T266M variants of ANGPTL4 improve lipid metabolism by modifying their binding affinity to acetyl-CoA carboxylase in obstructive sleep apnea

Angiopoietin-like protein 4 (ANGPTL4) is recognized as a crucial regulator in lipid metabolism. Acetyl-CoA carboxylases (ACACAs) play a role in the β-oxidation of fatty acids. Yet, the functions of ANGPTL4 and ACACA in dyslipidemia of obstructive sleep apnea (OSA) remain unclear. This study included...

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Published inAnnals of medicine (Helsinki) Vol. 56; no. 1; p. 2337740
Main Authors Li, Xinyi, Li, Chenyang, Xue, Wenjun, Wei, Zhicheng, Shen, Hangdong, Wu, Kejia, Zhu, Huaming, Xu, Huajun, Wu, Xiaolin, Yi, Hongliang, Guan, Jian, Yin, Shankai
Format Journal Article
LanguageEnglish
Published England Taylor & Francis Group 01.12.2024
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Online AccessGet full text
ISSN0785-3890
1365-2060
1365-2060
DOI10.1080/07853890.2024.2337740

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Abstract Angiopoietin-like protein 4 (ANGPTL4) is recognized as a crucial regulator in lipid metabolism. Acetyl-CoA carboxylases (ACACAs) play a role in the β-oxidation of fatty acids. Yet, the functions of ANGPTL4 and ACACA in dyslipidemia of obstructive sleep apnea (OSA) remain unclear. This study included 125 male OSA subjects from the Shanghai Sleep Health Study (SSHS) who were matched for age, body mass index (BMI), and lipid profile. Serum ANGPTL4 levels were measured ELISA. The ANGPTL4 T266M variants of 4455 subjects along with their anthropometric, fasting biochemical, and standard polysomnographic parameters were collected. Linear regression was used to analyze the associations between quantitative traits and ANGPTL4 T266M. Molecular docking and molecular dynamic simulation were employed to compare the effects of the wild-type ANGPTL4 and its T266M mutation on ACACA. Serum ANGPTL4 levels significantly decreased with increasing OSA severity (non-OSA: 59.6 ± 17.4 ng/mL, mild OSA: 50.0 ± 17.5 ng/mL, moderate OSA: 46.3 ± 15.5 ng/mL, severe OSA: 19.9 ± 14.3 ng/mL, respectively,  = 6.02 × 10 ). No associations were found between T266M and clinical characteristics. Molecular docking indicated that mutant ANGTPL4 T266M had stronger binding affinity for the ACACA protein, compared with wild-type ANGPTL4. In terms of protein secondary structure, mutant ANGTPL4 T266M demonstrated greater stability than wild-type ANGPTL4. Serum ANGTPL4 levels were significantly decreased in OSA patients, particularly among individuals with severe OSA. Although functional ANGTPL4 T266M variants were not associated with lipid levels in OSA, ANGTPL4 T266M could enhance binding affinity for the ACACA protein, potentially regulating lipid metabolism.
AbstractList Angiopoietin-like protein 4 (ANGPTL4) is recognized as a crucial regulator in lipid metabolism. Acetyl-CoA carboxylases (ACACAs) play a role in the β-oxidation of fatty acids. Yet, the functions of ANGPTL4 and ACACA in dyslipidemia of obstructive sleep apnea (OSA) remain unclear. This study included 125 male OSA subjects from the Shanghai Sleep Health Study (SSHS) who were matched for age, body mass index (BMI), and lipid profile. Serum ANGPTL4 levels were measured ELISA. The ANGPTL4 T266M variants of 4455 subjects along with their anthropometric, fasting biochemical, and standard polysomnographic parameters were collected. Linear regression was used to analyze the associations between quantitative traits and ANGPTL4 T266M. Molecular docking and molecular dynamic simulation were employed to compare the effects of the wild-type ANGPTL4 and its T266M mutation on ACACA. Serum ANGPTL4 levels significantly decreased with increasing OSA severity (non-OSA: 59.6 ± 17.4 ng/mL, mild OSA: 50.0 ± 17.5 ng/mL, moderate OSA: 46.3 ± 15.5 ng/mL, severe OSA: 19.9 ± 14.3 ng/mL, respectively,  = 6.02 × 10 ). No associations were found between T266M and clinical characteristics. Molecular docking indicated that mutant ANGTPL4 T266M had stronger binding affinity for the ACACA protein, compared with wild-type ANGPTL4. In terms of protein secondary structure, mutant ANGTPL4 T266M demonstrated greater stability than wild-type ANGPTL4. Serum ANGTPL4 levels were significantly decreased in OSA patients, particularly among individuals with severe OSA. Although functional ANGTPL4 T266M variants were not associated with lipid levels in OSA, ANGTPL4 T266M could enhance binding affinity for the ACACA protein, potentially regulating lipid metabolism.
Angiopoietin-like protein 4 (ANGPTL4) is recognized as a crucial regulator in lipid metabolism. Acetyl-CoA carboxylases (ACACAs) play a role in the β-oxidation of fatty acids. Yet, the functions of ANGPTL4 and ACACA in dyslipidemia of obstructive sleep apnea (OSA) remain unclear.BACKGROUNDAngiopoietin-like protein 4 (ANGPTL4) is recognized as a crucial regulator in lipid metabolism. Acetyl-CoA carboxylases (ACACAs) play a role in the β-oxidation of fatty acids. Yet, the functions of ANGPTL4 and ACACA in dyslipidemia of obstructive sleep apnea (OSA) remain unclear.This study included 125 male OSA subjects from the Shanghai Sleep Health Study (SSHS) who were matched for age, body mass index (BMI), and lipid profile. Serum ANGPTL4 levels were measured via ELISA. The ANGPTL4 T266M variants of 4455 subjects along with their anthropometric, fasting biochemical, and standard polysomnographic parameters were collected. Linear regression was used to analyze the associations between quantitative traits and ANGPTL4 T266M. Molecular docking and molecular dynamic simulation were employed to compare the effects of the wild-type ANGPTL4 and its T266M mutation on ACACA.METHODSThis study included 125 male OSA subjects from the Shanghai Sleep Health Study (SSHS) who were matched for age, body mass index (BMI), and lipid profile. Serum ANGPTL4 levels were measured via ELISA. The ANGPTL4 T266M variants of 4455 subjects along with their anthropometric, fasting biochemical, and standard polysomnographic parameters were collected. Linear regression was used to analyze the associations between quantitative traits and ANGPTL4 T266M. Molecular docking and molecular dynamic simulation were employed to compare the effects of the wild-type ANGPTL4 and its T266M mutation on ACACA.Serum ANGPTL4 levels significantly decreased with increasing OSA severity (non-OSA: 59.6 ± 17.4 ng/mL, mild OSA: 50.0 ± 17.5 ng/mL, moderate OSA: 46.3 ± 15.5 ng/mL, severe OSA: 19.9 ± 14.3 ng/mL, respectively, p = 6.02 × 10-16). No associations were found between T266M and clinical characteristics. Molecular docking indicated that mutant ANGTPL4 T266M had stronger binding affinity for the ACACA protein, compared with wild-type ANGPTL4. In terms of protein secondary structure, mutant ANGTPL4 T266M demonstrated greater stability than wild-type ANGPTL4.RESULTSSerum ANGPTL4 levels significantly decreased with increasing OSA severity (non-OSA: 59.6 ± 17.4 ng/mL, mild OSA: 50.0 ± 17.5 ng/mL, moderate OSA: 46.3 ± 15.5 ng/mL, severe OSA: 19.9 ± 14.3 ng/mL, respectively, p = 6.02 × 10-16). No associations were found between T266M and clinical characteristics. Molecular docking indicated that mutant ANGTPL4 T266M had stronger binding affinity for the ACACA protein, compared with wild-type ANGPTL4. In terms of protein secondary structure, mutant ANGTPL4 T266M demonstrated greater stability than wild-type ANGPTL4.Serum ANGTPL4 levels were significantly decreased in OSA patients, particularly among individuals with severe OSA. Although functional ANGTPL4 T266M variants were not associated with lipid levels in OSA, ANGTPL4 T266M could enhance binding affinity for the ACACA protein, potentially regulating lipid metabolism.CONCLUSIONSSerum ANGTPL4 levels were significantly decreased in OSA patients, particularly among individuals with severe OSA. Although functional ANGTPL4 T266M variants were not associated with lipid levels in OSA, ANGTPL4 T266M could enhance binding affinity for the ACACA protein, potentially regulating lipid metabolism.
AbstractBackground Angiopoietin-like protein 4 (ANGPTL4) is recognized as a crucial regulator in lipid metabolism. Acetyl-CoA carboxylases (ACACAs) play a role in the β-oxidation of fatty acids. Yet, the functions of ANGPTL4 and ACACA in dyslipidemia of obstructive sleep apnea (OSA) remain unclear.Methods This study included 125 male OSA subjects from the Shanghai Sleep Health Study (SSHS) who were matched for age, body mass index (BMI), and lipid profile. Serum ANGPTL4 levels were measured via ELISA. The ANGPTL4 T266M variants of 4455 subjects along with their anthropometric, fasting biochemical, and standard polysomnographic parameters were collected. Linear regression was used to analyze the associations between quantitative traits and ANGPTL4 T266M. Molecular docking and molecular dynamic simulation were employed to compare the effects of the wild-type ANGPTL4 and its T266M mutation on ACACA.Results Serum ANGPTL4 levels significantly decreased with increasing OSA severity (non-OSA: 59.6 ± 17.4 ng/mL, mild OSA: 50.0 ± 17.5 ng/mL, moderate OSA: 46.3 ± 15.5 ng/mL, severe OSA: 19.9 ± 14.3 ng/mL, respectively, p = 6.02 × 10−16). No associations were found between T266M and clinical characteristics. Molecular docking indicated that mutant ANGTPL4 T266M had stronger binding affinity for the ACACA protein, compared with wild-type ANGPTL4. In terms of protein secondary structure, mutant ANGTPL4 T266M demonstrated greater stability than wild-type ANGPTL4.Conclusions Serum ANGTPL4 levels were significantly decreased in OSA patients, particularly among individuals with severe OSA. Although functional ANGTPL4 T266M variants were not associated with lipid levels in OSA, ANGTPL4 T266M could enhance binding affinity for the ACACA protein, potentially regulating lipid metabolism.
Author Yin, Shankai
Shen, Hangdong
Guan, Jian
Yi, Hongliang
Wei, Zhicheng
Zhu, Huaming
Xu, Huajun
Li, Chenyang
Xue, Wenjun
Wu, Kejia
Wu, Xiaolin
Li, Xinyi
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Cites_doi 10.1093/sleep/zsy236
10.1016/S0002-9440(10)64285-X
10.1186/s12953-022-00198-y
10.1038/nrdp.2015.15
10.1136/jmedgenet-2015-103439
10.1073/pnas.0705041104
10.1098/rsob.150272
10.1006/abbi.1996.0031
10.1007/s00018-010-0414-7
10.1161/ATVBAHA.110.212209
10.1194/jlr.M400138-JLR200
10.1159/000327774
10.1042/BST20060223
10.1016/S0140-6736(13)60734-5
10.1164/rccm.202109-2044OC
10.1161/ATVBAHA.108.176917
10.1073/pnas.0408452102
10.1093/eurheartj/ehr097
10.1194/jlr.M034272
10.2174/1381612829666221219123937
10.1186/s12944-016-0231-6
10.1042/BSR20110102
10.3389/fendo.2018.00651
10.1038/ng1984
10.1164/rccm.201209-1688OC
10.1210/en.2005-0476
10.3390/biomedicines10112754
10.1136/thoraxjnl-2015-207403
10.1152/japplphysiol.00984.2016
10.1056/NEJM199304293281704
10.1016/s0065-2571(98)00016-8
10.1152/japplphysiol.00522.2005
10.1586/epr.12.12
10.1016/j.atherosclerosis.2014.10.028
10.1016/j.metop.2022.100177
10.1016/j.bbalip.2015.02.008
10.1016/j.metabol.2007.12.007
10.1186/1471-2350-12-89
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Keywords obstructive sleep apnea
molecular docking
molecular dynamic simulation
T266M, ACACA
Angiopoietin-like protein 4
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References e_1_3_6_30_1
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e_1_3_6_32_1
e_1_3_6_33_1
e_1_3_6_11_1
e_1_3_6_10_1
e_1_3_6_15_1
e_1_3_6_38_1
e_1_3_6_14_1
e_1_3_6_39_1
e_1_3_6_13_1
e_1_3_6_12_1
e_1_3_6_19_1
Iber C (e_1_3_6_29_1) 2007
e_1_3_6_34_1
e_1_3_6_18_1
e_1_3_6_35_1
e_1_3_6_17_1
e_1_3_6_36_1
e_1_3_6_16_1
e_1_3_6_37_1
e_1_3_6_20_1
e_1_3_6_21_1
e_1_3_6_22_1
e_1_3_6_2_1
e_1_3_6_40_1
e_1_3_6_6_1
e_1_3_6_5_1
e_1_3_6_4_1
e_1_3_6_3_1
e_1_3_6_9_1
e_1_3_6_8_1
e_1_3_6_7_1
e_1_3_6_27_1
e_1_3_6_28_1
e_1_3_6_23_1
e_1_3_6_24_1
e_1_3_6_25_1
e_1_3_6_26_1
References_xml – ident: e_1_3_6_5_1
  doi: 10.1093/sleep/zsy236
– ident: e_1_3_6_14_1
  doi: 10.1016/S0002-9440(10)64285-X
– ident: e_1_3_6_24_1
  doi: 10.1186/s12953-022-00198-y
– ident: e_1_3_6_4_1
  doi: 10.1038/nrdp.2015.15
– ident: e_1_3_6_17_1
  doi: 10.1136/jmedgenet-2015-103439
– ident: e_1_3_6_12_1
  doi: 10.1073/pnas.0705041104
– ident: e_1_3_6_9_1
  doi: 10.1098/rsob.150272
– ident: e_1_3_6_25_1
  doi: 10.1006/abbi.1996.0031
– ident: e_1_3_6_30_1
  doi: 10.1007/s00018-010-0414-7
– ident: e_1_3_6_39_1
  doi: 10.1161/ATVBAHA.110.212209
– ident: e_1_3_6_36_1
  doi: 10.1194/jlr.M400138-JLR200
– ident: e_1_3_6_32_1
  doi: 10.1159/000327774
– ident: e_1_3_6_21_1
  doi: 10.1042/BST20060223
– ident: e_1_3_6_3_1
  doi: 10.1016/S0140-6736(13)60734-5
– volume-title: The AASM manual for the scoring of sleep and associated events: rules, terminology and technical specifications
  year: 2007
  ident: e_1_3_6_29_1
– ident: e_1_3_6_28_1
  doi: 10.1164/rccm.202109-2044OC
– ident: e_1_3_6_18_1
  doi: 10.1161/ATVBAHA.108.176917
– ident: e_1_3_6_35_1
  doi: 10.1073/pnas.0408452102
– ident: e_1_3_6_13_1
  doi: 10.1093/eurheartj/ehr097
– ident: e_1_3_6_33_1
  doi: 10.1194/jlr.M034272
– ident: e_1_3_6_40_1
  doi: 10.2174/1381612829666221219123937
– ident: e_1_3_6_19_1
  doi: 10.1186/s12944-016-0231-6
– ident: e_1_3_6_8_1
  doi: 10.1042/BSR20110102
– ident: e_1_3_6_15_1
  doi: 10.3389/fendo.2018.00651
– ident: e_1_3_6_16_1
  doi: 10.1038/ng1984
– ident: e_1_3_6_34_1
  doi: 10.1164/rccm.201209-1688OC
– ident: e_1_3_6_37_1
  doi: 10.1210/en.2005-0476
– ident: e_1_3_6_6_1
  doi: 10.3390/biomedicines10112754
– ident: e_1_3_6_7_1
  doi: 10.1136/thoraxjnl-2015-207403
– ident: e_1_3_6_23_1
  doi: 10.1152/japplphysiol.00984.2016
– ident: e_1_3_6_2_1
  doi: 10.1056/NEJM199304293281704
– ident: e_1_3_6_22_1
  doi: 10.1016/s0065-2571(98)00016-8
– ident: e_1_3_6_27_1
  doi: 10.1152/japplphysiol.00522.2005
– ident: e_1_3_6_10_1
  doi: 10.1586/epr.12.12
– ident: e_1_3_6_11_1
  doi: 10.1016/j.atherosclerosis.2014.10.028
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  doi: 10.1016/j.metop.2022.100177
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  doi: 10.1016/j.bbalip.2015.02.008
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  doi: 10.1016/j.metabol.2007.12.007
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Snippet Angiopoietin-like protein 4 (ANGPTL4) is recognized as a crucial regulator in lipid metabolism. Acetyl-CoA carboxylases (ACACAs) play a role in the β-oxidation...
AbstractBackground Angiopoietin-like protein 4 (ANGPTL4) is recognized as a crucial regulator in lipid metabolism. Acetyl-CoA carboxylases (ACACAs) play a role...
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SubjectTerms Angiopoietin-like protein 4
molecular docking
molecular dynamic simulation
obstructive sleep apnea
T266M, ACACA
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Title T266M variants of ANGPTL4 improve lipid metabolism by modifying their binding affinity to acetyl-CoA carboxylase in obstructive sleep apnea
URI https://www.ncbi.nlm.nih.gov/pubmed/38574398
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