THE EFFECT OF ACUTE CONTINUOUS HYPOXIA ON POSTPRANDIAL LIPID METABOLISM

Abstract

INTRODUCTION: Blood lipids, more precisely triglycerides (TG), are important fuel sources that are highly regulated since an exaggerate amount can lead to cardiovascular diseases. TG breakdown after a meal is mainly controlled by an enzyme expressed in adipose tissue called lipoprotein lipase (LPL). Recent evidence in animals report that adipose tissue LPL is inhibited after an exposure to an environment with reduced oxygen content, leading to a raised level of plasmatic TG. The objective of this thesis was to characterize the effects of an acute exposure to hypoxia on the plasmatic lipolytic activity level and on postprandial TG levels in humans. It was hypothesized that postprandial TG level and plasmatic lipolytic activity, a proxy of LPL activity, would be negatively affected by hypoxia. METHODS: Postprandial TG, non-esterified fatty acid (NEFA), glucose levels, and postheparin plasmatic lipolytic activity were measured on healthy young men (n=7) exposed for 6 h to either control (FiO2=0.2093) or hypoxia (FiO2=0.1200) in a randomized crossover fashion. RESULTS: Exposure to acute hypoxia led to a close to significant (p = .06) increase in postprandial plasmatic TG level and significant postprandial NEFA levels. Postprandial glucose levels were not affected by acute exposure to hypoxia. A significant increase in postheparin plasmatic lipolytic activity was observed after acute hypoxia exposure as compared to the control condition. CONCLUSION: Acute hypoxia in healthy men tend to negatively affects postprandial TG level while increasing plasmatic lipolytic activity. These results lend support to the increased blood lipid levels reported in individuals exposed to lower partial pressure of oxygen during sojourn at high altitude.