2005 Fiscal Year Final Research Report Summary
GENETIC PREDISPOSITION, INFLAMMATION, INTERMITTENT HYPOXIA AND CARDIOVASCULAR COMPLICATIONS IN SLEEP APNEA SYNDROME
| Project/Area Number |
16590735
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Chiba University |
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Principal Investigator |
TATSUMI Koichiro Chiba University, Department of Respirology, Graduate School of Medicine, Associate Professor, 大学院・医学研究院, 助教授 (10207061)
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| Co-Investigator(Kenkyū-buntansha) |
KASAHARA Yasunori Chiba University, Department of Respirology, Graduate School of Medicine, Assistant, 大学院・医学研究院, 助手 (60343092)
KUROSU Katushi Chiba University, Department of Respirology, Graduate School of Medicine, Assistant, 大学院・医学研究院, 助手 (20291106)
TANABE Nobuhiro Chiba University, Department of Respirology, Chiba University Hospital, Assistant Professor, 医学部付属病院, 講師 (40292700)
TAKIGUCHI Yuichi Chiba University, Department of Respirology, Chiba University Hospital, Assistant Professor, 医学部付属病院, 講師 (30272321)
KURIYAMA Takayuki Chiba University, Department of Respirology, Graduate School of Medicine, Professor, 大学院・医学研究院, 教授 (20009723)
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| Project Period (FY) |
2004 – 2005
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| Keywords | sleep apnea syndrome / hypoxemia / visceral fat accumulation / leptin / obesity |
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| Research Abstract |
Background : Obstructive sleep apnea-hypopnea syndrome (OSAHS) is characterized by repeated oxygen desaturation. Obesity and visceral fat accumulation (VFA) are risk factors for the development of OSAHS. Circulating leptin increases in accordance with body mass index (BMI), and under experimental conditions intermittent hypoxia stimulates leptin production.
Methods : The primary objective of this study was to investigate whether hypoxemia during sleep influences the levels of circulating leptin and whether the location of body fat deposits, i.e. the distribution of VFA and subcutaneous fat accumulation (SFA), affects circulating leptin levels in patients with OSAHA who are not obese. We assessed VFA and SFA by abdominal CT scan and measured circulating levels of leptin in 96 male patients with OSAHS and 52 male patients without OSAHS matched for BMI. To be matched for BMI in the two groups, patients whose BMI was less than 27 kg/m^2 were selected for the OSAHS group.
Results : In the whole study group, circulating leptin levels correlated with BMI (r=0.30), VFA (r=0.44), SFA (r=0.28), apnea-hypopnea index (AHI) (r=0.48), sleep mean SaO_2 (r=0.59) and sleep lowest SaO_2 (r=037). Multiple regression analysis showed that average SaO_2 (P<0.01) and lowest SaO_2 (P=0.03) were explanatory variables for serum leptin values, but AHI (P=0.054), BMI (P=0.33), VFA (P=0.11) and SFA (P=0.36) were not.
Conclusions : These results suggest that sleep hypoxemia may be the main determinant of circulating leptin levels, although the location of body fat deposits could contribute to the elevated circulating leptin levels in patients with OSAHS who are not obese.
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Research Products
(4 results)
