Fatty Acid Pattern of Lipids in Normal and Dystrophic Human Muscle

Kunze, D; Reichmann, G.; Egger, E; Olthoff, D; Döhler, K.-D.

doi:10.1111/j.1365-2362.1975.tb02311.x

Cited by 24 publications

(5 citation statements)

References 18 publications

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“…Additionally, membrane vesicles possess the ability to transport lipid droplets in human astrocytes and rat adipocytes (Muller et al, 2009;Falchi et al, 2013). Cell membrane dysfunction could lead to fatty acid metabolism disturbances (Kunze et al, 1975). Our results suggest that bdmew may play a key role in fatty acid metabolism.…”

Section: Discussionmentioning

confidence: 79%

Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR‐associated 9‐mediated mutagenesis of the multiple edematous wings gene induces muscle weakness and flightlessness in Bactrocera dorsalis (Diptera: Tephritidae)

Zheng

Sun

et al. 2018

Insect Molecular Biology

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The clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR‐associated 9 (Cas9) system is a versatile, efficient and heritable gene editing tool that can be useful for genome engineering. Bactrocera dorsalis (Hendel) is a major pest of agriculture that causes great economic losses. We used the B. dorsalis multiple edematous wings (Bdmew) gene as the target gene to explore the effectiveness of CRISPR/Cas9 for B. dorsalis genome manipulation. We studied the physiological functions of the Bdmew gene, particularly those related to muscle development. Site‐specific genome editing was feasible using direct microinjection of specific guide RNA and the Cas9‐plasmid into B. dorsalis embryos. Mutation frequencies ranged from 12.1 to 30.2% in the injected generation. Mosaic G0, with the mew mutation, was heritable to the next generation. The G1 displayed a series of defective phenotypes including muscle weakness, flightlessness, failure to eclose, wing folds and unbalanced movement. These results demonstrated that CRISPR/Cas9 can act as a highly specific, efficient, heritable tool for genome manipulation in B. dorsalis and this has significance for gene function research and genetic control of pests. The Bdmew gene possesses key functions in muscle development of B. dorsalis. Bdmew mutations cause a series of serious defects by interfering with muscle development and may provide a means for controlling B. dorsalis via a gene‐based method such as gene drive.

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Section: Discussionmentioning

confidence: 79%

Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR‐associated 9‐mediated mutagenesis of the multiple edematous wings gene induces muscle weakness and flightlessness in Bactrocera dorsalis (Diptera: Tephritidae)

Zheng

Sun

et al. 2018

Insect Molecular Biology

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“…This applies particularly to choline phosphoglyceride, ethanolamine phosphoglyceride and sphingomyelin. Takagi et al (1968) and Kunze et al (1975) reported an increase in the fatty acid 18:1 and a decrease in 18:2 in phosphatidylcholine in dystrophic muscle. Kunze et al (1975) also analysed phosphatidylethanolamine and sphingomyelin, but their profiles even for normal muscle were unusual.…”

Section: Discussionmentioning

confidence: 96%

“…Takagi et al (1968) and Kunze et al (1975) reported an increase in the fatty acid 18:1 and a decrease in 18:2 in phosphatidylcholine in dystrophic muscle. Kunze et al (1975) also analysed phosphatidylethanolamine and sphingomyelin, but their profiles even for normal muscle were unusual. A similar criticism has been levelled at their data for erythrocytes (Plishker and Appel, 1980) and suggests that there is some problem in their methodology.…”

Section: Discussionmentioning

confidence: 96%

“…Phospholipids are important components of cell membranes and have been the subject of numerous biochemical studies in both muscle and erythrocytes in muscular dystrophy (Rowland (1980) and Plishker and Appel (1980), respectively, for reviews). Takagi et al (1968), Kunze and Olthoff (1970), Hughes (1972) and Kunze et al (1975) have reported changes in the phospholipid composition of dystrophic muscle, but Takagi, Schodand and Rowland (1973) have since stressed the problems arising from the infiltration of the muscle with fat and connective tissue. Furthermore, workers from several laboratories (Kobayashi, Mawatari and Kuroiwa, 1978;Koski, Jungalwala and Kolodny, 1978;Ruitenbeek, 1978;McLaughlin and Engel, 1979) have described discrepancies between their work and that of Kunze et al (1973) on the phospholipid composition of erythrocytes, and they have been unable to substantiate the reports of Kunze et al (1973) and Kaiofoutis, Jullien and Spanos (1977) about alterations in erythrocyte lipids in muscular dystrophy.…”

Section: Introductionmentioning

confidence: 99%

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Muscle Lipids in Duchenne Muscular Dystrophy

Pearce

Johnsen

Wysocki

et al. 1981

Aust J Exp Biol Med

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Summary The lipids of muscle and adipose tissue from normal males and of muscle from males with Duchenne muscular dystrophy were investigated. Triglyceride, the major neutral lipid, showed similar fatty acid compositions in all tissues examined. When the phospholipids of dystrophic muscle and of normal adipose tissue were compared with those of normal muscle, it was found that there was an increase in the proportion of sphingomyelin in dystrophic muscle, while adipose tissue had higher proportions of sphingomyelin and lysophosphatidylcholine but lower choline phosphoglyceride. In dystrophic muscle only small alterations from normal were observed in the fatty acid compositions of the individual phospholipids, whereas the phospholipids of adipose tissue had quite distinctive fatty acid compositions. An atrophic muscle sample resulting from poliomyelitis consisted almost entirely of connective tissue and fat and had a phospholipid composition similar to that of adipose tissue. From a comparison of the results for all the types of tissue studied, it is evident that the increase in sphingomyelin in dystrophic muscle biopsies and the changes in the fatty acid compositions of individual phospholipids may be accounted for by the increased amounts of fat and connective tissue which are present in dystrophic muscle samples. In a case each of polymyositis, limb girdle muscular dystrophy and an autosomal recessive form of muscular dystrophy, the results obtained for the phospholipid composition of the muscle sample were also normal or consistent with some contamination from fat and connective tissue.

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“…Compared with those in their wild-type counterparts on the same diet, skeletal muscle phospholipid (PL) in mdx mice exhibit increased oleic acid (18 : 1) and linoleic acid (18 : 2) abundances and reduced DHA (22 : 6) abundance ( 3 ) . Results from similar assessments of fatty acid (FA) composition in the muscle of human subjects with DMD are unclear due to a lack of dietary control in these studies ( 4 – 6 ) as well as issues related to age matching and sample handling ( 5 ) . In DMD and the mdx mouse, the skeletal muscle sarcolemma is destabilised as a result of a mutation in the dystrophin gene ( 2 ) .…”

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confidence: 99%

Compared with that of MUFA, a high dietary intake ofn-3 PUFA does not reduce the degree of pathology in mdx mice

et al. 2014

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Duchenne muscular dystrophy (DMD) is a severe muscle disease that affects afflicted males from a young age, and the mdx mouse is an animal model of this disease. Although new drugs are in development, it is also essential to assess potential dietary therapies that could assist in the management of DMD. In the present study, we compared two diets, high-MUFA diet v. high-PUFA diet, in mdx mice. To generate the high-PUFA diet, a portion of dietary MUFA (oleic acid) was replaced with the dietary essential n-3 PUFA a-linolenic acid (ALA). We sought to determine whether ALA, compared with oleic acid, was beneficial in mdx mice. Consumption of the high-PUFA diet resulted in significantly higher n-3 PUFA content and reduced arachidonic acid content in skeletal muscle phospholipids (PL), while the high-MUFA diet led to higher oleate content in PL. Mdx mice on the high-MUFA diet exhibited 2-fold lower serum creatine kinase activity than those on the high-PUFA diet (P,0·05) as well as a lower body fat percentage (P, 0·05), but no significant difference in skeletal muscle histopathology results. There was no significant difference between the dietary groups with regard to phosphorylated p65 (an inflammatory marker) in skeletal muscle.In conclusion, alteration of PL fatty acid (FA) composition by the high-PUFA diet made mdx muscle more susceptible to sarcolemmal leakiness, while the high-MUFA diet exhibited a more favourable impact. These results may be important for designing dietary treatments for DMD patients, and future work on dietary FA profiles, such as comparing other FA classes and dose effects, is needed.Key words: Dystrophic muscle: n-3 Fatty acids: Olive oil: Flaxseed oil Duchenne muscular dystrophy (DMD) is an X-linked, recessive, degenerative muscle disease, and the mdx mouse is an animal model of DMD (1) . Approximately one in 3500 boys are afflicted with the disease (2) . Compared with those in their wild-type counterparts on the same diet, skeletal muscle phospholipid (PL) in mdx mice exhibit increased oleic acid (18 : 1) and linoleic acid (18 : 2) abundances and reduced DHA (22 : 6) abundance (3) . Results from similar assessments of fatty acid (FA) composition in the muscle of human subjects with DMD are unclear due to a lack of dietary control in these studies (4 -6) as well as issues related to age matching and sample handling (5) . In DMD and the mdx mouse, the skeletal muscle sarcolemma is destabilised as a result of a mutation in the dystrophin gene (2) . Corticosteroid treatment is useful but not sufficiently effective (7) , and lifestyle changes could be additionally useful to favourably alter the trajectory of disease progression. Little is known regarding appropriate dietary recommendations for patients with DMD. However, based on known dysfunction in dystrophic muscle, hypotheses can be generated. The skeletal muscle of DMD patients (8,9) and mdx mice (10 -14) exhibits high levels of inflammation and membrane permeability or leakiness. Therefore, dietary treatments that could alter the...

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Fatty Acid Pattern of Lipids in Normal and Dystrophic Human Muscle

Cited by 24 publications

References 18 publications

Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR‐associated 9‐mediated mutagenesis of the multiple edematous wings gene induces muscle weakness and flightlessness in Bactrocera dorsalis (Diptera: Tephritidae)

Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR‐associated 9‐mediated mutagenesis of the multiple edematous wings gene induces muscle weakness and flightlessness in Bactrocera dorsalis (Diptera: Tephritidae)

Muscle Lipids in Duchenne Muscular Dystrophy

Compared with that of MUFA, a high dietary intake ofn-3 PUFA does not reduce the degree of pathology in mdx mice

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