Diabetic nephropathy induces alterations in the glomerular and tubule lipid profiles

Diabetic nephropathy (DN) is a major life-threatening complication of diabetes. Renal lesions affect glomeruli and tubules, but the pathogenesis is not completely understood. Phospholipids and glycolipids are molecules that carry out multiple cell functions in health and disease, and their role in D...

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Vydané v:Journal of lipid research Ročník 55; číslo 7; s. 1375
Hlavní autori: Grove, Kerri J, Voziyan, Paul A, Spraggins, Jeffrey M, Wang, Suwan, Paueksakon, Paisit, Harris, Raymond C, Hudson, Billy G, Caprioli, Richard M
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 01.07.2014
Predmet:
Animals
Diabetic Nephropathies - genetics
Diabetic Nephropathies - metabolism
Diabetic Nephropathies - pathology
Glycolipids - genetics
Glycolipids - metabolism
Kidney Glomerulus - metabolism
Kidney Glomerulus - pathology
Kidney Tubules - metabolism
Kidney Tubules - pathology
Mice
Mice, Knockout
Phospholipids - genetics
Phospholipids - metabolism
kidney
glucose
mass spectrometry
diabetes
imaging
glomerulus
oxidative stress
ISSN:1539-7262, 1539-7262
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Abstract Diabetic nephropathy (DN) is a major life-threatening complication of diabetes. Renal lesions affect glomeruli and tubules, but the pathogenesis is not completely understood. Phospholipids and glycolipids are molecules that carry out multiple cell functions in health and disease, and their role in DN pathogenesis is unknown. We employed high spatial resolution MALDI imaging MS to determine lipid changes in kidneys of eNOS(-/-) db/db mice, a robust model of DN. Phospholipid and glycolipid structures, localization patterns, and relative tissue levels were determined in individual renal glomeruli and tubules without disturbing tissue morphology. A significant increase in the levels of specific glomerular and tubular lipid species from four different classes, i.e., gangliosides, sulfoglycosphingolipids, lysophospholipids, and phosphatidylethanolamines, was detected in diabetic kidneys compared with nondiabetic controls. Inhibition of nonenzymatic oxidative and glycoxidative pathways attenuated the increase in lipid levels and ameliorated renal pathology, even though blood glucose levels remained unchanged. Our data demonstrate that the levels of specific phospho- and glycolipids in glomeruli and/or tubules are associated with diabetic renal pathology. We suggest that hyperglycemia-induced DN pathogenic mechanisms require intermediate oxidative steps that involve specific phospholipid and glycolipid species.
AbstractList Diabetic nephropathy (DN) is a major life-threatening complication of diabetes. Renal lesions affect glomeruli and tubules, but the pathogenesis is not completely understood. Phospholipids and glycolipids are molecules that carry out multiple cell functions in health and disease, and their role in DN pathogenesis is unknown. We employed high spatial resolution MALDI imaging MS to determine lipid changes in kidneys of eNOS(-/-) db/db mice, a robust model of DN. Phospholipid and glycolipid structures, localization patterns, and relative tissue levels were determined in individual renal glomeruli and tubules without disturbing tissue morphology. A significant increase in the levels of specific glomerular and tubular lipid species from four different classes, i.e., gangliosides, sulfoglycosphingolipids, lysophospholipids, and phosphatidylethanolamines, was detected in diabetic kidneys compared with nondiabetic controls. Inhibition of nonenzymatic oxidative and glycoxidative pathways attenuated the increase in lipid levels and ameliorated renal pathology, even though blood glucose levels remained unchanged. Our data demonstrate that the levels of specific phospho- and glycolipids in glomeruli and/or tubules are associated with diabetic renal pathology. We suggest that hyperglycemia-induced DN pathogenic mechanisms require intermediate oxidative steps that involve specific phospholipid and glycolipid species.
Diabetic nephropathy (DN) is a major life-threatening complication of diabetes. Renal lesions affect glomeruli and tubules, but the pathogenesis is not completely understood. Phospholipids and glycolipids are molecules that carry out multiple cell functions in health and disease, and their role in DN pathogenesis is unknown. We employed high spatial resolution MALDI imaging MS to determine lipid changes in kidneys of eNOS(-/-) db/db mice, a robust model of DN. Phospholipid and glycolipid structures, localization patterns, and relative tissue levels were determined in individual renal glomeruli and tubules without disturbing tissue morphology. A significant increase in the levels of specific glomerular and tubular lipid species from four different classes, i.e., gangliosides, sulfoglycosphingolipids, lysophospholipids, and phosphatidylethanolamines, was detected in diabetic kidneys compared with nondiabetic controls. Inhibition of nonenzymatic oxidative and glycoxidative pathways attenuated the increase in lipid levels and ameliorated renal pathology, even though blood glucose levels remained unchanged. Our data demonstrate that the levels of specific phospho- and glycolipids in glomeruli and/or tubules are associated with diabetic renal pathology. We suggest that hyperglycemia-induced DN pathogenic mechanisms require intermediate oxidative steps that involve specific phospholipid and glycolipid species.Diabetic nephropathy (DN) is a major life-threatening complication of diabetes. Renal lesions affect glomeruli and tubules, but the pathogenesis is not completely understood. Phospholipids and glycolipids are molecules that carry out multiple cell functions in health and disease, and their role in DN pathogenesis is unknown. We employed high spatial resolution MALDI imaging MS to determine lipid changes in kidneys of eNOS(-/-) db/db mice, a robust model of DN. Phospholipid and glycolipid structures, localization patterns, and relative tissue levels were determined in individual renal glomeruli and tubules without disturbing tissue morphology. A significant increase in the levels of specific glomerular and tubular lipid species from four different classes, i.e., gangliosides, sulfoglycosphingolipids, lysophospholipids, and phosphatidylethanolamines, was detected in diabetic kidneys compared with nondiabetic controls. Inhibition of nonenzymatic oxidative and glycoxidative pathways attenuated the increase in lipid levels and ameliorated renal pathology, even though blood glucose levels remained unchanged. Our data demonstrate that the levels of specific phospho- and glycolipids in glomeruli and/or tubules are associated with diabetic renal pathology. We suggest that hyperglycemia-induced DN pathogenic mechanisms require intermediate oxidative steps that involve specific phospholipid and glycolipid species.
Author Grove, Kerri J
Voziyan, Paul A
Harris, Raymond C
Hudson, Billy G
Paueksakon, Paisit
Wang, Suwan
Caprioli, Richard M
Spraggins, Jeffrey M
Author_xml – sequence: 1
  givenname: Kerri J
  surname: Grove
  fullname: Grove, Kerri J
  organization: Departments of Chemistry, Vanderbilt University Medical Center, Nashville, TN 37232 Mass Spectrometry Research Center, Vanderbilt University Medical Center, Nashville, TN 37232 Center for Matrix Biology, Vanderbilt University Medical Center, Nashville, TN 37232
– sequence: 2
  givenname: Paul A
  surname: Voziyan
  fullname: Voziyan, Paul A
  organization: Center for Matrix Biology, Vanderbilt University Medical Center, Nashville, TN 37232 Division of Nephrology, Vanderbilt University Medical Center, Nashville, TN 37232 Medicine, Vanderbilt University Medical Center, Nashville, TN 37232
– sequence: 3
  givenname: Jeffrey M
  surname: Spraggins
  fullname: Spraggins, Jeffrey M
  organization: Mass Spectrometry Research Center, Vanderbilt University Medical Center, Nashville, TN 37232 Biochemistry, Vanderbilt University Medical Center, Nashville, TN 37232
– sequence: 4
  givenname: Suwan
  surname: Wang
  fullname: Wang, Suwan
  organization: Division of Nephrology, Vanderbilt University Medical Center, Nashville, TN 37232 Medicine, Vanderbilt University Medical Center, Nashville, TN 37232
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  givenname: Paisit
  surname: Paueksakon
  fullname: Paueksakon, Paisit
  organization: Pathology, Microbiology, and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232
– sequence: 6
  givenname: Raymond C
  surname: Harris
  fullname: Harris, Raymond C
  organization: Center for Matrix Biology, Vanderbilt University Medical Center, Nashville, TN 37232 Division of Nephrology, Vanderbilt University Medical Center, Nashville, TN 37232 Medicine, Vanderbilt University Medical Center, Nashville, TN 37232
– sequence: 7
  givenname: Billy G
  surname: Hudson
  fullname: Hudson, Billy G
  organization: Center for Matrix Biology, Vanderbilt University Medical Center, Nashville, TN 37232 Division of Nephrology, Vanderbilt University Medical Center, Nashville, TN 37232 Medicine, Vanderbilt University Medical Center, Nashville, TN 37232 Biochemistry, Vanderbilt University Medical Center, Nashville, TN 37232
– sequence: 8
  givenname: Richard M
  surname: Caprioli
  fullname: Caprioli, Richard M
  organization: Departments of Chemistry, Vanderbilt University Medical Center, Nashville, TN 37232 Mass Spectrometry Research Center, Vanderbilt University Medical Center, Nashville, TN 37232 Medicine, Vanderbilt University Medical Center, Nashville, TN 37232 Biochemistry, Vanderbilt University Medical Center, Nashville, TN 37232
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glucose
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diabetes
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glomerulus
oxidative stress
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Snippet Diabetic nephropathy (DN) is a major life-threatening complication of diabetes. Renal lesions affect glomeruli and tubules, but the pathogenesis is not...
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SubjectTerms Animals
Diabetic Nephropathies - genetics
Diabetic Nephropathies - metabolism
Diabetic Nephropathies - pathology
Glycolipids - genetics
Glycolipids - metabolism
Kidney Glomerulus - metabolism
Kidney Glomerulus - pathology
Kidney Tubules - metabolism
Kidney Tubules - pathology
Mice
Mice, Knockout
Phospholipids - genetics
Phospholipids - metabolism
Title Diabetic nephropathy induces alterations in the glomerular and tubule lipid profiles
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