0.05) between eNO and triglycerides or systemic inflammatory markers for any time point in either condition. Pulmonary function did not differ (p>0.05) between any condition.CONCLUSION: These results demonstrate that an acute bout of moderate intensity exercise 12 hours before a HFM does not attenuate postprandial airway inflammation or lipemia in healthy college-aged men.v

show abstract

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

Cited by 27 publications

References 20 publications

Exercise Prevents the Accumulation of Triglyceride-Rich Lipoproteins and Their Remnants Seen When Changing to a High-Carbohydrate Diet

Exercise Prevents the Accumulation of Triglyceride-Rich Lipoproteins and Their Remnants Seen When Changing to a High-Carbohydrate Diet

Dietary Taurine Reduces Hepatic Secretion of Cholesteryl Ester and Enhances Fatty Acid Oxidation in Rats Fed a High-Cholesterol Diet

Effects of an acute bout of moderate-intensity exercise on postprandial lipemia and airway inflammation

Contact Info

Product

Resources

About