Journal
ACTA PHYSIOLOGICA
Volume 232, Issue 1, Pages -Publisher
WILEY
DOI: 10.1111/apha.13610
Keywords
1-deoxyceramide; lipid metabolism; lipidomics; serum; Type 2 diabetes in lean and obese subjects; visceral adipose tissue
Categories
Funding
- SNSF [310030B_166686, 31003A_166700/1, 310030-184708]
- Vontobel Foundation
- Olga Mayenfisch Foundation
- Novartis Foundation for Medical-Biological Research
- EFSD/Novonordisk Programme for Diabetes Research in Europe
- Leenaards Foundation
- Fondation Ernst et Lucie Schmidheiny
- Jubilaumsstiftung Swiss Life Foundation
- Fondation pour la Recherche sur le Cancer
- SNSF grant [310030B_166686, CRSII3_154405, CRSII3_160741]
- NCCR Chemical Biology - SNSF
- Bo & Kerstin Hjelt diabetes Foundation
- Young Independent Investigator Grant SGED/SSED
- Swiss National Science Foundation (SNF) [310030B_166686, CRSII3_154405, CRSII3_160741] Funding Source: Swiss National Science Foundation (SNF)
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This study analyzed the lipid profile of lean and obese individuals with T2D and non-T2D, revealing significant alterations in lipid homeostasis in a disease- and tissue-specific manner. These lipid changes, including sphingolipids, will aid in identifying T2D patient subgroups and advancing personalized medicine in diabetes.
Aim: The worldwide increase in obesity and type 2 diabetes (T2D) represents a major health challenge. Chronically altered lipids induced by obesity further promote the development of T2D, and the accumulation of toxic lipid metabolites in serum and peripheral organs may contribute to the diabetic phenotype. Methods: To better understand the complex metabolic pattern of lean and obese T2D and non-T2D individuals, we analysed the lipid profile of human serum, skeletal muscle and visceral adipose tissue of two cohorts by systematic mass spectrometry-based lipid analysis. Results: Lipid homeostasis was strongly altered in a disease- and tissue-specific manner, allowing us to define T2D signatures associated with obesity from those that were obesity independent. Lipid changes encompassed lyso-, diacyl- and ether-phospholipids. Moreover, strong changes in sphingolipids included cytotoxic 1-deoxyceramide accumulation in a disease-specific manner in serum and visceral adipose tissue. The high amounts of non-canonical 1-deoxyceramide present in human adipose tissue most likely come from cell-autonomous synthesis because 1-deoxyceramide production increased upon differentiation to adipocytes in mouse cell culture experiments. Conclusion: Taken together, the observed lipidome changes in obesity and T2D will facilitate the identification of T2D patient subgroups and represent an important step towards personalized medicine in diabetes.
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