Journal
HIGH ALTITUDE MEDICINE & BIOLOGY
Volume 15, Issue 3, Pages 388-395Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/ham.2013.1134
Keywords
blood lipids; chronic hypoxia; high altitude; HMG-CoA reductase; SCD-1
Funding
- GORE-Tarapaca [BIP 30125349-0]
- Universidad Arturo Prat, Iquique, Chile
- ALMEDFIS, CYTED
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Lipid metabolism under chronic hypoxia (CH) has not received equal attention as intermittent hypoxia (IH). To determine the CH-induced changes in plasma and liver, as well as the mRNA and protein expression of two key enzymes in the triglyceride and cholesterol biosynthesis pathways, SREBP-1 (HMG-CoA reductase) and SREBP-2 (SCD-1), we exposed adult male Wistar rats to CH (4600 m; n = 15) for 30 days compared to normoxic rats (n = 15). The CH rats exhibited weight loss (p < 0.001), higher hematocrit (%), and higher hemoglobin (g/dL) (p < 0.01). In the plasma of CH rats, total cholesterol and LDL-cholesterol increased at day 15. VLDL-cholesterol and triglycerides (p < 0.01) greatly increased (35%), while HDL-cholesterol decreased (p < 0.01). Triglycerides and VLDL-cholesterol remained elevated by 28% at day 30 (p < 0.01). Hepatic triglycerides increased two-fold, while total cholesterol increased by 51% (p < 0.001; p < 0.05). Upregulation of SCD-1 mRNA and protein was observed in the CH rats (p < 0.01); however, no differences were observed in HMG-CoA reductase mRNA or protein expression in both groups. In conclusion, CH, like IH, alters lipid profiles by increasing triglycerides in the plasma and liver and upregulating triglyceride biosynthesis without affecting the cholesterol biosynthetic pathway. Additional involved mechanisms require further study because of the importance of lipids in cardiovascular risk.
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