Obese Mice with Dyslipidemia Exhibit Meibomian Gland Hypertrophy and Alterations in Meibum Composition and Aqueous Tear Production
Background: Dyslipidemia may be linked to meibomian gland dysfunction (MGD) and altered meibum lipid composition. The purpose was to determine if plasma and meibum cholesteryl esters (CE), triglycerides (TG), ceramides (Cer) and sphingomyelins (SM) change in a mouse model of diet-induced obesity whe...
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| Vydané v: | International journal of molecular sciences Ročník 21; číslo 22; s. 8772 |
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20.11.2020
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| Abstract | Background: Dyslipidemia may be linked to meibomian gland dysfunction (MGD) and altered meibum lipid composition. The purpose was to determine if plasma and meibum cholesteryl esters (CE), triglycerides (TG), ceramides (Cer) and sphingomyelins (SM) change in a mouse model of diet-induced obesity where mice develop dyslipidemia. Methods: Male C57/BL6 mice (8/group, age = 6 wks) were fed a normal (ND; 15% kcal fat) or an obesogenic high-fat diet (HFD; 42% kcal fat) for 10 wks. Tear production was measured and meibography was performed. Body and epididymal adipose tissue (eAT) weights were determined. Nano-ESI-MS/MS and LC-ESI-MS/MS were used to detect CE, TG, Cer and SM species. Data were analyzed by principal component analysis, Pearson’s correlation and unpaired t-tests adjusted for multiple comparisons; significance set at p ≤ 0.05. Results: Compared to ND mice, HFD mice gained more weight and showed heavier eAT and dyslipidemia with higher levels of plasma CE, TG, Cer and SM. HFD mice had hypertrophic meibomian glands, increased levels of lipid species acylated by saturated fatty acids in plasma and meibum and excessive tear production. Conclusions: The majority of meibum lipid species with saturated fatty acids increased with HFD feeding with evidence of meibomian gland hypertrophy and excessive tearing. The dyslipidemia is associated with altered meibum composition, a key feature of MGD. |
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| AbstractList | Background: Dyslipidemia may be linked to meibomian gland dysfunction (MGD) and altered meibum lipid composition. The purpose was to determine if plasma and meibum cholesteryl esters (CE), triglycerides (TG), ceramides (Cer) and sphingomyelins (SM) change in a mouse model of diet-induced obesity where mice develop dyslipidemia. Methods: Male C57/BL6 mice (8/group, age = 6 wks) were fed a normal (ND; 15% kcal fat) or an obesogenic high-fat diet (HFD; 42% kcal fat) for 10 wks. Tear production was measured and meibography was performed. Body and epididymal adipose tissue (eAT) weights were determined. Nano-ESI-MS/MS and LC-ESI-MS/MS were used to detect CE, TG, Cer and SM species. Data were analyzed by principal component analysis, Pearson’s correlation and unpaired t-tests adjusted for multiple comparisons; significance set at p ≤ 0.05. Results: Compared to ND mice, HFD mice gained more weight and showed heavier eAT and dyslipidemia with higher levels of plasma CE, TG, Cer and SM. HFD mice had hypertrophic meibomian glands, increased levels of lipid species acylated by saturated fatty acids in plasma and meibum and excessive tear production. Conclusions: The majority of meibum lipid species with saturated fatty acids increased with HFD feeding with evidence of meibomian gland hypertrophy and excessive tearing. The dyslipidemia is associated with altered meibum composition, a key feature of MGD. Dyslipidemia may be linked to meibomian gland dysfunction (MGD) and altered meibum lipid composition. The purpose was to determine if plasma and meibum cholesteryl esters (CE), triglycerides (TG), ceramides (Cer) and sphingomyelins (SM) change in a mouse model of diet-induced obesity where mice develop dyslipidemia. Male C57/BL6 mice (8/group, age = 6 wks) were fed a normal (ND; 15% kcal fat) or an obesogenic high-fat diet (HFD; 42% kcal fat) for 10 wks. Tear production was measured and meibography was performed. Body and epididymal adipose tissue (eAT) weights were determined. Nano-ESI-MS/MS and LC-ESI-MS/MS were used to detect CE, TG, Cer and SM species. Data were analyzed by principal component analysis, Pearson's correlation and unpaired -tests adjusted for multiple comparisons; significance set at ≤ 0.05. Compared to ND mice, HFD mice gained more weight and showed heavier eAT and dyslipidemia with higher levels of plasma CE, TG, Cer and SM. HFD mice had hypertrophic meibomian glands, increased levels of lipid species acylated by saturated fatty acids in plasma and meibum and excessive tear production. The majority of meibum lipid species with saturated fatty acids increased with HFD feeding with evidence of meibomian gland hypertrophy and excessive tearing. The dyslipidemia is associated with altered meibum composition, a key feature of MGD. Dyslipidemia may be linked to meibomian gland dysfunction (MGD) and altered meibum lipid composition. The purpose was to determine if plasma and meibum cholesteryl esters (CE), triglycerides (TG), ceramides (Cer) and sphingomyelins (SM) change in a mouse model of diet-induced obesity where mice develop dyslipidemia.BACKGROUNDDyslipidemia may be linked to meibomian gland dysfunction (MGD) and altered meibum lipid composition. The purpose was to determine if plasma and meibum cholesteryl esters (CE), triglycerides (TG), ceramides (Cer) and sphingomyelins (SM) change in a mouse model of diet-induced obesity where mice develop dyslipidemia.Male C57/BL6 mice (8/group, age = 6 wks) were fed a normal (ND; 15% kcal fat) or an obesogenic high-fat diet (HFD; 42% kcal fat) for 10 wks. Tear production was measured and meibography was performed. Body and epididymal adipose tissue (eAT) weights were determined. Nano-ESI-MS/MS and LC-ESI-MS/MS were used to detect CE, TG, Cer and SM species. Data were analyzed by principal component analysis, Pearson's correlation and unpaired t-tests adjusted for multiple comparisons; significance set at p ≤ 0.05.METHODSMale C57/BL6 mice (8/group, age = 6 wks) were fed a normal (ND; 15% kcal fat) or an obesogenic high-fat diet (HFD; 42% kcal fat) for 10 wks. Tear production was measured and meibography was performed. Body and epididymal adipose tissue (eAT) weights were determined. Nano-ESI-MS/MS and LC-ESI-MS/MS were used to detect CE, TG, Cer and SM species. Data were analyzed by principal component analysis, Pearson's correlation and unpaired t-tests adjusted for multiple comparisons; significance set at p ≤ 0.05.Compared to ND mice, HFD mice gained more weight and showed heavier eAT and dyslipidemia with higher levels of plasma CE, TG, Cer and SM. HFD mice had hypertrophic meibomian glands, increased levels of lipid species acylated by saturated fatty acids in plasma and meibum and excessive tear production.RESULTSCompared to ND mice, HFD mice gained more weight and showed heavier eAT and dyslipidemia with higher levels of plasma CE, TG, Cer and SM. HFD mice had hypertrophic meibomian glands, increased levels of lipid species acylated by saturated fatty acids in plasma and meibum and excessive tear production.The majority of meibum lipid species with saturated fatty acids increased with HFD feeding with evidence of meibomian gland hypertrophy and excessive tearing. The dyslipidemia is associated with altered meibum composition, a key feature of MGD.CONCLUSIONSThe majority of meibum lipid species with saturated fatty acids increased with HFD feeding with evidence of meibomian gland hypertrophy and excessive tearing. The dyslipidemia is associated with altered meibum composition, a key feature of MGD. |
| Author | Brodesser, Susanne Rumbaut, Rolando E. Steven, Philipp Chintapalati, Madhavi Redfern, Rachel Hanlon, Samuel Burns, Alan R. Bullock, Tiffany Smith, C. Wayne Osae, Eugene A. |
| AuthorAffiliation | 1 College of Optometry, University of Houston, Houston, TX 77204, USA; sdhanlon@gmail.com (S.H.); rredfer2@central.uh.edu (R.R.); arburns2@central.uh.edu (A.R.B.) 5 Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX 77030, USA 3 CECAD Research Center, Lipidomics/Metabolomics Facility, University of Cologne, 50931 Cologne, Germany; susanne.brodesser@uk-koeln.de 4 Department of Ophthalmology, Division for Dry-Eye and Ocular GvHD, Medical Faculty, University of Cologne, 50937 Cologne, Germany; philipp.steven@uk-koeln.de 2 Children’s Nutrition Research Center, Baylor College of Medicine, Houston, TX 77030, USA; tbullock@bcm.edu (T.B.); chintala@bcm.edu (M.C.); cwsmith@bcm.edu (C.W.S.); rrumbaut@bcm.edu (R.E.R.) |
| AuthorAffiliation_xml | – name: 3 CECAD Research Center, Lipidomics/Metabolomics Facility, University of Cologne, 50931 Cologne, Germany; susanne.brodesser@uk-koeln.de – name: 5 Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX 77030, USA – name: 1 College of Optometry, University of Houston, Houston, TX 77204, USA; sdhanlon@gmail.com (S.H.); rredfer2@central.uh.edu (R.R.); arburns2@central.uh.edu (A.R.B.) – name: 4 Department of Ophthalmology, Division for Dry-Eye and Ocular GvHD, Medical Faculty, University of Cologne, 50937 Cologne, Germany; philipp.steven@uk-koeln.de – name: 2 Children’s Nutrition Research Center, Baylor College of Medicine, Houston, TX 77030, USA; tbullock@bcm.edu (T.B.); chintala@bcm.edu (M.C.); cwsmith@bcm.edu (C.W.S.); rrumbaut@bcm.edu (R.E.R.) |
| Author_xml | – sequence: 1 givenname: Eugene A. orcidid: 0000-0002-2059-7823 surname: Osae fullname: Osae, Eugene A. – sequence: 2 givenname: Tiffany surname: Bullock fullname: Bullock, Tiffany – sequence: 3 givenname: Madhavi surname: Chintapalati fullname: Chintapalati, Madhavi – sequence: 4 givenname: Susanne orcidid: 0000-0001-5631-0663 surname: Brodesser fullname: Brodesser, Susanne – sequence: 5 givenname: Samuel surname: Hanlon fullname: Hanlon, Samuel – sequence: 6 givenname: Rachel surname: Redfern fullname: Redfern, Rachel – sequence: 7 givenname: Philipp orcidid: 0000-0001-6892-3619 surname: Steven fullname: Steven, Philipp – sequence: 8 givenname: C. Wayne surname: Smith fullname: Smith, C. Wayne – sequence: 9 givenname: Rolando E. surname: Rumbaut fullname: Rumbaut, Rolando E. – sequence: 10 givenname: Alan R. surname: Burns fullname: Burns, Alan R. |
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| Keywords | lipids meibomian gland dysfunction mass spectrometry meibum dry eye dyslipidemia obesity |
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| Snippet | Background: Dyslipidemia may be linked to meibomian gland dysfunction (MGD) and altered meibum lipid composition. The purpose was to determine if plasma and... Dyslipidemia may be linked to meibomian gland dysfunction (MGD) and altered meibum lipid composition. The purpose was to determine if plasma and meibum... |
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| SubjectTerms | Adipose Tissue - chemistry Adipose Tissue - metabolism Animals Ceramides - classification Ceramides - isolation & purification Ceramides - metabolism Cholesterol Esters - classification Cholesterol Esters - isolation & purification Cholesterol Esters - metabolism Diet, High-Fat - adverse effects Dyslipidemias - etiology Dyslipidemias - metabolism Dyslipidemias - pathology Epididymis - chemistry Epididymis - metabolism Fasting Fatty acids Humans Hypertrophy - etiology Hypertrophy - metabolism Hypertrophy - pathology Lipids Male Mass spectrometry Meibomian Glands - metabolism Meibomian Glands - pathology Metabolic disorders Mice Mice, Inbred C57BL Mice, Obese Obesity Obesity - etiology Obesity - metabolism Obesity - pathology Plasma Principal Component Analysis Scientific imaging Sphingomyelins - classification Sphingomyelins - isolation & purification Sphingomyelins - metabolism Tears - chemistry Tears - metabolism Triglycerides Triglycerides - classification Triglycerides - isolation & purification Triglycerides - metabolism |
| Title | Obese Mice with Dyslipidemia Exhibit Meibomian Gland Hypertrophy and Alterations in Meibum Composition and Aqueous Tear Production |
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