Association between macro- and microvascular damage and sarcopenia index in individuals with type 2 diabetes mellitus.

Sarcopenia was recently reported to be relevant to an increased macro-and microvascular disease risk. Sarcopenia index (SI) has been identified as a surrogate marker for sarcopenia. The aim of the present study was to investigate the association between macro- and microvascular disease and SI in patients with type 2 diabetes mellitus (T2DM). A total of 783 patients with T2DM were enrolled in this cross-sectional study. The SI was calculated by (serum creatinine [mg/dL]/cystatin C [mg/L]) × 100. The subjects were divided into three groups according to SI tertiles: T1 (41.27-81.37), T2 (81.38- 99.55), and T3 (99.56-192.31). Parameters of macro- and microvascular complications, including diabetic retinopathy (DR), micro- and macroalbuminuria (MAU), diabetic peripheral neuropathy (DPN), and lower extremity peripheral artery disease (LEAD) were evaluated. Multivariate logistic regression analysis revealed that when taking the top tertile of SI as a reference, an increasing trend of the prevalence of DR, MAU, DPN, and LEAD were presented (all P for trend  < 0.05), where the OR (95% CI) for DR prevalence was 1.967 (1.252-3.090) in T2, 2.195 (1.278-3.769) in T1, for MAU was 1.805 (1.149-2.837) in T2, 2.537 (1.490-4.320) in T1, for DPN was 2.244 (1.485-3.391) in T2, 3.172 (1.884-5.341) in T1, and for LEAD was 2.017 (1.002-4.057) in T2, 2.405 (1.107-5.225) in T1 (all P < 0.05). Patients with lower SI were more inclined to have an increased risk of macro- and microvascular damage in T2DM population, which may be related to sarcopenia.

Postprandial Triglyceride-Rich Lipoproteins-Induced Lysosomal Dysfunction and Impaired Autophagic Flux Contribute to Inflammation in White Adipocytes.

BACKGROUND: Obesity and postprandial hypertriglyceridemia, characterized by an increase in triglyceride-rich lipoproteins (TRLs), cause chronic low-grade inflammation. It is unclear how postprandial TRLs affect inflammation in white adipocytes. OBJECTIVES: The objectives of the study were to explore the inflammatory response of postprandial TRLs in white adipocytes and investigate the possible mechanism. METHODS: We measured postprandial triglyceride (TG) and high-sensitivity C-reactive protein (hsCRP) concentrations in 204 recruited subjects and treated white adipocytes from mice with postprandial TRLs from above patients with hypertriglyceridemia. RESULTS: Serum hsCRP concentrations and BMI were positively related to TG concentrations in the postprandial state. Postprandial TRLs increased mRNA and protein expression of inflammatory factors, including interleukin-1ß, via the NOD-like receptor protein 3 (NLRP3)/Caspase-1 pathway, and impaired autophagy flux in white adipocytes of mice. TRLs also induced lysosomal damage as evidenced by the reduced protein expression of lysosome-associated membrane proteins-1 and Cathepsin L. Inhibition of Cathepsin B, NLRP3, and mTOR signaling improved autophagy/lysosome dysfunction and inhibited the activation of the NLRP3/Caspase-1 pathway and inflammatory factors induced by TRLs in white adipocytes. CONCLUSIONS: Our results suggest that postprandial hypertriglyceridemia causes chronic inflammation in adipocytes through TRL-induced lysosomal dysfunction and impaired autophagic flux in an mTOR-dependent manner.

Reply to Mahat, R.K.; Rathore, V. Comment on "Xiang et al. Association between the Triglyceride-Glucose Index and Vitamin D Status in Type 2 Diabetes Mellitus. Nutrients 2023, 15, 639".

We are pleased to see that Mahat and Rathore [...].

High serum Bhlhe40 levels are associated with subclinical atherosclerosis in patients with type 2 diabetes mellitus: A cross-sectional study.

BACKGROUND: Our previous studies have shown that the basic helix-loop-helix family member e40 (Bhlhe40) plays a critical role in regulating calcification and senescence of vascular smooth muscle cells induced by high glucose. In this study, we determined the association between serum Bhlhe40 levels and subclinical atherosclerosis in patients with type 2 diabetes mellitus (T2DM). METHODS: 247 patients with T2DM were included in this cross-sectional study between June 2021 and July 2022. The presence of subclinical atherosclerosis was evaluated by carotid ultrasonography. Serum Bhlhe40 concentrations were measured with an ELISA kit. RESULTS: Serum Bhlhe40 levels were remarkably higher in the subclinical atherosclerosis group than in the subjects without subclinical atherosclerosis (p < 0.001). Correlation analysis showed a positive correlation between serum Bhlhe40 and carotid intima-media thickness (C-IMT) (r = 0.155, p = 0.015). The optimal threshold of serum Bhlhe40 > 5.67 ng/mL had an area under the ROC curve (AUC) was 0.709 (p < 0.001). In addition, serum Bhlhe40 levels were associated with the prevalence of subclinical atherosclerosis (OR: 1.790, 95% CI: 1.414-2.266, p < 0.001). CONCLUSION: Serum Bhlhe40 levels were significantly higher in T2DM subjects with subclinical atherosclerosis and positively associated with C-IMT.

Comparison of SSS-CN and PHQ-15 in the evaluation of patients with suspected psychological disorders in cardiovascular medicine.

Aims: Somatic Symptom Scale-China (SSS-CN) has been applied to assess the presence and severity of somatization symptom disorders (SSD) in Chinese patients. However, there was no study comparing SSS-CN with Patient Health Questionnaire-15 (PHQ-15). The aim of this study was to compare the consistency of the SSS-CN with the PHQ-15 in evaluating SSD in patients with suspected psychological disorders in cardiovascular medicine and to explore the relationship between scores on the two SSD self-rating scales and scores on self-rating scales for anxiety or depression. Methods: In this study, 1,324 subjects were enrolled by using a "three-question method." Then, they completed four self-assessment scales, i.e., SSS-CN, PHQ-15, Patient Health Questionnaire-9 (PHQ-9), and General Anxiety Disorder-7 (GAD-7), in turn. The ability of SSS-CN to diagnose SSD was analyzed by the receiver operating characteristic (ROC) curve, and the area under the curve (AUC) value, sensitivity, and specificity were calculated. Reliability analysis was performed with the Kappa statistic to determine consistency between SSS-CN and PHQ-15. The relationship between two qualitative variables was analyzed by Spearman correlation analysis. Results: The proportions of SSD evaluated by SSS-CN and PHQ-15 were 83.2 and 87.0%, respectively. SSS-CN score was significantly correlated with PHQ-15 one (r = 0.709, p < 0.001). The AUC of the SSS-CN for the diagnosis of SSD was 0.891, with a high sensitivity and acceptable specificity. There was a moderate agreement between SSS-CN and PHQ-15 in assessing SSD, with a Kappa value of 0.512. Anxiety and/or depression were detected in about 70% of patients with SSD. There was significant correlation between the score of each SSD scale and that of GAD-7 or PHQ-9 (SSS-CN: r = 0.614 or 0.674; PHQ-15: r = 0.444 or 0.582, all p < 0.001). In addition, the SSS-CN score was more closely correlated with the GAD-7 or PHQ-9 score than the PHQ-15 score, and a higher proportion of patients with anxiety or depression was detected in those with moderate and severe SSD evaluated by SSS-CN. Conclusion: The SSS-CN could be one of the ideal scales for the rapid screening of patients with suspected psychological disorders in cardiovascular medicine.

Association between the Triglyceride-Glucose Index and Vitamin D Status in Type 2 Diabetes Mellitus.

BACKGROUND: Vitamin D deficiency (VDD) increases the risk for type 2 diabetes mellitus (T2DM), which might be related to insulin resistance (IR). We aimed to explore the association between the triglyceride-glucose (TyG) index, a reliable indicator of IR, and VDD in patients with T2DM. METHODS: There were 1034 participants with T2DM enrolled in the Second Xiangya Hospital of Central South University. The TyG index was calculated as ln (fasting triglyceride (TG, mg/dL) × fasting blood glucose (mg/dL)/2). VDD was defined as 25-hydroxyvitamin D [25(OH)D] level <50 nmol/L. RESULTS: Correlation analysis showed a negative association between the TyG index and 25(OH)D level. After adjustments for clinical and laboratory parameters, it was revealed that when taking the Q1 quartile of TyG index as a reference, an increasing trend of VDD prevalence was presented in the other three groups divided by TyG index quartiles, where the OR (95% CI) was 1.708 (1.132-2.576) for Q2, 2.041 (1.315-3.169) for Q3, and 2.543 (1.520-4.253) for Q4 (all p < 0.05). CONCLUSIONS: Patients with higher TyG index were more likely to have an increased risk of VDD in T2DM population, which may be related to IR.

BMF-AS1/BMF Promotes Diabetic Vascular Calcification and Aging both In Vitro and In Vivo.

Vascular calcification and aging often increase morbidity and mortality in patients with diabetes mellitus (DM); however, the underlying mechanisms are still unknown. In the present study, we found that Bcl-2 modifying factor (BMF) and BMF antisense RNA 1 (BMF-AS1) were significantly increased in high glucose-induced calcified and senescent vascular smooth muscle cells (VSMCs) as well as artery tissues from diabetic mice. Inhibition of BMF-AS1 and BMF reduced the calcification and senescence of VSMCs, whereas overexpression of BMF-AS1 and BMF generates the opposite results. Mechanistic analysis showed that BMF-AS1 interacted with BMF directly and up-regulated BMF at both mRNA and protein levels, but BMF did not affect the expression of BMF-AS1. Moreover, knocking down BMF-AS1 and BMF suppressed the calcification and senescence of VSMCs, and BMF knockout (BMF-/-) diabetic mice presented less vascular calcification and aging compared with wild type diabetic mice. In addition, higher coronary artery calcification scores (CACs) and increased plasma BMF concentration were found in patients with DM, and there was a positive correlation between CACs and plasma BMF concentration. Thus, BMF-AS1/BMF plays a key role in promoting high glucose-induced vascular calcification and aging both in vitro and in vivo. BMF-AS1 and BMF represent potential therapeutic targets in diabetic vascular calcification and aging.

Long noncoding RNA SNHG1 alleviates high glucose-induced vascular smooth muscle cells calcification/senescence by post-transcriptionally regulating Bhlhe40 and autophagy via Atg10

Long noncoding RNAs (lncRNAs) are emerging regulators of vascular diseases, yet their role in diabetic vascular calcification/aging remains poorly understood. In this study, we identified a down-expressed lncRNA SNHG1 in high glucose (HG)-induced vascular smooth muscle cells (HA-VSMCs), which induced excessive autophagy and promoted HA-VSMCs calcification/senescence. Overexpression of SNHG1 alleviated HG-induced HA-VSMCs calcification/senescence. The molecular mechanisms of SNHG1 in HA-VSMCs calcification/senescence were explored by RNA pull-down, RNA immunoprecipitation, RNA stability assay, luciferase reporter assay, immunoprecipitation and Western blot assays. In one mechanism, SNHG1 directly interacted with Bhlhe40 mRNA 3′-untranslated region and increased Bhlhe40 mRNA stability and expression. In another mechanism, SNHG1 enhanced Bhlhe40 protein SUMOylation by serving as a scaffold to facilitate the binding of SUMO E3 ligase PIAS3 and Bhlhe40 protein, resulting in increased nuclear translocation of Bhlhe40 protein. Moreover, Bhlhe40 suppressed the expression of Atg10, which is involved in the process of autophagosome formation. Collectively, the protective effect of SNHG1 on HG-induced HA-VSMCs calcification/senescence is accomplished by stabilizing Bhlhe40 mRNA and promoting the nuclear translocation of Bhlhe40 protein. Our study could provide a novel approach for diabetic vascular calcification/aging. (AU)

Postprandial triglyceride-rich lipoproteins promote the adipogenic differentiation of adipose-derived mesenchymal stem cells via the LRP1/caveolin-1/AKT1 pathway.

Diet-induced obesity (OB) is usually accompanied by hypertriglyceridemia, which is characterized by the accumulation of triglyceride (TG)-rich lipoprotein (TRL) particles in the circulation. We previously found that postprandial TRL combined with insulin induced the adipogenic differentiation of 3T3-L1 preadipocytes, which may represent a key mechanism underlying obesity. However, the specific mechanism and signaling pathway involved in this process remain to be fully elucidated. In this study, we found that, in the postprandial state, patients with obesity had significantly higher levels of TG and remnant cholesterol (RC) than normal-weight controls. In vitro, we found that postprandial TRL, together with insulin, promoted the adipogenic differentiation of adipose-derived mesenchymal stem cells (AMSCs), as evidenced by the increased expression of lipogenesis-related genes and their protein products, including low-density lipoprotein related protein 1 (LRP1). Besides, caveolin-1 (Cav-1) expression was also significantly upregulated under this condition. Cav-1 and LRP1 were observed to interact, and then led to the activation of the PI3K/AKT1 signaling pathway. Meanwhile, the inhibition of LRP1 or Cav-1 significantly attenuated the adipogenic differentiation of AMSCs and downregulated AKT1 phosphorylation levels. Moreover, treatment with a selective AKT1 inhibitor significantly suppressed postprandial TRL and insulin-induced adipogenesis in AMSCs. Combined, our results demonstrated that, in association with insulin, postprandial TRL can promote the adipogenic differentiation of AMSCs in a manner that is dependent on the LRP1/Cav-1-mediated activation of the PI3K/AKT1 signaling pathway. Our findings indicated that a postprandial increase in TRL content is a critical factor in the pathogenesis of hypertriglyceridemia and diet-induced obesity.

Long noncoding RNA SNHG1 alleviates high glucose-induced vascular smooth muscle cells calcification/senescence by post-transcriptionally regulating Bhlhe40 and autophagy via Atg10.

Long noncoding RNAs (lncRNAs) are emerging regulators of vascular diseases, yet their role in diabetic vascular calcification/aging remains poorly understood. In this study, we identified a down-expressed lncRNA SNHG1 in high glucose (HG)-induced vascular smooth muscle cells (HA-VSMCs), which induced excessive autophagy and promoted HA-VSMCs calcification/senescence. Overexpression of SNHG1 alleviated HG-induced HA-VSMCs calcification/senescence. The molecular mechanisms of SNHG1 in HA-VSMCs calcification/senescence were explored by RNA pull-down, RNA immunoprecipitation, RNA stability assay, luciferase reporter assay, immunoprecipitation and Western blot assays. In one mechanism, SNHG1 directly interacted with Bhlhe40 mRNA 3'-untranslated region and increased Bhlhe40 mRNA stability and expression. In another mechanism, SNHG1 enhanced Bhlhe40 protein SUMOylation by serving as a scaffold to facilitate the binding of SUMO E3 ligase PIAS3 and Bhlhe40 protein, resulting in increased nuclear translocation of Bhlhe40 protein. Moreover, Bhlhe40 suppressed the expression of Atg10, which is involved in the process of autophagosome formation. Collectively, the protective effect of SNHG1 on HG-induced HA-VSMCs calcification/senescence is accomplished by stabilizing Bhlhe40 mRNA and promoting the nuclear translocation of Bhlhe40 protein. Our study could provide a novel approach for diabetic vascular calcification/aging.

The accuracy of four formulas for LDL-C calculation at the fasting and postprandial states.

Background: Elevated level of low-density lipoprotein cholesterol (LDL-C) is concerned as one of the main risk factors for cardiovascular disease, in both the fasting and postprandial states. This study aimed to compare the measured LDL-C with LDL-C calculated by the Friedewald, Martin-Hopkins, Vujovic, and Sampson formulas, and establish which formula could provide the most reliable LDL-C results for Chinese subjects, especially at the postprandial state. Methods: Twenty-six subjects were enrolled in this study. The blood samples were collected from all the subjects before and after taking a daily breakfast. The calculated LDL-C results were compared with LDL-C measured by the vertical auto profile method, at both the fasting and postprandial states. The percentage difference between calculated and measured LDL-C (total error) and the number of results exceeding the total error goal of 12% were established. Results: The calculated LDL-CF levels showed no significant difference from LDL-CVAP levels at the fasting state. The calculated LDL-CS were significantly higher than LDL-CVAP at the fasting state (P < 0.05), while the calculated LDL-Cs were very close to LDL-CVAP levels after a daily meal. At the fasting state, the median total error of calculated LDL-CF was 0 (quartile: -3.8 to 6.0), followed by LDL-CS, LDL-CMH, and LDL-CV. At the postprandial states, the median total errors of LDL-CS were the smallest, 1.0 (-7.5, 8.5) and -0.3 (-10.1, 10.9) at 2 and 4 h, respectively. The calculated LDL-CF levels showed the highest correlation to LDL-CVAP and accuracy in evaluating fasting LDL-C levels, while the Sampson formula showed the highest accuracy at the postprandial state. Conclusion: The Friedewald formula was recommended to calculate fasting LDL-C, while the Sampson formula seemed to be a better choice to calculate postprandial LDL-C levels in Chinese subjects.

New insight into dyslipidemia-induced cellular senescence in atherosclerosis.

Atherosclerosis, characterized by lipid-rich plaques in the arterial wall, is an age-related disorder and a leading cause of mortality worldwide. However, the specific mechanisms remain complex. Recently, emerging evidence has demonstrated that senescence of various types of cells, such as endothelial cells (ECs), vascular smooth muscle cells (VSMCs), macrophages, endothelial progenitor cells (EPCs), and adipose-derived mesenchymal stem cells (AMSCs) contributes to atherosclerosis. Cellular senescence and atherosclerosis share various causative stimuli, in which dyslipidemia has attracted much attention. Dyslipidemia, mainly referred to elevated plasma levels of atherogenic lipids or lipoproteins, or functional impairment of anti-atherogenic lipids or lipoproteins, plays a pivotal role both in cellular senescence and atherosclerosis. In this review, we summarize the current evidence for dyslipidemia-induced cellular senescence during atherosclerosis, with a focus on low-density lipoprotein (LDL) and its modifications, hydrolysate of triglyceride-rich lipoproteins (TRLs), and high-density lipoprotein (HDL), respectively. Furthermore, we describe the underlying mechanisms linking dyslipidemia-induced cellular senescence and atherosclerosis. Finally, we discuss the senescence-related therapeutic strategies for atherosclerosis, with special attention given to the anti-atherosclerotic effects of promising geroprotectors as well as anti-senescence effects of current lipid-lowering drugs.

Roles and mechanisms of exosomal non-coding RNAs in human health and diseases.

Exosomes play a role as mediators of cell-to-cell communication, thus exhibiting pleiotropic activities to homeostasis regulation. Exosomal non-coding RNAs (ncRNAs), mainly microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), are closely related to a variety of biological and functional aspects of human health. When the exosomal ncRNAs undergo tissue-specific changes due to diverse internal or external disorders, they can cause tissue dysfunction, aging, and diseases. In this review, we comprehensively discuss the underlying regulatory mechanisms of exosomes in human diseases. In addition, we explore the current knowledge on the roles of exosomal miRNAs, lncRNAs, and circRNAs in human health and diseases, including cancers, metabolic diseases, neurodegenerative diseases, cardiovascular diseases, autoimmune diseases, and infectious diseases, to determine their potential implication in biomarker identification and therapeutic exploration.

Determination of the Optimal Cutoff Value of Triglyceride That Corresponds to Fasting Levels in Chinese Subjects With Marked Hypertriglyceridemia.

The level of triglyceride (TG) ≥ 2. 3 mmol/L is suggestive of marked hypertriglyceridemia (HTG) and requires treatment with a triglyceride-lowering agent in high-risk and very high-risk patients as recommended by the 2019 ESC/EAS guidelines for the management of dyslipidemia. However, the optimal cutoff value required to diagnose non-fasting HTG that corresponds to the fasting goal level of 2.3 mmol/L in Chinese subjects is unknown. This study enrolled 602 cardiology inpatients. Blood lipid levels, including calculated non-high-density lipoprotein cholesterol (non-HDL-C) and remnant cholesterol (RC), were measured at 0, 2, and 4 h after a daily Chinese breakfast. Of these, 482 inpatients had TG levels of <2.3 mmol/L (CON group) and 120 inpatients had TG levels of ≥2.3 mmol/L (HTG group). Receiver operating characteristic (ROC) curve analysis was used to determine the cutoff values for postprandial HTG that corresponded to a target fasting level of 2.3 mmol/L. Marked hypertriglyceridemia (≥2.3 mmol/L) was found in 120 (19.9%) patients in this study population. The levels of non-fasting TG and RC increased significantly in both groups and reached the peak at 4 h after a daily meal, especially in the HTG group (p < 0.05). The optimal cutoff value of TG at 4 h, which corresponds to fasting TG of ≥2.3 mmol/L, that can be used to predict HTG, was 2.66 mmol/L. According to the new non-fasting cutoff value, the incidence of non-fasting HTG is close to its fasting level. In summary, this is the first study to determine the non-fasting cutoff value that corresponds to a fasting TG of ≥2.3 mmol/L in Chinese patients. Additionally, 2.66 mmol/l at 4 h after a daily meal could be an appropriate cutoff value that can be used to detect non-fasting marked HTG in Chinese subjects.

Non-fasting lipid profile for cardiovascular risk assessments using China ASCVD risk estimator and Europe SCORE risk charts in Chinese participants.

BACKGROUND: Previous studies have shown that non-fasting lipids have similar values in cardiovascular risk estimation as fasting, but it is not clear whether this could also be applicable to Chinese participants. METHODS: A total of 127 (76 men, 51 women) participants without atherosclerotic cardiovascular diseases (ASCVD) were enrolled in the study. Serum levels of blood lipids were monitored at 0 h, 2 h and 4 h after a daily breakfast. Ten-year cardiovascular disease (CVD) risk was estimated with China ASCVD risk estimator and European SCORE risk charts. Kappa statistic was used to determine agreement among estimators. RESULTS: China ASCVD risk estimator assessed half of the participants as low risk, while European risk charts assessed half of the participants as moderate risk in the same participants. Reliability analysis in China ASCVD risk estimator and Europe SCORE risk charts based on fasting and or non-fasting lipids profile were relatively high (Kappa =0.731 or 0.718, P<0.001), (Kappa =0.922 or 0.935, P<0.001) (Kappa =0.886 or 0.874, P<0.001), but agreement between two were relatively poor in both fasting and non-fasting states (Kappa =0.339 or 0.300, P<0.001), (Kappa =0.364 or 0.286, P<0.001). CONCLUSIONS: Promoting use of non-fasting lipids in diagnosis, evaluation, and prediction of CVD are feasible. Furthermore, non-fasting lipids could be used in China ASCVD risk estimator to evaluate 10-year risk of ASCVD among Chinese general participants.

Comparison of the Reductions in LDL-C and Non-HDL-C Induced by the Red Yeast Rice Extract Xuezhikang Between Fasting and Non-fasting States in Patients With Coronary Heart Disease.

Background: Xuezhikang, an extract of red yeast rice, effectively lowers fasting blood lipid levels. However, the influence of Xuezhikang on the non-fasting levels of low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non-HDL-C) has not been explored in Chinese patients with coronary heart disease (CHD). Methods: Fifty CHD patients were enrolled and randomly divided into two groups (n = 25 each) to receive 1,200 mg/d of Xuezhikang or a placebo for 6 weeks as routine therapy. Blood lipids were repeatedly measured before and after 6 weeks of treatment at 0, 2, 4, and 6 h after a standard breakfast containing 800 kcal and 50 g of fat. Results: The serum LDL-C levels significantly decreased, from a fasting level of 3.88 mmol/L to non-fasting levels of 2.99, 2.83, and 3.23 mmol/L at 2, 4, and 6 h, respectively, after breakfast (P < 0.05). The serum non-HDL-C level mildly increased from a fasting level of 4.29 mmol/L to non-fasting levels of 4.32, 4.38, and 4.34 mmol/L at 2, 4, and 6 h post-prandially, respectively, and the difference reached statistical significance only at 4 and 6 h after breakfast (P < 0.05). After 6 weeks of Xuezhikang treatment, the patients had significantly lower fasting and non-fasting serum levels of LDL-C and non-HDL-C (P < 0.05) than at pretreatment. The LDL-C levels were reduced by 27.8, 28.1, 26.2, and 25.3% at 0, 2, 4, and 6 h, respectively, and the non-HDL-C levels were reduced by 27.6, 28.7, 29.0, and 28.0% at 0, 2, 4, and 6 h, respectively, after breakfast. No significant difference was found in the percent reductions in the LDL-C and non-HDL-C levels among the four different time-points. Conclusions: Six weeks of Xuezhikang treatment significantly decreased LDL-C and non-HDL-C levels, with similar percent reductions in fasting and non-fasting states in CHD patients, indicating that the percent change in non-fasting LDL-C or non-HDL-C could replace that in the fasting state for evaluation the efficacy of cholesterol control in CHD patients who are unwilling or unable to fast.

Change in Postprandial Level of Remnant Cholesterol After a Daily Breakfast in Chinese Patients With Hypertension.

Background: Hypertension (HBP) is usually accompanied by hypertriglyceridemia that represents the increased triglyceride-rich lipoproteins and cholesterol content in remnant lipoproteins [i.e., remnant cholesterol (RC)]. According to the European Atherosclerosis Society (EAS), high RC (HRC) is defined as fasting RC ≥0.8 mmol/L and/or postprandial RC ≥0.9 mmol/L. However, little is known about postprandial change in RC level after a daily meal in Chinese patients with HBP. Methods: One hundred thirty-five subjects, including 90 hypertensive patients (HBP group) and 45 non-HBP controls (CON group), were recruited in this study. Serum levels of blood lipids, including calculated RC, were explored at 0, 2, and 4 h after a daily breakfast. Receiver operating characteristic (ROC) curve analysis was used to determine the cutoff point of postprandial HRC. Results: Fasting TG and RC levels were significantly higher in the HBP group (P < 0.05), both of which increased significantly after a daily meal in the two groups (P < 0.05). Moreover, postprandial RC level was significantly higher in the HBP group (P < 0.05). ROC curve analysis showed that the optimal cutoff point for RC after a daily meal to predict HRC corresponding to fasting RC of 0.8 mmol/L was 0.91 mmol/L, which was very close to that recommended by the EAS, i.e., 0.9 mmol/L. Fasting HRC was found in 31.1% of hypertensive patients but not in the controls. According to the postprandial cutoff point, postprandial HRC was found in approximately half of hypertensive patients and ~1-third of the controls. Conclusion: Postprandial RC level increased significantly after a daily meal, and hypertensive patients had higher percentage of HRC at both fasting and postprandial states. More importantly, the detection of postprandial lipids could be helpful to find HRC.

Non-HDL-C Is More Stable Than LDL-C in Assessing the Percent Attainment of Non-fasting Lipid for Coronary Heart Disease Patients.

This study aimed to compare the percentage attainment of fasting and non-fasting LDL-C and non-HDL-C target levels in coronary heart disease (CHD) patients receiving short-term statin therapy. This study enrolled 397 inpatients with CHD. Of these, 197 patients took statins for <1 month (m) or did not take any statin before admission (CHD1 group), while 204 patients took statins for ≥1 m before admission (CHD2 group). Blood lipid levels were measured at 0, 2, and 4 h after a daily breakfast. Non-fasting LDL-C and non-HDL-C levels significantly decreased after a daily meal (P < 0.05). Both fasting and non-fasting LDL-C or non-HDL-C levels were significantly lower in the CHD2 group. The percentage attainment of LDL-C <1.4 mmol/L at 2 and 4 h after a daily breakfast was significantly higher than that during fasting (P < 0.05), but the percent attainment of non-fasting non-HDL-C <2.2 mmol/L was close to its fasting value (P > 0.05). Analysis of c-statistic showed that non-fasting cut-off points for LDL-C and non-HDL-C were 1.19 and 2.11 mmol/L, corresponding to their fasting goal levels of 1.4 and 2.2 mmol/L, respectively. When post-prandial LDL-C and non-HDL-C goal attainments were re-evaluated using non-fasting cut-off points, there were no significant differences in percentage attainment between fasting and non-fasting states. Non-HDL-C is more stable than LDL-C in assessing the percent attainment of non-fasting lipid for coronary heart disease patients. If we want to use LDL-C to assess the percent attainment of post-prandial blood lipids, we may need to determine a lower non-fasting cut-off point.

A rare case of thymic carcinoid presenting with gastrointestinal symptoms and pericardium effusion.

BACKGROUND: Thymic carcinoid is one of an extremely rare type of malignant neuroendocrine tumor with a poor prognosis. Invasion of thymic carcinoid to other organs could lead to devastating consequences. It has been reported that thymic carcinoid mainly invaded to the pleura, lungs, liver, pancreas and bone, while rarely to the cardiac, especially to the ventricle. CASE PRESENTATION: A 53-year-old man presented with gastrointestinal symptoms and persistent pericardial effusion. Multiple imaging tools, including chest computed tomography (CT), magnetic resonance imaging (MRI), 18F-Fluorodeoxyglucose positron emission tomography/CT (18F-FDG PET/CT) showed a malignant neoplasm arising from the thymus invading into the biventricular myocardium, pericardium, and left superior pulmonary veins. The tumor was finally diagnosed as a thymic carcinoid through pathological examination. CONCLUSION: This is a rare case of thymic carcinoid invading the ventricular myocardium, which presented as subacute heart failure. The observations in this case would be useful for differential diagnosis of primary heart disease and invasion of heart due to thymic carcinoid.

Postprandial triglyceride-rich lipoproteins-induced premature senescence of adipose-derived mesenchymal stem cells via the SIRT1/p53/Ac-p53/p21 axis through oxidative mechanism.

The accumulation of senescent adipose-derived mesenchymal stem cells (AMSCs) in subcutaneous white adipose tissue (WAT) is the main cause for the deterioration of WAT and the subsequent age-related disorders in obesity. The number of AMSCs staining positively for senescence-associated-ß-galactosidase (SA-ß-Gal) increased significantly after incubation with postprandial triglyceride-rich lipoproteins (TRL), accompanied by an impaired cell proliferation capacity and increased expression of inflammatory factors. Besides, the expression of anti-aging protein, silent mating-type information regulation 2 homolog 1 (SIRT1), was downregulated significantly, while those of acetylated p53 (Ac-p53), total p53, and p21 proteins were upregulated significantly during postprandial TRL-induced premature senescence of AMSCs. Furthermore, the production of intracellular reactive oxygen species (ROS) in the TRL group increased significantly, while pretreatment with the ROS scavenger N-acetyl-L-cysteine effectively attenuated the premature senescence of AMSCs by decreasing ROS production and upregulating SIRT1 level. Thus, postprandial TRL induced premature senescence of AMSCs through the SIRT1/p53/Ac-p53/p21 axis, partly through increased oxidative stress.