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Acute Intermittent Hypoxia Inhibits Triglycerides Clearance And Has a Tissue‐Specific Effect on Lipoprotein Lipase Activity
Author(s) -
Drager Luciano F.,
Reinke Christian,
Jun Jonathan C.,
BevansFonti Shan,
Polotsky Vsevolod Y.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1103.4
Subject(s) - lipoprotein lipase , endocrinology , medicine , adipose tissue , triglyceride , intermittent hypoxia , clearance rate , chemistry , adipose triglyceride lipase , skeletal muscle , lipase , hypoxia (environmental) , lipolysis , cholesterol , enzyme , oxygen , biochemistry , organic chemistry , obstructive sleep apnea
Background We have recently shown that chronic intermittent hypoxia (IH) decreases triglycerides (TG) clearance due to the inhibition of lipoprotein lipase (LPL) activity in adipose tissue. However, the impact of acute IH on TG clearance and LpL activity remains unknown. Methods Male C57BL/6J mice were exposed to 7hs of IH with FiO2 decreasing from 20.9% to 5% once per minute or to intermittent air (IA). During the exposure, intralipid (20%, 7.5 ml/kg) was administered and serum triglyceride levels were measured over the 2 hr time course. In a separate batch of mice, fasting (5 hrs) LPL activity was measured in the epididymal fat pads, heart and skeletal muscle. Results Compared to IA, IH increased TG levels throughout the 2 hr time course of intralipid (p <0.01). Exposure to IH for 7 hrs resulted in a significant decrease in adipose LPL activity (IA: 5.83±0.51 vs. IH: 4.40±0.29 umol FFA released/g/hr; P<0.05) and a significant increase in the heart LPL activity (IA: 42.61±2.28 vs. IH: 60.70±3.05 umol FFA released/g/hr; P<0.01). No difference was observed in the skeletal muscle. Conclusions Acute IH inhibits TG clearance, possibly by suppressing adipose LpL activity. A simultaneous increase in heart LpL may be attributable to the heightened myocardial demand in fatty acids as a source of energy. Research Support: R01 HL80105, AHA 10GRNT3360001, 5P50HL084945, FAPESP 2010/11681‐0