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Investigation of the prognostic predictive value of serum lipid profiles in amyotrophic lateral sclerosis: roles of sex and hypermetabolism.

NAKAMURA Ryutaro KURIHARA Mika 90467374 OGAWA Nobuhiro KITAMURA Akihiro 80636019 YAMAKAWA Isamu BAMBA Shigeki 40422901 0000-0002-4108-5894 SANADA Mitsuru 10418759 SASAKI Masaya 40242979 URUSHITANI Makoto 60332326 0000-0003-2773-9836 滋賀医科大学

2022.02.03

概要

The prognostic predictive value of lipid profiling in amyotrophic lateral sclerosis (ALS) remains unclear. Here, we aimed to clarify the value of the levels of serum lipids, including high-density lipoprotein cholesterol (HDL), low-density lipoprotein cholesterol (LDL), and triglycerides (TG), for predicting the prognosis in ALS. This was a single-center retrospective study of 78 patients with ALS. The serum lipid profiles at the first hospital visit after symptom onset were analyzed to determine the correlations of lipids with survival and physical parameters, including nutritional, respiratory, and metabolic conditions. The cutoff level for high HDL was defined as the third quartile, while that of low LDL and TG, as the first quartile. Hypermetabolism was defined as the ratio of resting energy expenditure to lean soft tissue mass ≥ 38 kcal/kg. High HDL was an independent factor for poor prognosis in all patients (hazards ratio [HR]: 9.87, p < 0.001) in the Cox proportional hazard model, including %vital capacity and the monthly decline rate in body mass index and the Revised Amyotrophic Lateral Functional Rating Scale score from symptom onset to diagnosis. Low LDL was a factor for poor prognosis (HR: 6.59, p = 0.017) only in women. Moreover, subgroup analyses with log-rank tests revealed that the prognostic predictive value of high HDL was evident only in the presence of hypermetabolism (p = 0.005). High HDL predicts poor prognosis in all patients, whereas low LDL, only in women. Hypermetabolism and high HDL synergistically augment the negative effect on prognosis.

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参考文献

1. Chiò, A. et al. Prognostic factors in ALS: A critical review. Amyotroph Lateral Scler 10, 310–323. https://​doi.​org/​10.​3109/​17482​

96080​25668​24 (2009).

2. Ludolph, A. C. et al. Effect of high-caloric nutrition on survival in amyotrophic lateral sclerosis. Ann Neurol 2020(87), 206–216.

https://​doi.​org/​10.​1002/​ana.​25661​[publi​shedO​nline​First:​19Dec​ember (2019).

3. Khamankar, N. et al. Associative increases in amyotrophic lateral sclerosis Survival duration with non-invasive ventilation initiation and usage protocols. Front Neurol 9, 578. https://​doi.​org/​10.​3389/​fneur.​2018.​00578 (2018).

4. Bouteloup, C. et al. Hypermetabolism in ALS patients: an early and persistent phenomenon. J Neurol 2009(256), 1236–1242.

https://​doi.​org/​10.​1007/​s00415-​009-​5100-​z[publi​shedO​nline​First:​24Mar​ch (2009).

5. Steyn, F. J. et al. Hypermetabolism in ALS is associated with greater functional decline and shorter survival. J Neurol Neurosurg

Psychiatry 2018(89), 1016–1023. https://​doi.​org/​10.​1136/​jnnp-​2017-​31788​7[publi​shedO​nline​First:​1May (2018).

6. He, J. et al. Hypermetabolism associated with worse prognosis of amyotrophic lateral sclerosis. J Neurol https://​doi.​org/​10.​1007/​

s00415-​021-​10716-1 (2021).

7. Steyn, F. J. et al. Altered skeletal muscle glucose-fatty acid flux in amyotrophic lateral sclerosis. Brain Commun 2, fcaa154. https://​

doi.​org/​10.​1093/​brain​comms/​fcaa1​54(2020) (2020).

8. Nakamura, R. et al. Prognostic prediction by hypermetabolism varies depending on the nutritional status in early amyotrophic

lateral sclerosis. Sci Rep 11, 17943. https://​doi.​org/​10.​1038/​s41598-​021-​97196-5 (2021).

9. Marin, B. et al. Alteration of nutritional status at diagnosis is a prognostic factor for survival of amyotrophic lateral sclerosis patients.

J Neurol Neurosurg Psychiatry 2011(82), 628–634. https://​doi.​org/​10.​1136/​jnnp.​2010.​21147​4[publi​shedO​nline​First:​19Nov​ember

(2010).

10. Dorst, J. et al. Patients with elevated triglyceride and cholesterol serum levels have a prolonged survival in amyotrophic lateral

sclerosis. J Neurol 2011(258), 613–617. https://​doi.​org/​10.​1007/​s00415-​010-​5805-z (2010).

11. Huang, R. et al. The serum lipid profiles of amyotrophic lateral sclerosis patients: a study from south-west China and a metaanalysis. Amyotroph Lateral Scler Frontotemporal Degener 2015(16), 359–365. https://​doi.​org/​10.​3109/​21678​421.​2015.​10474​54

(2015).

12. Mandrioli, J. et al. Changes in routine laboratory tests and survival in amyotrophic lateral sclerosis. Neurol Sci 2017(38), 2177–2182.

https://​doi.​org/​10.​1007/​s10072-​017-​3138-8 (2017).

13. Rafiq, M. K. et al. Effect of lipid profile on prognosis in the patients with amyotrophic lateral sclerosis: insights from the olesoxime

clinical trial. Amyotroph Lateral Scler Frontotemporal Degener 2015(16), 478–484. https://​doi.​org/​10.​3109/​21678​421.​2015.​10625​

17[publi​shedO​nline​First:​10July (2015).

14. Ikeda, K. et al. Relationships between disease progression and serum levels of lipid, urate, creatinine and ferritin in Japanese patients

with amyotrophic lateral sclerosis: a cross-sectional study. Intern Med 2012(51), 1501–1508. https://​doi.​org/​10.​2169/​inter​nalme​

dicine.​51.​7465[publi​shedO​nline​First:​15June (2012).

Scientific Reports |

Vol:.(1234567890)

(2022) 12:1826 |

https://doi.org/10.1038/s41598-022-05714-w

www.nature.com/scientificreports/

15. Wuolikainen, A. et al. Cholesterol, oxysterol, triglyceride, and coenzyme Q homeostasis in ALS. Evidence against the hypothesis

that elevated 27-hydroxycholesterol is a pathogenic factor. PLoS ONE 9, e113619. https://​doi.​org/​10.​1371/​journ​al.​pone.​01136​19

(2014).

16. Chiò, A. et al. Lower serum lipid levels are related to respiratory impairment in patients with ALS. Neurology 73, 1681–1685.

https://​doi.​org/​10.​1212/​WNL.​0b013​e3181​c1df1e (2009).

17. Chiò, A. et al. Amyotrophic lateral sclerosis outcome measures and the role of albumin and creatinine: a population-based study.

JAMA Neurol 71, 1134–1142. https://​doi.​org/​10.​1001/​jaman​eurol.​2014.​1129 (2014).

18. Barros, A. N. A. B. et al. Association of copper status with lipid profile and functional status in patients with amyotrophic lateral

sclerosis. J Nutr Metab 2018, 5678698. https://​doi.​org/​10.​1155/​2018/​56786​98 (2018).

19. Liu, J. et al. Lipid profile in patients with amyotrophic lateral sclerosis: a systematic review and meta-analysis. Front Neurol 11,

567753. https://​doi.​org/​10.​3389/​fneur.​2020.​567753 (2020).

20. Ingre, C. et al. Lipids, apolipoproteins, and prognosis of amyotrophic lateral sclerosis. Neurology 2020(94), e1835–e1844. https://​

doi.​org/​10.​1212/​WNL.​00000​00000​009322 (2020).

21. Brooks, B. R. et al. El Escorial revisited: revised criteria for the diagnosis of amyotrophic lateral sclerosis. Amyotroph Lateral Scler

Other Motor Neuron Disord 1, 293–299. https://​doi.​org/​10.​1080/​14660​82003​00079​536 (2000).

22. Cedarbaum, J. M. et al. The ALSFRS-R: a revised ALS functional rating scale that incorporates assessments of respiratory function.

BDNF ALS Study Group (Phase III). J Neurol Sci 169, 13–21. https://​doi.​org/​10.​1016/​s0022-​510x(99)​00210-5 (1999).

23. Nordestgaard, B. G. et al. Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications

including flagging at desirable concentration cut-points-a joint consensus statement from the European Atherosclerosis Society

and European Federation of Clinical Chemistry and Laboratory Medicine. Eur Heart J 2016(37), 1944–1958. https://​doi.​org/​10.​

1093/​eurhe​artj/​ehw15​2[publi​shedO​nline​First:​26Apr​il (2016).

24. Takaoka, A. et al. Comparison of energy metabolism and nutritional status of hospitalized patients with Crohn’s disease and those

with ulcerative colitis. J Clin Biochem Nutr 2015(56), 208–214. https://​doi.​org/​10.​3164/​jcbn.​14-​95[publi​shedO​nline​First:​14Apr​il

(2015).

25. Desport, J. C. et al. Factors correlated with hypermetabolism in patients with amyotrophic lateral sclerosis. Am J Clin Nutr 74,

328–334. https://​doi.​org/​10.​1093/​ajcn/​74.3.​328 (2001).

26. Harris, J. A. & Benedict, F. G. A biometric study of human basal metabolism. Proc Natl Acad Sci USA 4, 370–373. https://​doi.​org/​

10.​1073/​pnas.4.​12.​370 (1918).

27. Miyake, R. et al. Validity of predictive equations for basal metabolic rate in Japanese adults. J Nutr Sci Vitaminol (Tokyo) 57,

224–232. https://​doi.​org/​10.​3177/​jnsv.​57.​224 (2011).

28. Kanda, Y. Investigation of the freely available easy-to-use software “EZR” for medical statistics. Bone Marrow Transplant 2013(48),

452–458. https://​doi.​org/​10.​1038/​bmt.​2012.​244 (2012).

29. Dedic, S. I. et al. Is hyperlipidemia correlated with longer survival in patients with amyotrophic lateral sclerosis?. Neurol Res

2012(34), 576–580. https://​doi.​org/​10.​1179/​17431​32812Y.​00000​00049 (2012).

30. Andersson, S. et al. Inactivation of liver X receptor beta leads to adult-onset motor neuron degeneration in male mice. Proc Natl

Acad Sci USA 2005(102), 3857–3862. https://​doi.​org/​10.​1073/​pnas.​05006​34102 (2005).

31. Choi, C. I. et al. Effects of estrogen on lifespan and motor functions in female hSOD1 G93A transgenic mice. J Neurol Sci 2008(268),

40–47. https://​doi.​org/​10.​1016/j.​jns.​2007.​10.​024 (2007).

32. Tang, S. et al. Apolipoprotein A-I enhances insulin-dependent and insulin-independent glucose uptake by skeletal muscle. Sci Rep

9, 1350. https://​doi.​org/​10.​1038/​s41598-​018-​38014-3 (2019).

33. Lehti, M. et al. High-density lipoprotein maintains skeletal muscle function by modulating cellular respiration in mice. Circulation

2013(128), 2364–2371. https://​doi.​org/​10.​1161/​CIRCU​LATIO​NAHA.​113.​001551 (2013).

34. Wang, S. & Peng, D. Regulation of adipocyte autophagy–the potential anti-obesity mechanism of high density lipoprotein and

apolipoproteinA-I. Lipids Health Dis 11, 131. https://​doi.​org/​10.​1186/​1476-​511X-​11-​131 (2012).

35. Manzo, E. et al. Glycolysis upregulation is neuroprotective as a compensatory mechanism in ALS. Elife https://​doi.​org/​10.​7554/​

eLife.​45114 (2019).

36. Ferri, A. & Coccurello, R. What is “hyper” in the ALS hypermetabolism?. Mediators Inflamm 2017, 7821672. https://​doi.​org/​10.​

1155/​2017/​78216​72 (2017).

37. Bruckert, E. et al. High prevalence of low HDL-cholesterol in a pan-European survey of 8545 dyslipidaemic patients. Curr Med

Res Opin 21, 1927–1934. https://​doi.​org/​10.​1185/​03007​9905X​74871 (2005).

Acknowledgements

We appreciate the support of Jun Matsubayashi and Shoji Momokawa from the Center for Clinical Research

and Advanced Medicine at the Shiga University of Medical Science. We thank all the patients with ALS who

participated in this study.

Author contributions

R.N. and M.U. designed the research, analyzed the data, and wrote the manuscript. M. S., A. K., I. Y., and N. O.

analyzed the data. M.K. and M.S. measured the RQ and REE and analyzed the data. All authors reviewed the

manuscript.

Funding

This study was supported by an intramural research fund from the Shiga University of Medical Science.

Competing interests The authors declare no competing interests.

Additional information

Supplementary Information The online version contains supplementary material available at https://​doi.​org/​

10.​1038/​s41598-​022-​05714-w.

Correspondence and requests for materials should be addressed to M.U.

Reprints and permissions information is available at www.nature.com/reprints.

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and

institutional affiliations.

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