Astaxanthin improves muscle lipid metabolism in exercise via inhibitory effect of oxidative CPT I modification

Aoi, Wataru; Naito, Yuji; Takanami, Yoichi; Ishii, Takeshi; Kawai, Yukari; Akagiri, Satomi; Kato, Yoji; Osawa, Toshihiko; Yoshikawa, Toshikazu

doi:10.1016/j.bbrc.2007.12.019

Cited by 142 publications

(134 citation statements)

References 33 publications

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“…The results showed that astaxanthin inhibited weight gain, reduced liver weight, hepatic triglycerides as well as triglycerides and plasma cholesterol. Aoi et al 47 found that H. pluvialis astaxanthin added to the diet of rats for 4 weeks accelerated the use of lipids during exercise, leading to better physical performance and reduced body fat. These observations demonstrate that the antioxidant effect of astaxanthin can modify muscular metabolism, resulting in improved muscular function during exercise.…”

Section: Astaxanthin and Chronic Diseasesmentioning

confidence: 99%

Astaxanthin: structural and functional aspects

Seabra

Pedrosa

2010

Rev. Nutr.

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1 Article based on L.M.J. SEABRA' s thesis project entitled "Litopenaeus vannamei shrimp: components of nutritional importance in meat and processing waste. A B S T R A C TAstaxanthin, a carotenoid belonging to the xanthophyll class, has stirred great interest due to its antioxidant capacity and its possible role in reducing the risk of some diseases. Astaxanthin occurs naturally in microalgae, such as Haematococcus pluvialis and the yeast Phaffia rhodozyma, and has also been considered to be the major carotenoid in salmon and crustaceans. Shrimp processing waste, which is generally discarded, is also an important source of astaxanthin. The antioxidant activity of astaxanthin has been observed to modulate biological functions related to lipid peroxidation, having beneficial effects on chronic diseases such as cardiovascular disease, macular degeneration and cancer. Researches have shown that both astaxanthin obtained from natural sources and its synthetic counterpart produce satisfactory effects, but studies in humans are limited to natural sources. There is no established nutritional recommendation regarding astaxanthin daily intake but most studies reported beneficial results from a daily intake of 4mg. Thus, this review discusses some aspects of the carotenoid astaxanthin, highlighting its chemical structure and antioxidant activity, and some studies that report its use in humans.Indexing terms: Antioxidants. Astaxanthin. Carotenoids. Chronic diseases. R E S U M O

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Section: Astaxanthin and Chronic Diseasesmentioning

confidence: 99%

Astaxanthin: structural and functional aspects

Seabra

Pedrosa

2010

Rev. Nutr.

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“…The current study and those previously completed by ours and other laboratories have consistently observed FAT/CD36 on both SS and IMF mitochondria (12,23,38). In addition, it has been observed that this transport protein regulates FA uptake and oxidation in mitochondria (2,23,24,37,38). Not all laboratories have identified the presence of FAT/CD36 on the mitochondria or demonstrated its ability to increase FA oxidation (25,28).…”

Section: Fa Transport As a Regulator Of Lipid Accumulationmentioning

confidence: 74%

Recovered insulin response by 2 weeks of leptin administration in high-fat fed rats is associated with restored AS160 activation and decreased reactive lipid accumulation

Stefanyk

Gulli

Ritchie

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Stefanyk LE, Gulli RA, Ritchie IR, Chabowski A, Snook LA, Bonen A, Dyck DJ. Recovered insulin response by 2 weeks of leptin administration in high-fat fed rats is associated with restored AS160 activation and decreased reactive lipid accumulation. Am J Physiol Regul Integr Comp Physiol 301: R159 -R171, 2011. First published April 27, 2011 doi:10.1152/ajpregu.00636.2010.-Leptin is an adipokine that increases fatty acid (FA) oxidation, decreases intramuscular lipid stores, and improves insulin response in skeletal muscle. In an attempt to elucidate the underlying mechanisms by which these metabolic changes occur, we administered leptin (Lep) or saline (Sal) by miniosmotic pumps to rats during the final 2 wk of a 6-wk low-fat (LF) or high-fat (HF) diet. Insulin-stimulated glucose transport was impaired by the HF diet (HF-Sal) but was restored with leptin administration (HF-Lep). This improvement was associated with restored phosphorylation of Akt and AS160 and decreased in reactive lipid species (ceramide, diacylglycerol), known inhibitors of the insulin-signaling cascade. Total muscle citrate synthase (CS) activity was increased by both leptin and HF diet, but was not additive. Leptin increased subsarcolemmal (SS) and intramyofibrillar (IMF) mitochondria CS activity. Total muscle, sarcolemmal, and mitochondrial (SS and IMF) FA transporter (FAT/CD36) protein content was significantly increased with the HF diet, but not altered by leptin. Therefore, the decrease in reactive lipid stores and subsequent improvement in insulin response, secondary to leptin administration in rats fed a HF diet was not due to a decrease in FA transport protein content or altered cellular distribution. fatty acid transport proteins; insulin signaling; diacylglycerol; ceramide; mitochondria; leptin OBESITY IS CHARACTERIZED by increased lipid availability, increased fatty acid (FA) uptake into skeletal muscle, increased intramuscular lipid stores, and insulin resistance (22,34,54). Leptin is an adipokine known to improve insulin response in skeletal muscle (27) and insulin-stimulated glucose disposal (56, 59), an effect largely attributed to an increase in FA oxidation and a decrease in intramuscular triacylglycerol (TAG) content (31). Skeletal muscle expresses all leptin receptor isoforms, and leptin's effects on FA oxidation are mediated, at least in part, by the activation of AMP-activated protein kinase (AMPK) (47). Leptin administration improves insulin signaling in skeletal muscle in obese and high-fat (HF) fed rodents; in particular, leptin administration can restore muscle glucose transport protein (GLUT4) content and Akt phosphorylation in rats fed a chronic HF diet (57). Leptin can also rapidly restore insulin-stimulated GLUT4 translocation in isolated muscle acutely exposed to high concentrations of palmitate, an effect strongly associated with the recovery of AS160 (Akt substrate of 160 kDa) phosphorylation (1). AS160 is one of the distal proteins in the insulin-signaling cascade, and its phosphorylation has been shown to have...

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“…In addition, a number of studies suggest that exercise stimulates fatty acid oxidation in the gastrocnemius muscle of mice (16,(25)(26)(27)(28). Therefore, we finally examined the effects of ESG and exercise on the mRNA levels of lipid metabolism-related genes in the gastrocnemius muscle in HFD-fed mice (Fig.…”

Section: Resultsmentioning

confidence: 99%

Effects of Enzymatically Synthesized Glycogen and Exercise on Abdominal Fat Accumulation in High-Fat Diet-Fed Mice

Tamura

Honda

Morinaga

et al. 2017

J Nutr Sci Vitaminol

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SummaryThe combination of diet and exercise is the first choice for the treatment of obesity and metabolic syndrome. We previously reported that enzymatically synthesized glycogen (ESG) suppresses abdominal fat accumulation in obese rats. However, the effect of the combination of ESG and exercise on abdominal fat accumulation has not yet been investigated. Our goal in this study was therefore to evaluate the effects of dietary ESG and its combination with exercise on abdominal fat accumulation in high-fat diet (HFD)-fed mice. Male ICR mice were assigned to four groups: HFD, HFD containing 20% ESG, HFD with exercise, HFD containing 20% ESG with exercise. Treadmill exercise was performed for 3 wk (25 m/ min, 30 min/d, 3 d/wk) after 5-d adaption to running at that speed. Both ESG and exercise significantly reduced the weights of abdominal adipose tissues. In addition, the combination of ESG and exercise significantly suppressed abdominal fat accumulation, suggesting that ESG and exercise showed an additive effect. Exercise significantly increased the mRNA levels of lipid metabolism-related genes such as lipoprotein lipase, peroxisome proliferator-activated receptor delta; factor-delta (PPARd), carnitin palmitoyltransferase b, adipose triglyceride lipase (ATGL), and uncoupling protein-3 in the gastrocnemius muscle. On the other hand, dietary ESG significantly decreased the mRNA levels of PPARd and ATGL in the gastrocnemius muscle. These results suggest that the combined treatment of ESG and exercise effectively suppresses abdominal fat accumulation in HFD-fed mice by different mechanisms.

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Astaxanthin improves muscle lipid metabolism in exercise via inhibitory effect of oxidative CPT I modification

Cited by 142 publications

References 33 publications

Astaxanthin: structural and functional aspects

Astaxanthin: structural and functional aspects

Recovered insulin response by 2 weeks of leptin administration in high-fat fed rats is associated with restored AS160 activation and decreased reactive lipid accumulation

Effects of Enzymatically Synthesized Glycogen and Exercise on Abdominal Fat Accumulation in High-Fat Diet-Fed Mice

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