Department of Clinical and Medical Therapy, Unit of Medical Therapy, University La Sapienza of Rome, Azienda Policlinico Umberto I, Viale del Policlinico 155, 00161 Rome, Italy.
Nutr Metab Cardiovasc Dis. 2009 Nov;19(9):660-6. doi: 10.1016/j.numecd.2008.11.008. Epub 2009 Jul 24.
Hypoadiponectinemia has been reported in patients with familial combined hyperlipidemia (FCHL) presenting increased waist circumference and insulin resistance. However, no studies have evaluated this association in non-obese FCHL patients. Moreover, it is unclear whether correction of lipoprotein abnormalities may influence adiponectin levels in FCHL.
We have compared serum levels of adiponectin in 199 non-obese FCHL patients (BMI 25.96+/-3.7), 116 normolipaemic (NL) non-affected relatives (BMI 24.4+/-4.0) and 192 controls (BMI 28.0+/-7.4). In a subgroup of FCHL patients, changes in adiponectin levels after treatment with atorvastatin (n=22) or fenofibrate (n=26) were also evaluated. FCHL patients as well as their NL relatives showed lower serum adiponectin levels compared to controls (9.7+/-5.4 microg/mL, 10.7+/-5.3 microg/mL and 17.3+/-13.7microg/mL, respectively; p<0.0001 for all comparisons). After controlling for confounders, the strongest association with hypoadiponectinemia was observed with family history of FCHL, followed by HDL-C (negatively) and age (positively). These variables jointly explained 15% of the total variance of serum adiponectin levels. After 24-week of treatment, adiponectin was increased by 12.5% (p<0.05) by atorvastatin and was reduced by 10% by fenofibrate, resulting in a treatment difference of 22.5% in favor of atorvastatin (p<0.017).
FCHL patients showed lower serum adiponectin levels compared to controls. Also normolipaemic relatives of FCHL patients presented decreased levels of adiponectin, suggesting a possible common background in the determination of this abnormality. Overall, these observations indicate that hypoadiponectinemia may be an inherent characteristic of the FCHL phenotype. In FCHL patients hypoadiponectinemia may be partially corrected by atorvastatin but not by fenofibrate treatment.
家族性混合型高脂血症(FCHL)患者存在低脂联素血症,表现为腰围增加和胰岛素抵抗。然而,尚无研究评估非肥胖型 FCHL 患者的这种相关性。此外,脂蛋白异常的纠正是否会影响 FCHL 患者的脂联素水平尚不清楚。
我们比较了 199 例非肥胖型 FCHL 患者(BMI 25.96±3.7)、116 例非脂代谢异常的 FCHL 无亲缘关系亲属(BMI 24.4±4.0)和 192 例对照者(BMI 28.0±7.4)的血清脂联素水平。在 FCHL 患者亚组中,还评估了阿托伐他汀(n=22)或非诺贝特(n=26)治疗后脂联素水平的变化。与对照组相比,FCHL 患者及其 NL 亲属的血清脂联素水平均较低(分别为 9.7±5.4μg/mL、10.7±5.3μg/mL 和 17.3±13.7μg/mL;所有比较均 P<0.0001)。校正混杂因素后,与低脂联素血症相关性最强的因素是 FCHL 家族史,其次是 HDL-C(负相关)和年龄(正相关)。这些变量共同解释了血清脂联素水平总变异的 15%。阿托伐他汀治疗 24 周后,脂联素增加 12.5%(P<0.05),非诺贝特降低 10%,阿托伐他汀治疗的脂联素差值为 22.5%(P<0.017)。
与对照组相比,FCHL 患者的血清脂联素水平较低。FCHL 无亲缘关系亲属的脂联素水平也较低,提示这种异常可能存在共同的决定因素。总体而言,这些观察结果表明,低脂联素血症可能是 FCHL 表型的固有特征。在 FCHL 患者中,脂联素血症可能部分通过阿托伐他汀纠正,但不能通过非诺贝特治疗纠正。