Obstructive sleep apnoea syndrome, plasma adiponectin levels, and insulin resistance

Department of Internal Medicine, Osaka Gyomeikan Hospital, Kasugade-naka, Osaka, Japan.
Clinical Endocrinology (Impact Factor: 3.46). 02/2006; 64(1):12-9. DOI: 10.1111/j.1365-2265.2005.02407.x
Source: PubMed


To investigate whether sleep-disordered breathing and/or plasma adiponectin levels are associated with insulin resistance independent of obesity or fat distribution in obstructive sleep apnoea syndrome (OSAS).
Cross-sectional clinical study.
Two-hundred and thirteen Japanese patients with OSAS aged 27-80 years were divided into three groups: 30 with mild OSAS [apnoea-hypopnoea index (AHI) = 10.3 +/- 0.9 episodes/h, minimum oxygen saturation (min SpO2) = 87.3 +/- 0.9%], 98 with moderate OSAS (AHI = 28.9 +/- 0.6 episodes/h, min SpO2 = 82.1 +/- 0.7%), and 85 with severe OSAS (AHI = 68.1 +/- 2.8 episodes/h, min SpO2 = 72.3 +/- 1.6%). Twenty-one patients undergoing diabetic treatments (two mild, nine moderate and 10 severe) were excluded from the assessment of insulin resistance and plasma adiponectin measurements.
Fat distribution [evaluated according to visceral (V) and subcutaneous (S) fat areas using computed tomography scanning at the umbilical level], blood pressure, metabolic parameters and hormones including insulin and adiponectin were measured. After full polysomnography, venous blood was collected between 0600 and 0700 h.
Severe OSAS patients were more hypertensive than mild and moderate OSAS. Fasting plasma glucose (FPG) and fasting plasma insulin and homeostasis model assessment of insulin resistance (HOMA-IR) levels were all higher in severe OSAS than mild and moderate OSAS patients. HOMA-IR was correlated not only with obesity [body mass index (BMI), V and S areas] but also with apnoea (AHI, min SpO2 and desaturation time). Additionally, HOMA-IR was correlated positively with haemoglobin (Hb)A1c, systolic (SBP) and diastolic blood pressure (DBP), triglycerides and free fatty acids (FFA), and negatively with high density lipoprotein (HDL)-cholesterol, suggesting that insulin resistance is a key component of the metabolic syndrome in OSAS. Plasma adiponectin levels were not different between mild, moderate and severe OSAS groups. Plasma adiponectin levels were correlated with HOMA-IR and V area, but not AHI or min SpO2. Stepwise multiple regression analysis, however, revealed that BMI, AHI and plasma adiponectin were independently associated with HOMA-IR.
Sleep-disordered breathing was associated with insulin resistance independent of obesity. Although plasma adiponectin was also an independent determinant of HOMA-IR in OSAS patients, plasma adiponectin was more closely related to obesity than to sleep apnoea. Although treatment of sleep-disordered breathing with nasal continuous positive airway pressure reportedly improves insulin sensitivity, our findings suggest that treatment of obesity is also essential in ameliorating insulin resistance at least through increased plasma adiponectin levels in OSAS.

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    • "Zhang et al.[23] reported that serum adiponectin levels were significantly lower in the OSAS group than in the control. Makino et al.[24] examined that 213 patients with OSAS were divided into three groups: 30 with mild, 98 moderate, and 85 with severe OSAS. They determined plasma adiponectin levels were not different among mild, moderate, and severe OSAS groups. "
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    ABSTRACT: The aim of this study was to investigate the relationship among plasma leptin, ghrelin, adiponectin, resistin levels, and obstructive sleep apnea syndrome (OSAS). Fifty-five consecutive newly diagnosed OSAS patients and 15 age-matched nonapneic controls were enrolled in this study. After sleep study between 8:00 AM and 9:00 AM on the morning, venous blood was obtained in the fasting state to measure ghrelin and adipokines. Serum ghrelin levels of OSAS group were significantly (P < 0.05) higher than those of the control group. No significant difference was noted in the levels of leptin, adiponectin, and resistin in OSAS group when compared to controls. There was a significant positive correlation between ghrelin and apnea-hypopnea index (AHI) (r = 0.237, P < 0.05) or the Epworth sleepiness scale (ESS) (r = 0.28, P < 0.05). There was also a significant positive correlation between leptin and body mass index (r = 0.592, P < 0.0001). No significant correlation was observed between leptin, adiponectin, resistin, and any polysomnographic parameters. Our findings demonstrated that serum ghrelin levels were higher in OSAS patients than those of control group and correlated with AHI and ESS. Further studies are needed to clarify the complex relation among OSAS, obesity, adipokines, and ghrelin.
    Full-text · Article · Jul 2010
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    • "IGF-1 n or ↓ ↓ ↓ [48] [49] [50] PRL ↓ n or ↑ [49, 51–53] ACTH ↑ ↑ [51] [54] [55] Cortisol ↑ n or ↑ [49, 53–60] Aldosterone ↑ ↑ [61] [62] fT 3 n n [ 51] fT 4 n n [ 49, 51] TSH n n or ↓ [49] [51] [56] [63] LH n or ↓ n or ↓ [49] [56] [64] FSH n or ↓ n or ↓ [49] Testosterone in ♂ ↓ ↓ [49, 65–68] Free Testosterone in ♂ n or ↓ ↓ [49] Testosterone in ♀ ↑ ? [ 69, 70] SHBG ↓ ↓ [49] Insulin ↑ ↑ ↑ [11, 31–33] Leptin ↑ ↑ ↑ [35, 37–40] Adiponectin ↓ ↓ ↓ [36] [37] [42] [43] [71] Ghrelin ↓ ? [ 39, 45] n "
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    ABSTRACT: Obstructive sleep apnea syndrome (OSAS) is a serious, prevalent condition that has significant morbidity and mortality when untreated. It is strongly associated with obesity and is characterized by changes in the serum levels or secretory patterns of several hormones. Obese patients with OSAS show a reduction of both spontaneous and stimulated growth hormone (GH) secretion coupled to reduced insulin-like growth factor-I (IGF-I) concentrations and impaired peripheral sensitivity to GH. Hypoxemia and chronic sleep fragmentation could affect the sleep-entrained prolactin (PRL) rhythm. A disrupted Hypothalamus-Pituitary-Adrenal (HPA) axis activity has been described in OSAS. Some derangement in Thyroid-Stimulating Hormone (TSH) secretion has been demonstrated by some authors, whereas a normal thyroid activity has been described by others. Changes of gonadal axis are common in patients with OSAS, who frequently show a hypogonadotropic hypogonadism. Altogether, hormonal abnormalities may be considered as adaptive changes which indicate how a local upper airway dysfunction induces systemic consequences. The understanding of the complex interactions between hormones and OSAS may allow a multi-disciplinary approach to obese patients with this disturbance and lead to an effective management that improves quality of life and prevents associated morbidity or death.
    Full-text · Article · Feb 2010 · International Journal of Endocrinology
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    • "In contrast to other adipokines, there is a strong negative correlation between adiponectin and adiposity, insulin resistance , diabetes, vascular inflammation and atherosclerosis (Pannacciulli et al., 2006). Remarkably, several studies have indicated an association between the adiponectin level and sleep apnea in relation to insulin resistance (Makino et al., 2006; Wolk et al., 2005; Zhang et al., 2006). But, an association between the plasma adiponectin level and the circadian and sleep ⁄ wake regulation is controversial (Gavrila et al., 2003; Shea et al., 2005). "
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    ABSTRACT: Adiponectin, an adipose tissue-derived hormone, has been negatively related to obstructive sleep apnea syndrome. Besides sleep apnea, children with Prader-Willi syndrome (PWS) may have excessive daytime sleepiness and rapid eye movement (REM) sleep abnormality. The aim of this study is to determine whether changes in sleep structures are related to plasma adiponectin levels in PWS. Correlations between adiponectin level and sleep variables were analyzed in 28 children with PWS and 18 controls. Overnight polysomnography was performed. The fasting plasma adiponectin levels were higher in the children with PWS than in the controls (P = 0.0006). In the PWS, Epworth sleepiness scale was significantly higher (P = 0.002); sleep latency (P = 0.003) and REM latency (P = 0.001) were significantly shortened; the apnea-hypopnea index (AHI) was significantly increased (P = 0.0001); and the duration of non-rapid eye movement (NREM) sleep stages 3 and 4 was decreased (P = 0.005). Multiple regression analysis revealed correlations between the adiponectin level and the total sleep time (beta = 0.688, P = 0.009), AHI (beta = 1.274, P = 0.010), REM latency (beta = -0.637, P = 0.021) and the percentage of NREM sleep (beta = -7.648, P = 0.002) in PWS. In children with PWS, higher plasma adiponectin levels were independently associated with several sleep variables, which was not observed in the control group. These results suggest a potential influence of elevated adiponectin level on the sleep structures in PWS.
    Full-text · Article · Nov 2009 · Journal of Sleep Research
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