Journal of Glycomics & Lipidomics
Open Access
ISSN: 2153-0637
+44 1223 790975
ISSN: 2153-0637
+44 1223 790975
Bimit Mahat
University of Ottawa, Canada
Posters-Accepted Abstracts: J Glycomics Lipidomics
Context: Recent animal studies suggest that acute exposure to intermittent hypoxia (IH), a phenomenon observed in obstructive sleep apnea, induces adipose tissue lipolysis and inhibits the activity of adipose tissue lipoprotein lipase (LPL). Objective: Determine if IH could adversely impact lipid metabolism, namely circulating triglyceride (TG) levels and adipose tissue lipolytic functions in humans. Design: In vitro primary cell culture of human preadipocytes and in vivo randomized crossover study design. Intervention: 10 healthy men were exposed to 6 hours of normoxia (21% oxygen) or IH (pulsed medical nitrogen) following the consumption of a high fat liquid meal. Results: Using differentiated human preadipocytes, hypoxia significantly inhibits lipoprotein lipase (P<0.05) and lipolysis activity. Postprandial TG levels increased in a significant (P<0.001) but comparable manner in normoxia and IH sessions. Non-esterified fatty acid (NEFA) levels were significantly reduced over 120 minutes following meal in both sessions. After 120 minutes, NEFA levels significantly rose in both sessions, but to greater extent during IH. Neither meal nor IH affected subcutaneous abdominal adipose tissue LPL activity. Lipolytic responses to catecholamine or isoproterenol (�?²-adrenergic agonist) and antilipolytic response to �?±2-agonist assessed in isolated subcutaneous abdominal adipocyte were similar between normoxia and IH sessions. Conclusions: In vitro results suggested that hypoxia significantly inhibits LPL and lipolysis activity. However, in vivo study concluded that an acute session of IH is sufficient to increase postprandial NEFA levels, but not circulating TG. Our results do not support impairment in subcutaneous abdominal adipose LPL activity nor intracellular lipolysis in young healthy men.
Email: bimitmahat@gmail.com