Ceramide and sphingosine 1-phosphate in adipose dysfunction

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

The increased adipose tissue mass of obese individuals enhances the risk of metabolic syndrome, type 2 diabetes and cardiovascular diseases. During pathological expansion of adipose tissue, multiple molecular controls of lipid storage, adipocyte turn-over and endocrine secretion are perturbed and abnormal lipid metabolism results in a distinct lipid profile. There is a role for ceramides and sphingosine 1-phosphate (S1P) in inducing adipose dysfunction. For instance, the alteration of ceramide biosynthesis, through the de-regulation of key enzymes, results in aberrant formation of ceramides (e.g. C16:0 and C18:0) which block insulin signaling and promote adipose inflammation. Furthermore, S1P can induce defective adipose tissue phenotypes by promoting chronic inflammation and inhibiting adipogenesis. These abnormal changes are discussed in the context of possible therapeutic approaches to re-establish normal adipose function and to, thereby, increase insulin sensitivity in type 2 diabetes. Such novel approaches include blockade of ceramide biosynthesis using inhibitors of sphingomyelinase or dihydroceramide desaturase and by antagonism of S1P receptors, such as S1P2.
LanguageEnglish
Pages145-159
Number of pages15
JournalProgress in Lipid Research
Volume74
Early online date2 Apr 2019
DOIs
Publication statusPublished - 30 Apr 2019

Fingerprint

Ceramides
Adipose Tissue
Type 2 Diabetes Mellitus
Biosynthesis
Tissue
Medical problems
Lysosphingolipid Receptors
Inflammation
Lipids
Sphingomyelin Phosphodiesterase
Adipogenesis
Insulin
Lipid Metabolism
Adipocytes
Deregulation
Insulin Resistance
Cardiovascular Diseases
Phenotype
Enzymes
sphingosine 1-phosphate

Keywords

  • adipose tissue mass
  • obesity
  • type 2 diabetes
  • cardiovascular diseaes

Cite this

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title = "Ceramide and sphingosine 1-phosphate in adipose dysfunction",
abstract = "The increased adipose tissue mass of obese individuals enhances the risk of metabolic syndrome, type 2 diabetes and cardiovascular diseases. During pathological expansion of adipose tissue, multiple molecular controls of lipid storage, adipocyte turn-over and endocrine secretion are perturbed and abnormal lipid metabolism results in a distinct lipid profile. There is a role for ceramides and sphingosine 1-phosphate (S1P) in inducing adipose dysfunction. For instance, the alteration of ceramide biosynthesis, through the de-regulation of key enzymes, results in aberrant formation of ceramides (e.g. C16:0 and C18:0) which block insulin signaling and promote adipose inflammation. Furthermore, S1P can induce defective adipose tissue phenotypes by promoting chronic inflammation and inhibiting adipogenesis. These abnormal changes are discussed in the context of possible therapeutic approaches to re-establish normal adipose function and to, thereby, increase insulin sensitivity in type 2 diabetes. Such novel approaches include blockade of ceramide biosynthesis using inhibitors of sphingomyelinase or dihydroceramide desaturase and by antagonism of S1P receptors, such as S1P2.",
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Ceramide and sphingosine 1-phosphate in adipose dysfunction. / Fang, Zijian; Pyne, Susan; Pyne, Nigel J.

In: Progress in Lipid Research, Vol. 74, 30.04.2019, p. 145-159.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Ceramide and sphingosine 1-phosphate in adipose dysfunction

AU - Fang, Zijian

AU - Pyne, Susan

AU - Pyne, Nigel J.

PY - 2019/4/30

Y1 - 2019/4/30

N2 - The increased adipose tissue mass of obese individuals enhances the risk of metabolic syndrome, type 2 diabetes and cardiovascular diseases. During pathological expansion of adipose tissue, multiple molecular controls of lipid storage, adipocyte turn-over and endocrine secretion are perturbed and abnormal lipid metabolism results in a distinct lipid profile. There is a role for ceramides and sphingosine 1-phosphate (S1P) in inducing adipose dysfunction. For instance, the alteration of ceramide biosynthesis, through the de-regulation of key enzymes, results in aberrant formation of ceramides (e.g. C16:0 and C18:0) which block insulin signaling and promote adipose inflammation. Furthermore, S1P can induce defective adipose tissue phenotypes by promoting chronic inflammation and inhibiting adipogenesis. These abnormal changes are discussed in the context of possible therapeutic approaches to re-establish normal adipose function and to, thereby, increase insulin sensitivity in type 2 diabetes. Such novel approaches include blockade of ceramide biosynthesis using inhibitors of sphingomyelinase or dihydroceramide desaturase and by antagonism of S1P receptors, such as S1P2.

AB - The increased adipose tissue mass of obese individuals enhances the risk of metabolic syndrome, type 2 diabetes and cardiovascular diseases. During pathological expansion of adipose tissue, multiple molecular controls of lipid storage, adipocyte turn-over and endocrine secretion are perturbed and abnormal lipid metabolism results in a distinct lipid profile. There is a role for ceramides and sphingosine 1-phosphate (S1P) in inducing adipose dysfunction. For instance, the alteration of ceramide biosynthesis, through the de-regulation of key enzymes, results in aberrant formation of ceramides (e.g. C16:0 and C18:0) which block insulin signaling and promote adipose inflammation. Furthermore, S1P can induce defective adipose tissue phenotypes by promoting chronic inflammation and inhibiting adipogenesis. These abnormal changes are discussed in the context of possible therapeutic approaches to re-establish normal adipose function and to, thereby, increase insulin sensitivity in type 2 diabetes. Such novel approaches include blockade of ceramide biosynthesis using inhibitors of sphingomyelinase or dihydroceramide desaturase and by antagonism of S1P receptors, such as S1P2.

KW - adipose tissue mass

KW - obesity

KW - type 2 diabetes

KW - cardiovascular diseaes

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