Lipid transfer to HDL and HDL-c levels impaired in long-term bedridden patients
Lipid transfers to HDL are diminished in long-term bedridden patients: association with low HDL-cholesterol and increased inflammatory markersLiterature - de Oliveira WPC, Tavoni TM, Freitas FR et al., - Lipids. 2017. doi: 10.1007/s11745-017-4274-x.[Epub ahead of print]
- Mean BMI was lower in the bedridden than in the sedentary group (21.9 ± 3.0 vs. 25.4 ± 2.7, P<0.001).
- Bedridden patients showed lower levels than sedentary subjects of total cholesterol (160 ± 43 vs. 193 ± 36 mg/dL, P=0.005), non-HDL-c (125 ± 40 vs. 148 ± 36 mg/dL, P=0.034), LDL-c (96 ± 33 vs. 1124 ± 31 mg/dL, P=0.003), HDL-c (36 ± 13 vs 45 ± 10 mg/dL, P=0.008), oxidized LDL (43 ± 12 vs. 53 ± 13 mg/dL, P=0.011) and Apo A-1 (111 ± 24 vs. 134 ± 20 mg/dL, P=0.001).
No differences were seen in levels of apoB, CETP and LCAT, as well as glucose, insulin and leptin.
- Transfer of all four lipids from the lipid nanoparticles to the HDL fraction was lower in bedridden patients compared to sedentary subjects (cholesteryl esters: 4.8 ± 1.27 vs. 6.24 ± 1.10%, P=0.0001, unesterified cholesterol: 3.05 ±1.10 ± 4.04 ± 1.07, P=0.0022, phospholipids: 17.32 ± 2.02 vs. 19.06 ± 1.31, P=0.0007, triglycerides: 3.06 ± 0.65 vs. 3.65 ± 0.71, P=0.0037).
- When these date were normalized by either HDL-c or apo A-I plasma levels, the transfer of cholesterol esters, unesterified cholesterol and triglycerides was no longer significantly different between the two groups. Phospholipid transfer corrected by HDL-c was higher in bedridden patients than in sedentary subjects (0.537 ± 0.157 vs. 0.444 ± 0.093, P=0.0134), as well as when corrected by Apo A-I (0.161 ± 0.026 vs. 0.145 ± 0.019, P=0.0166).
- Serum concentrations of inflammatory markers IL-1β, IL-6, IL-8, HGF and NGF were significantly higher in bedridden patients, while no differences were seen between groups in levels of MCP-1 and TNF-α.
This study showed that the transfer of all four lipids to HDL was impaired in bedridden patients, as compared with sedentary subjects. This may be related to their lower HDL-c levels, as suggested by disappearance of the effect upon normalization by HDL-c levels or Apo A-I. Thus, the diminished lipid transfer does not seem to be the consequence of impaired ability of HDL particles to receive cholesterol. The data suggest that even low levels of physical activity exerted in the day-to-day life of sedentary subjects support HDL concentration and lipid transfer rates, as compared with complete inactivity.
The unexpected finding that LDL-c was lower in bedridden patients, may be explained by the standard infirmary diet that the patients received, with presumably lower calorie and fat intake compared with the free-living control sedentary subjects.