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.     

The triglyceride-glucose index,a predictor of type 2 diabetes development: A retrospective cohort study

AimsThe triglycerides-glucose (TyG) index, the product of fasting plasma glucose (FPG) and triglycerides (TG) is a novel index. Many previous studies have reported that the TyG index might be a strong predictor of incident type 2 diabetes. We determined whether the TyG index could be a useful predictor for diabetes diagnosis and compared it to the FPG and TG as predictors of type 2 diabetes.MethodsA total of 617 subjects without baseline diabetes were examined and followed up for a median period of 9.2 years. We performed a mixed effect cox regression analysis to evaluate the risk of developing diabetes across the quartiles of the TyG index, calculated as ln[triglyceride (mg/dl) × FPG (mg/dl)/2], and plotted a receiver operating characteristic (ROC) curve to assess discrimination among TyG, FPG and TG.ResultsDuring 4,871.56 person-years of follow-up, there were 163 incident cases of diabetes. The risk of diabetes increased across the quartiles of the TyG index. Those in the highest quartile of TyG had a higher risk of developing diabetes (adjusted HR 3.38 95% CI 2.38–4.8, ptrend < 0.001) than those in the lowest quartile. The area under the curve (AUC) of the ROC plots were 0.79 (95% CI 0.74–0.83) for FPG, 0.64 (95% CI 0.60–0.69) for TyG and 0.59 (95% CI 0.54–0.64) for TG.ConclusionThe TyG index was significantly associated with risk of incident diabetes and could be a valuable biomarker of developing diabetes. However, FPG appeared to be a more robust predictor of diabetes.     

Medium Chain Triglycerides induce mild ketosis and may improve cognition in Alzheimer’s disease. A systematic review and meta-analysis of human studies

Introduction/aimThe brain in Alzheimer’s disease shows glucose hypometabolism but may utilize ketones for energy production. Ketone levels can potentially be boosted through oral intake of Medium Chain Triglycerides (MCTs). The aim of this meta-analysis is to investigate the effect of MCTs on peripheral ketone levels and cognitive performance in patients with mild cognitive impairment and Alzheimer’s disease.MethodsMedline, Scopus and Web of Science were searched for literature up to March 1, 2019. Meta-analyses were performed by implementing continuous random-effects models and outcomes were reported as weighted Mean Differences (MDs) or Standardized Mean Differences (SMDs).ResultsTwelve records (422 participants) were included. Meta-analysis of RCTs showed that, compared with placebo, MCTs elevated beta-hydroxybutyrate [MD = 0.355; 95 % CI (0.286, 0.424), I² = 0 %], showed a trend towards cognitive improvement on ADAS-Cog [MD = −0.539; 95% CI (−1.239, −0.161), I² = 0 %], and significantly improved cognition on a combined measure (ADAS-Cog with MMSE) [SMD = −0.289; 95 % CI (−0.551, −0.027), I² = 0 %].ConclusionsIn this meta-analysis, we demonstrated that MCTs can induce mild ketosis and may improve cognition in patients with mild cognitive impairment and Alzheimer’s disease. However, risk of bias of existing studies necessitates future trials.     

妊娠期三酰甘油代谢的研究进展

三酰甘油是人体脂质的组成部分,可被脂蛋白脂肪酶水解为游离脂肪酸和甘油并加以利用,在妊娠期参与母儿的能量供应及胎儿生长发育等多个环节。近年来研究表明,妊娠期三酰甘油水平由于受到妊娠期特有激素、胰岛素等多种因素影响,相较于非妊娠期妇女显著增加,并随妊娠期的进展而逐渐升高,同时在多种妊娠期并发症如妊娠期糖尿病、子痫前期、妊娠期肝内胆汁淤积症、早产、妊娠期急性胰腺炎等中观察到三酰甘油水平发生相应的改变。本文就三酰甘油与妊娠期糖尿病、子痫前期、妊娠期肝内胆汁淤积症等妊娠期并发症之间的关系和可能的发生机制以及监测随访等进行综述。寻求一个国际认可的、具有地区差异性的参考范围,确定有效的个体化监测及治疗指南,对妊娠期三酰甘油水平的管理具有重要意义。     

Defect of insulin signal in peripheral tissues: important role of ceramide

In healthy people,balance between glucose production and its utilization is precisely controlled.When circulating glucose reaches a critical threshold level,pancreaticβcells secrete insulin that has two major actions:to lower circulating glucose levels by facilitating its uptake mainly into skeletal muscle while inhibiting its production by the liver.Interestingly,dietary triglycerides are the main source of fatty acids to fulfill energy needs of oxidative tissues.Normally,the unconsumed fraction of excess of fatty acids is stored in lipid droplets that are localized in adipocytes to provide energy during fasting periods.Thus,adipose tissue acts as a trap for fatty acid excess liberated from plasma triglycerides.When the buffering action of adipose tissue to store fatty acids is impaired,fatty acids that build up in othertissues are metabolized as sphingolipid derivatives such as ceramides.Several studies suggest that ceramides are among the most active lipid second messengers to inhibit the insulin signaling pathway and this review describes the major role played by ceramide accumulation in the development of insulin resistance of peripherals tissues through the targeting of specific proteins of the insulin signaling pathway.     

A novel mutation in GPIHBP1 causes familial chylomicronemia syndrome

Familial chylomicronemia syndrome is characterized by severe elevation in serum triglycerides and an increased risk of acute pancreatitis. Although familial chylomicronemia syndrome is mainly caused by mutations in the lipoprotein lipase (LPL) gene, few causal mutations in other genes (ie, APOC2, APOA5, LMF1, and GPIHBP1) have also been reported. In this case report, we present the discovery of a novel mutation in the glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) gene and discuss its pathogenicity through a familial segregation study.