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Table 1 Lipidomics data from liver biopsies of patients

From: How does hepatic lipid accumulation lead to lipotoxicity in non-alcoholic fatty liver disease?

References Year Study cohort Technique Main findings
[43] 2007 Normal (n = 9)
NAFL (n = 9)
NASH (n = 9)
TLC 1. Increased TG and DG, but unaltered FFAs in both NAFL and NASH cohorts compared with control
2. FC and TG/DG ratio progressively increased from normal liver to NAFL to NASH. However, the total CE content was not significantly changed in either NAFL or NASH
3. n-6 and n-3 PUFAs within hepatic FFAs exhibited trends of stepwise decrease from control to NAFL to NASH
4. PUFAs in DG and TG decreased significantly, meanwhile, SFAs and MUFAs in DG and TG showed trends for increase in NAFL and NASH
5. The total PC decreased in both NAFL and NASH, but no significant changes in PS or CL
6. AA was relatively depleted from most lipid species
[44] 2015 Normal (n = 31) Steatosis (n = 17) NASH (n = 20) Cirrhosis (n = 20) LC–MS 1. TG was higher in NASH and steatosis cohorts compared with normal
2. TG contained higher amounts of short-chain FA- and SFA, lower amounts of PUFA in NASH compared with steatosis
3. PUFA-containing LyPEs were significantly increased in steatosis, but not in NASH
4. Almost all lipids except for eicosanoids and certain GPLs (e.g. PIs, ether-linked PEs) were lower in the cirrhotic than in normal samples
5. NASH demonstrated higher amounts of many sphingolipids and the greatest distinction between NASH and steatosis was in very-long-chain dihydroceramides and 1-deoxydihydroceramides
[45] 2017 Control (n = 7)
NAFL (n = 39)
NASH (n = 15)
GC/LC–MS 1. The increased FAs in NASH (14:0, 16:0, 16:1 n-7, 18:1 n-7, 18:1 n-9 and 18:2 n-6) belong to the long-chain FA synthesis pathway and related to the decreased ELOVL6 activity and increased FADS2 and SCD1 activities
2. The significantly decreased eicosanoid precursors (AA, EPA and DHA) is related to the decrease in FADS1 activity in NASH compared with control
3. The deficiency in the synthesis of polyunsaturated long-chain FA causes a decrease in phospholipids in NASH patients
[46] Focused on mitochondrial lipids 2018 Control (n = 16)
NAFL (n = 10)
NASH (n = 32)
LC–MS 1. The levels of TG, DG, dihydroceramide, cholesterol, CE, acylcarnitine, dihexosylceramide, CL and ubiquinone were significantly higher in NAFL and/or NASH compared with control
2. SFAs (e.g., 14:0, 17:0, and 18:0) in TG increased significantly in NASH compared with control
3. Only acylcarnitine and dihexosylceramide demonstrated a significant increase in NASH compared with NAFL
4. Hepatic CL and ubiquinone accumulated in NAFL and NASH, and levels of acylcarnitine increased in NASH, indicating the mitochondrial dysfunction. However, the percentage of 18:2 FA in CL, the most abundant FA composition in CL, was lower in NASH
5. Among the most abundant FAs in CEs, 16:1 and 18:2 FAs were increased, while 16:0 and 18:1 FAs were decreased in NASH compared with control. Meanwhile, 16:0 FA in CEs was also significantly lower in NAFL compared with control
6. The percentage of polyunsaturated AA in TG showed a stepwise decrease from Control to NAFL to NASH
7. Only dihydroceramide and dihexosylceramide were significantly different (increased) in the sphingolipids class between the control and NAFL/NASH
8. NAFL and NASH demonstrated higher amounts of MUFAs (16:1 and 18:1), however lower amounts of SFA (18:0), diunsaturated (DUFA, 18:2), and long-chain PUFAs (20:4, 22:5, and 22:6) in DGs
9. Several phospholipid species comprising DHA decreased during the progression of NAFLD, including PC(P-16:0/22:6), LyPC (22:6), and PE(18:1, 22:6)
  1. NAFL non-alcoholic fatty liver, TLC thin-layer chromatography, FC free cholesterol, CE cholesterol ester, PC phosphatidylcholine, CL cardiolipin, PUFAs polyunsaturated fatty acids, SFAs saturated fatty acids, MUFAs monounsaturated fatty acids, AA arachidonic acid, DHA docosahexaenoic acid (22:6 n-3), EPA eicosapentaenoic acid (20:5 n-3), PE phosphatidylethanolamine, LyPC lysophosphatidylcholine, PS phosphatidylserine, SM sphingomyelin, LyPE lysophosphatidylethanolamine, GPL glycerophospholipid, PI phosphatidylinositol, FA fatty acid, ELOVL6 elongation of very long chain fatty acids protein 6, FADS fatty acid desaturase, SCD1 stearoyl-CoA desaturase 1