肥胖型PCOS患者的生物学特征和临床特征

多囊卵巢综合征（polycystic ovary syndrome,PCOS）是一种内分泌代谢紊乱综合征,临床表现高度异质性。肥胖是PCOS异质性临床表现之一,超过50%的PCOS患者超重或肥胖。肥胖型PCOS主要表现为高雄激素血症、中心型肥胖和糖脂代谢紊乱,非肥胖型PCOS主要表现为黄体生成激素（luteinizing hormone,LH）水平异常升高。尽管肥胖型和非肥胖型PCOS均存在内分泌代谢异常,然而肥胖可加重PCOS糖脂代谢紊乱;肥胖型PCOS还表现脂肪代谢的异常。综述肥胖型PCOS患者的临床特征、性激素水平、糖脂代谢特征,旨在为肥胖型和非肥胖型PCOS患者新的分型诊治提供参考。     

甲状旁腺激素对大鼠牵张成骨过程中O NC、OPN、C-FOS、COL1、VEGF、RUNX2、ALP基因表达的影响

目的：探讨甲状旁腺激素（PTH）对大鼠牵张成骨（DO）过程中ONC、OPN、C-FOS、COL1、VEGF、RUNX2、ALP基因表达的影响。方法30只雄性大鼠制备大鼠下颌骨DO模型。随机分5组，每组6只。第1组（只有牵张无PTH），术后8周取材，应用HE染色及微CT检测，以确定成骨情况。第2组（有牵张无PTH），第3组（有牵张有PTH），第4组（无牵张有PTH），第5组（对照组：无牵张无PTH）。2、3、4组及对照组术后1周取材，RT-PCR测定ONC、OPN、C-FOS、COL1、VEGF、RUNX2、ALP基因的表达。结果第1组，新骨形成，骨质充满牵张区，骨质连续，大鼠建模成功。RT-PCR检测结果显示，2、3、4组与对照组比较，OPN、COL1、RUNX2、ALP基因表达有明显提高（P＜0．05），其中第3组最为明显。ONC、C-FOS、VEGF基因2、3、4组与对照组比较差异无统计学意义（P＞0．05）。结论 PTH在 DO 过程中，间歇性给以 PTH的作用只有在牵张期发挥作用，其对 OPN、COL1、RUNX2、ALP基因表达能够获得理想的协同作用。     

Could non-HDL-cholesterol be a better marker of atherogenic dyslipidemia in obstructive sleep apnea?

Background/objectiveObstructive sleep apnea (OSA) is independently associated with dyslipidemia, a surrogate marker of atherosclerosis. Low-density lipoprotein (LDL)-cholesterol is accepted as a major independent risk factor for cardiovascular disease. However, non-high-density lipoprotein (HDL)-cholesterol is a better marker of atherogenic dyslipidemia and recommended as a target of lipid lowering therapy. We aimed to assess the prevalence of atherogenic dyslipidemia, and relationship between OSA severity and serum LDL-cholesterol and non-HDL cholesterol levels in OSA patients.MethodsWe retrospectively evaluated treatment naïve 2361 subjects admitted to the sleep laboratory of a university hospital for polysomnography. All subjects’ lipid profile including total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, and non-HDL-cholesterol were measured.ResultsOut of 2361 patients (mean age 49.6 ± 11.9 years; 68.9% male, apnea-hypopnea index 36.6 ± 28.4/h), 185 (7.8%) had no OSA and 2176 (92.2%) had OSA. Atherogenic dyslipidemia prevalence was high (57–66%) in OSA patients, and especially increased in severe OSA compared to other groups (p < 0.05). Though total and LDL-cholesterol did not differ between those with and without OSA, non-HDL-cholesterol (p = 0.020), and triglycerides (p = 0.001) were higher and HDL-cholesterol levels (p = 0.018) were lower in OSA patients than non-OSA. Non-HDL-cholesterol was significantly correlated with OSA severity (p < 0.001) and hypoxia parameters (p < 0.01), whereas LDL-cholesterol showed no correlation.ConclusionsAtherogenic dyslipidemia is highly prevalent and non-HDL-cholesterol levels are significantly increased, predominantly in severe OSA patients. Non-HDL-cholesterol but not LDL-cholesterol, is significantly correlated with OSA severity and hypoxia parameters. Therefore, it could be better to use non-HDL-cholesterol, which is a guideline recommended target of lipid therapy, as a marker of atherosclerotic cardiovascular risk in OSA patients.