PT  - JOURNAL ARTICLE
AU  - Qian Xiaosen
AU  - Liu Yi
TI  - The impact of obstructive sleep apnea on glucose regulation and liver injury in nondiabetic men
DP  - 2011 Sep 01
TA  - European Respiratory Journal
PG  - p2224
VI  - 38
IP  - Suppl 55
4099  - http://erj.ersjournals.com/content/38/Suppl_55/p2224.short
4100  - http://erj.ersjournals.com/content/38/Suppl_55/p2224.full
SO  - Eur Respir J2011 Sep 01; 38
AB  - Objective: We explored the effect of Obstructive sleep apnea syndrome (OSAS) on glucose regulation and liver injury in nondiabetic men.Research design and methods: We enrolled 49 non diabetic men of the OSAS patients without concomitant diseases/medications based on overnight polysomnography and blood tests. We measured fasting serum glucose (FPG), fasting insulin (FIS), C-reactive protein (CRP), liver enzymes such as alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) and calculated new homeostasis model assessment estimates of insulin resistance (HOMA2-IR), insulin sensitivity (HOMA2-IS) and pancreatic beta-cell function (HOMA2-B).Results: Median fasting insulin level, HOMA2-IS, and HOMA2-IR of the severe OSAS group were significantly higher than those of the other OSAS subgroups and controls. No significant differences were observed for FPG and HOMA2-B. CRP levels were significantly correlated with BMI, with AHI, with minimum SpO2, with HOMA2-IR and with LDH during sleep. Both levels of ALT and LDH were significantly positively correlated with insulin and HOMA2-IR (p =0.001 respectively). Significant elevations in HOMA2-IR (p=0.001), fasting serum insulin (p=0.001), levels of CRP (p=0.024) levels of ALT (p=0.040) and levels of LDH (p=0.047) and significant reductions in HOMA2-IS (p=0.002) were found in subjects with AHI>15/h compared to those with AHI<15/h matched by BMI, sex and age.Conclusions: We demonstrated that OSAS contribute to the development of insulin resistance and liver injury. Insulin resistance may be the first key effect of OSAS on glucose regulation. Insulin resistance may be the pathophysiologic basis of liver injury in OSAS.