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.

Overexpression of miR-146a promotes cell proliferation and migration in a model of diabetic foot ulcers by regulating the AKAP12 axis.

In the current study, we aimed to study the effect of miR-146a on proliferation and migration in an in vitro diabetic foot ulcer (DFU) model by targeting A-kinase-anchoring protein 12 (AKAP12). An in vitro DFU model was initially established using HaCaT cells derived from human keratinocytes and induced by advanced glycation end products (AGEs). The effects of overexpression of miR-146a on proliferation and migration ability were analysed. The expression levels of miR-146a and AKAP12 were measured by quantitative real-time polymerase chain reaction (qRT-PCR), and AKAP12, hypoxia-inducible factor-1α (HIF-1α), Wnt3a and ß-catenin protein levels were measured by western blotting. The cell proliferation ability was measured by MTT, and the migration ability was analysed by a cell scratch assay. The binding between miR-146a and AKAP12 was identified using a luciferase reporter assay. The results demonstrated that AGEs significantly suppressed cell proliferation and migration, while the expression of miR-146a decreased and the expression of AKAP12 increased. A luciferase reporter assay revealed that miR-146a could directly target AKAP12. Overexpression of miR-146a promoted cell proliferation and migration in an in vitro DFU model and also promoted the expression of HIF-1α, Wnt3a and ß-catenin but suppressed the expression of AKAP12. Co-overexpression of miR-146a and AKAP12 reversed the effect of miR-146a on cell proliferation and migration. Our findings revealed that miR-146a directly targeted AKAP12 and promoted cell proliferation and migration in an in vitro DFU model. This study provides a new perspective for the study of miR-146a in the treatment of DFU.

Thamnolia vermicularis extract improves learning ability in APP/PS1 transgenic mice by ameliorating both Aß and Tau pathologies.

Considering the complicated pathogenesis of Alzheimer's disease (AD), multi-targets have become a focus in the discovery of drugs for treatment of this disease. In the current work, we established a multi-target strategy for discovering active reagents capable of suppressing both Aß level and Tau hyperphosphorylation from natural products, and found that the ethanol extract of Thamnolia vermicularis (THA) was able to improve learning ability in APP/PS1 transgenic mice by inhibiting both Aß levels and Tau hyperphosphorylation. SH-SY5Y and CHO-APP/BACE1 cells and primary astrocytes were used in cell-based assays. APP/PS1 transgenic mice [B6C3-Tg(APPswe, PS1dE9)] were administered THA (300 mg·kg-1·d-1, ig) for 100 d. After the administration was completed, the learning ability of the mice was detected using a Morris water maze (MWM) assay; immunofluorescence staining, Congo red staining and Thioflavine S staining were used to detect the senile plaques in the brains of the mice. ELISA was used to evaluate Aß and sAPPß contents, and Western blotting and RT-PCR were used to investigate the relevant signaling pathway regulation in response to THA treatment. In SH-SY5Y cells, THΑ (1, 10, 20 µg/mL) significantly stimulated PI3K/AKT/mTOR and AMPK/raptor/mTOR signaling-mediated autophagy in the promotion of Aß clearance as both a PI3K inhibitor and an AMPK indirect activator, and restrained Aß production as a suppressor against PERK/eIF2α-mediated BACE1 expression. Additionally, THA functioned as a GSK3ß inhibitor with an IC50 of 1.32±0.85 µg/mL, repressing Tau hyperphosphorylation. Similar effects on Aß accumulation and Tau hyperphosphorylation were observed in APP/PS1 transgenic mice treated with THA. Furthermore, administration of THA effectively improved the learning ability of APP/PS1 transgenic mice, and markedly reduced the number of senile plaques in their hippocampus and cortex. The results highlight the potential of the natural product THA for the treatment of AD.

Comparison between Fasting and Non-Fasting Cut-Off Values of Triglyceride in Diagnosing High Triglyceride in Chinese Hypertensive Outpatients.

Background: Hypertension (HBP) often occurs together with hypertriglyceridemia which indicates elevated triglyceride (TG) and remnant cholesterol (RC) levels. Non-fasting (i.e., postprandial) blood lipid test after a daily meal has been recommended by the European Atherosclerosis Society (EAS). However, little is known about the difference between fasting and non-fasting cut-off values in assessing high TG (HTG) and high RC (HRC) in HBP outpatients. Methods: 225 Chinese outpatients with HBP, including 119 fasting patients (i.e., fasting group) and 106 non-fasting patients (i.e., non-fasting group) were enrolled in this study. Non-fasting levels of blood lipids at 2 h after a daily breakfast were also tested in 33 patients among the fasting group. Venous blood samples were collected. Results: The non-fasting group had significantly higher levels of TG and RC while lower levels of total cholesterol, low-density lipoprotein cholesterol, and non-high-density lipoprotein cholesterol than the fasting group (p < 0.05). According to the TG and RC cut-off values of the EAS, the percentages of HTG and HRC in the non-fasting group were 72.6% and 70.8%, respectively, whereas those in the fasting group were 57.1% and 52.9%, respectively. According to the cut-off value of marked HTG commonly used in the Chinese population in clinical practice, the percentage of marked HTG in the non-fasting group was 57.5%, whereas that in the fasting group was 34.5%. However, the percentages of HTG (57.6% vs. 51.5%) and HRC (51.5% vs. 51.5%) marked HTG (30.3% vs. 33.3%) in the fasting state and at 2 h after a daily breakfast in 33 outpatients did not reach statistical significance. Conclusion: Non-fasting blood lipid tests could find more individuals with HTG as well as those with marked HTG among Chinese outpatients with HBP. It indicates that non-fasting blood lipid tests are worth being recommended in patients with HBP.

Effects of Xuezhikang versus Pravastatin on Triglyceride Level in Patients with T2DM and Dyslipidemia: Study Protocol for a Multicenter Randomized Controlled Trial.

BACKGROUND: Hypertriglyceridemia, is commonly found in patients with diabetes. Xuezhikang, an extract of red yeast rice, is effective in reducing cardiovascular events in Chinese patients with diabetes and coronary heart disease (CHD). Xuezhikang has been reported to significantly decrease the level of triglycerides (TG), a potential causal risk factor for myocardial infarction. On the basis of a similar reduction in low-density lipoprotein cholesterol, this study will evaluate the effect of xuezhikang on TG levels compared with pravastatin in patients with type 2 diabetes mellitus (T2DM) and dyslipidemia. METHODS: This is an open-label, multicenter, randomized controlled study to assess the effects of xuezhikang (1.2 g/day) and pravastatin (20 mg/day) on TG and other blood lipid parameters in patients with T2DM and dyslipidemia. A total of 114 patients will be enrolled and randomly assigned 1:1 to receive xuezhikang or pravastatin treatment for 6 weeks. RESULT: The primary outcome measure is the change from baseline in fasting TG levels after 6 weeks. The change from baseline in other fasting and postprandial lipid parameters, and glucose profiles at 1, 2, and 4 h after a nutritious breakfast will also be explored. CONCLUSION: This study will evaluate the effect of a 6-week treatment with xuezhikang compared with pravastatin on fasting and postprandial TG levels and other blood lipid parameters in patients with T2DM and dyslipidemia without atherosclerotic cardiovascular disease (ASCVD). The results will provide more information on optimizing the lipid control of patients with diabetes in the primary prevention of ASCVD.

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.

Determination of the postprandial cut-off value of triglyceride after a daily meal corresponding to fasting optimal triglyceride level in Chinese subjects.

Background: According to the 2021 consensus statement about triglyceride (TG)-rich lipoproteins and their remnants from the European Atherosclerosis Society (EAS), fasting TG level < 1.2 mmol/L is regarded as optimal, otherwise considered as non-optimal TG (NoTG). However, the postprandial cut-off value after a daily meal corresponding to a fasting TG level of 1.2 mmol/L has not been explored. Materials and methods: Six hundred and eighteen inpatients aged 18 to 70 were recruited in this study. Among them, 219 subjects had fasting TG levels < 1.2 mmol/L (i.e., OTG group), and 399 subjects had fasting TG levels ≥ 1.2 mmol/L (i.e., NoTG group). Serum levels of blood lipids, including calculated non-high-density lipoprotein cholesterol (non-HDL-C) and remnant cholesterol (RC), were monitored at 0, 2, and 4 h after a daily Chinese breakfast according to their dietary habits. Receiver operating characteristic (ROC) curve analysis was used to determine the postprandial cut-off value corresponding to the fasting TG level of 1.2 mmol/L. Kappa statistics were performed to determine the consistency between fasting and postprandial cut-off values in determining whether TG was optimal. Univariate and multivariate logistic regression analyses were conducted to evaluate the associations between NoTG and potential confounders. Subgroup analyses were performed to explore the association between postprandial TG levels at 4h (pTG4h) and NoTG in greater detail. Results: Postprandial levels of TG and RC significantly elevated and peaked at 4h after a daily breakfast in two groups (P < 0.05). The optimal cut-off value at 4h corresponding to fasting TG of 1.2 mmol/L was 1.56 mmol/L. According to the fasting cut-off value, the percentage of patients with NoTG was 64.6% in the fasting state while increasing obviously to 73.3-78.4% at 2 and 4h, respectively, after a daily Chinese breakfast. According to the postprandial cut-off value, the percentage of patients with NoTG at 4h after a daily Chinese breakfast was 62.6% which was close to 64.6% in the fasting state. The Kappa coefficient was 0.551, indicating a moderate consistency between the fasting and postprandial cut-off values in the diagnosis of NoTG. Moreover, the subjects with NoTG determined by the postprandial TG cut-off value had an obviously higher postprandial level of RC (1.2 vs. 0.8 mmol/L) and percentage of HRC (37.1 vs. 32.1%) than those determined by the fasting TG cut-off value. Multivariate logistic regression analyses demonstrated that except for BMI, pTG4h emerged as an independent predictor of not. Subgroup analyses revealed that the association between pTG4h and NoTG was consistent across subgroups. Conclusion: Taken together, we for the first time determined TG 1.56 mmol/L as the postprandial cut-off value corresponding to fasting TG 1.2 mmol/L in Chinese subjects. This could make it more convenient to determine whether TG is optimal or not in the fasting or postprandial state.

Myocardial Damage in a Highly Suspected Case With Paraneoplastic Pemphigus: A Case Report and Literature Review.

Paraneoplastic pemphigus (PNP) is a rare mucocutaneous autoimmune disease. It has multiple clinical accompanied symptoms by affecting various types of epithelia, including the gastrointestinal and respiratory tract. However, an extensive review of the literature found no cases of PNP associated with myocardial damage. Here, we present a 56-year-old male patient with clinically and histopathologically typical paraneoplastic pemphigus (PNP), who had sustained myocardial injury due to non-cardiac disease involvement. Therefore, we suppose that, when persistent cardiac necrosis markers are elevated in patients with paraneoplastic pemphigus (PNP), the possibility of concomitant myocardial damage should get more attention from clinicians to obtain quick diagnosis and treatment.

The complete chloroplast genome of Stichorkis gibbosa (Orchidaceae: Malaxideae).

Stichorkis gibbosa is a rare orchid species of the tribe Malaxideae mainly distributed in tropical Asia. This is the only species of the genus Stichorkis Thouars which has been reported to occur in China. Despite the importance of this genus, previous molecular studies based on few markers have resulted in limited phylogenetic resolution. With the decline of habitats, the wild population of S. gibbosa has decreased in recent years. In this study, we first reported the complete chloroplast (cp) genome of S. gibbosa. The entire cp genome was determined to be 158,056 bp in length with overall GC content of 36.9%, containing a pair of inverted repeat regions (IRs) of 27,006 bp, separated by a large single-copy (LSC, 86,280 bp) and a small single-copy (SSC, 17,764 bp). A total of 133 unique genes were annotated, including 87 protein-coding genes, 38 tRNA genes, and eight rRNA genes. The phylogenetic tree indicated that S. gibbosa was a sister group of the genus Oberonia and the epiphytic Liparis alliance with strong support.

Non-fasting Changes in Blood Lipids After Three Daily Meals Within a Day in Chinese Inpatients With Cardiovascular Diseases.

Background: Non-fasting (i.e., postprandial) lipid detection is recommended in clinical practice. However, the change in blood lipids in Chinese patients with cardiovascular diseases after three daily meals has never been reported yet. Methods: Serum levels of blood lipids were measured or calculated in 77 inpatients (48 men and 29 women) at high or very high risk of atherosclerotic cardiovascular disease (ASCVD) in the fasting state and at 4 h after three meals within a day according to their diet habits. Results: Female patients showed significantly higher level of high-density lipoprotein cholesterol (HDL-C) than male patients, and the gender difference in other lipid parameters did not reach statistical significance at any time-point. Levels of triglyceride (TG) and remnant cholesterol (RC) increased, while that of low-density lipoprotein cholesterol (LDL-C) decreased significantly after three meals (p < 0.05). Levels of HDL-C, total cholesterol (TC), and non-high-density lipoprotein cholesterol (non-HDL-C) showed smaller changes after three meals. Percent reductions in the non-fasting LDL-C levels after lunch and supper were around 20%, which were greater than that after breakfast. The percent reductions in the non-fasting non-HDL-C levels after three meals were smaller than those in the non-fasting LDL-C levels. Patients with TG level ≥ 2.0 mmol/L (177 mg/dL) after lunch had significantly greater absolute reduction of LDL-C level than those with TG level < 2.0 mmol/L (177 mg/dL) after lunch [-0.69 mmol/L (-27 mg/dL) vs. -0.36 mmol/L (-14 mg/dL), p<0.01]. There was a significant and negative correlation between absolute change in LDL-C level and that in TG level (r = -0.32) or RC level (r = -0.67) after lunch (both p<0.01). Conclusion: LDL-C level decreased significantly after three daily meals in Chinese patients at high or very high risk of ASCVD, especially when TG level reached its peak after lunch. Relatively, non-HDL-C level was more stable than LDL-C level postprandially. Therefore, when LDL-C level was measured in the non-fasting state, non-HDL-C level could be evaluated simultaneously to reduce the interference of related factors, such as postprandial hypertriglyceridemia, on detection.

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.

Deletion of Dcf1 Reduces Amyloid-ß Aggregation and Mitigates Memory Deficits.

BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disease. One of the pathologies of AD is the accumulation of amyloid-ß (Aß) to form senile plaques, leading to a decline in cognitive ability and a lack of learning and memory. However, the cause leading to Aß aggregation is not well understood. Dendritic cell factor 1 (Dcf1) shows a high expression in the entorhinal cortex neurons and neurofibrillary tangles in AD patients. OBJECTIVE: Our goal is to investigate the effect of Dcf1 on Aß aggregation and memory deficits in AD development. METHODS: The mouse and Drosophila AD model were used to test the expression and aggregation of Aß, senile plaque formation, and pathological changes in cognitive behavior during dcf1 knockout and expression. We finally explored possible drug target effects through intracerebroventricular delivery of Dcf1 antibodies. RESULTS: Deletion of Dcf1 resulted in decreased Aß42 level and deposition, and rescued AMPA Receptor (GluA2) levels in the hippocampus of APP-PS1-AD mice. In Aß42 AD Drosophila, the expression of Dcf1 in Aß42 AD flies aggravated the formation and accumulation of senile plaques, significantly reduced its climbing ability and learning-memory. Data analysis from all 20 donors with and without AD patients aged between 80 and 90 indicated a high-level expression of Dcf1 in the temporal neocortex. Dcf1 contributed to Aß aggregation by UV spectroscopy assay. Intracerebroventricular delivery of Dcf1 antibodies in the hippocampus reduced the area of senile plaques and reversed learning and memory deficits in APP-PS1-AD mice. CONCLUSION: Dcf1 causes Aß-plaque accumulation, inhibiting dcf1 expression could potentially offer therapeutic avenues.

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.

Diagnostic value of monocyte to high-density lipoprotein ratio in acute aortic dissection in a Chinese han population.

Background: Recently, considerable evidence pointed out monocyte to high-density lipoprotein ratio (MHR) is highly related to inflammatory related diseases. We aim to explore the level of MHR in acute aortic dissection (AAD) patients and determine whether MHR can be a novel diagnostic marker of AAD. Research design and methods: A total of 228 subjects including 128 AAD patients and 110 healthy control were enrolled. MHR levels and other serum samples were obtained at admission. Results: The baseline MHR levels were significantly higher in patients with AAD (p < 0.0001). A cutoff value of MHR >0.37 was associated with a sensitivity of 86.70% and a specificity of 93.60% for AAD. MHR levels were positively correlated with the time from symptom onset (R2 = 0.0318, p = 0.0003). Additionally, the area under the curve (AUC) was increased to 0.979 in patients whose time from onset of symptoms >24 h, with a sensitivity of 98.04% and a specificity of 93.64%. Multivariate logistic regression demonstrated that MHR levels, history of hypertension, and coronary artery disease (CHD) emerged as independent predictors of AAD. Expert Opinion: MHR has a high diagnostic value in AAD patients, especially in those whose time from onset of symptoms >24 h.

Comparison of remnant cholesterol levels estimated by calculated and measured LDL-C levels in Chinese patients with coronary heart disease.

BACKGROUND: Evidence about whether remnant cholesterol (RC), especially non-fasting RC, is a causal risk factor for coronary heart disease (CHD) in Chinese subjects is rare. Recently, estimated RC level (RCe) was applied in many studies with large population. We aimed to compare fasting and non-fasting RCe calculated by LDL-C level determined by different methods in Chinese subjects, and investigate their contributions to CHD. METHODS: Levels of TC, TG and HDL-C were measured directly in 273 CHD patients (CHD group) and 136 controls (CON group) before and at 4 h after a daily breakfast. LDL-C level was measured directly or calculated by Friedewald equation at TG < 4.5 mmol/L. RC level estimated by calculated or measured LDL-C was termed as RCe1 or RCe2. Contributions of different RC levels to CHD were evaluated by multivariable logistic regression analysis. RESULTS: Both RCe1 and RCe2 increased significantly at 4 h after breakfast (both p < 0.05). RCe1 was significantly higher than RCe2 in fasting or non-fasting state (p < 0.05). RCe1 was closely related to RCe2, especially in the highest quartile of RCe1 (p < 0.05). Non-fasting RCe1 or RCe2 and fasting RCe2 independently predicted CHD after adjustment for traditional risk factors (all p < 0.05). CONCLUSIONS: Although RCe1 was significantly higher than RCe2, non-fasting RCe, no matter RCe1 or RCe2, after a daily breakfast was an independent predictor for CHD risk in Chinese subjects, indicating that the non-fasting state is critical in the development of atherosclerosis.

Comparison of non-fasting LDL-C levels calculated by Friedewald formula with those directly measured in Chinese patients with coronary heart disease after a daily breakfast.

BACKGROUND: LDL-C level can be measured by direct methods (LDL-CM) or calculated by Friedewald formula (LDL-CC). The aim of this study was to investigate the difference between LDL-CM and LDL-CC after a daily breakfast in Chinese patients with coronary heart disease (CHD). METHODS: Three hundred and three inpatients, including 203 CHD patients (CHD group) and 100 non-CHD controls (CON group), were enrolled in this study. Serum levels of blood lipid parameters, including LDL-CC and LDL-CM, at 0, 2 and 4 h (h) were monitored after a daily breakfast in all subjects. RESULTS: LDL-CM was significantly higher than LDL-CC in fasting state in each group and at 4 h postprandially in CHD group (P < .05). Postprandial LDL-CM and LDL-CC significantly decreased in each group (P < .05). Postprandial decline in LDL-CM was significantly greater than that of LDL-CC (P < .05). For CHD patients taking statins for ≥1 month before admission, non-fasting percent attainment of LDL-CM or LDL-CC was significantly higher than its fasting value, especially at 4 h (P < .05). The percent deviation of LDL-CM from 1.8 mmol/L at 4 h was significantly different from its fasting value. However, there was no significant difference in percent deviation of LDL-CC from 1.8 mmol/L between fasting and non-fasting states. CONCLUSIONS: It indicated that the clinical monitoring of non-fasting LDL-C level in CHD patients could be relatively complex, and the judgement may depend not only on the method to acquire LDL-C level, but also on the evaluation method.

Changes in non-fasting concentrations of blood lipids after a daily Chinese breakfast in overweight subjects without fasting hypertriglyceridemia.

BACKGROUND: Overweight is always accompanied by hypertriglyceridemia (HTG), but the change in non-fasting triglyceride (TG) concentration in overweight subjects without postprandial hypertriglyceridemia was unknown. METHODS: Concentrations of serum lipids were measured at 2 and 4 h in matched overweight (OW group, n = 54) and control subjects (CON group, n = 55) after a daily meal. Concentrations of remnant cholesterol and non-HDL cholesterol were calculated according to the formulas. The diagnostic criteria for non-fasting HTG were based on 2 different consensus statement. ROC curve was used to determine the pointcut of postprandial HTG. RESULTS: OW group had higher fasting concentrations of RC and non-HDL-C than CON group. Non-fasting concentrations of triglyceride and RC significantly increased in 2 groups while were higher in OW group (p < .05). The proportion of non-fasting HTG increased after a daily meal in OW group was significantly higher than the percentage of fasting HTG (p < .05). There was a significant correlation between the postprandial concentrations of TG and RC. CONCLUSIONS: Overweight subjects were more likely to develop non-fasting hypertriglyceridemia and higher concentrations of RC and non-HDL-C. Additionally, 2.0 mmol/l at 4 h after breakfast could be a pointcut value to detect changes in lipid profile of Chinese overweight people.

Postprandial hypertriglyceridemia associated with inflammatory response and procoagulant state after a high-fat meal in hypertensive patients.

OBJECTIVE: To investigate the changes of inflammatory factors and hemostatic variable in plasma after a high-fat meal in normocholesterolemic patients with essential hypertension. METHODS: A total of 60 hypertensive patients were randomly assigned to accept a single high-fat meal (group 1, n=40) or not (group 2, n=20) in the morning after an overnight fast, and 20 healthy participants (group 3) consumed a single high-fat meal on the same day. Plasma lipid profiles, high-sensitivity C-reactive protein (hsCRP), tumor necrosis factor alpha (TNFalpha), soluble P-selectin and plasminogen activator inhibitor type 1 (PAI-1) antigen levels were measured at fasting and 4 h after meal ingestion. RESULTS: Postprandial triglyceride levels increased significantly in groups 1 and 3 (P<0.01), whereas levels were higher in group 1 (P<0.001). Postprandial plasma TNFalpha, hsCRP, soluble P-selectin and PAI-1 antigen levels increased in group 1 (P<0.001) but not in group 3. Postprandial plasma triglyceride level was correlated with log(hsCRP) (P<0.001), TNFalpha (P<0.001), soluble P-selectin (P<0.01) and PAI-1 antigen (P<0.05) levels, respectively. Both postprandial plasma level of soluble P-selectin and that of PAI-1 antigen were positively and significantly correlated with those of log(hsCRP) (P<0.01) and TNFalpha (P<0.001), respectively. CONCLUSION: Postprandial hypertriglyceridemia in hypertensive patients is associated with inflammatory response and procoagulant state.

[The relationship between apolipoprotein E genotype and hypertriglyceridemia-associated recurrent acute pancreatitis].

OBJECTIVE: To explore the relationship of apolipoprotein E (ApoE) genotype with hypertriglyceridemia-associated recurrent acute pancreatitis. METHODS: Taking the fasting serum triglyceride (TG) level > or = 2.3 mmol/L as hypertriglyceridemia, ApoE genotypes in 115 patients with hypertriglyceridemia-associated recurrent acute pancreatitis were assessed by polymerase chain reaction. According to the fasting serum TG level, all patients were divided into 3 groups: TG mild elevation group (2.3 mmol/L < or = TG < 5.5 mmol/L, Group A), TG moderate elevation group (5.5 mmol/L < or = TG < 11.3 mmol/L, Group B), and TG severe elevation group (TG > or = 11.3 mmol/L, Group C). RESULTS: Group C had significantly fewer patients with biliary tract disease, improper diet and heavy alcohol consumption, and significantly more patients with passed history of moderate-severe hypertriglyceridemia than Group A and B (P < 0.05). The proportion of patients with E3/4, E3/2, E2/4 and E2/2 genotypes and gene frequency for epsilon 2 and epsilon 4 alleles are significantly higher in Group C than in Group A and B(P < 0.05). Group B had significantly more patients with E3/2 genotype and higher gene frequency for epsilon 2 allele than Group A (P < 0.05). CONCLUSIONS: Apo epsilon 2 and epsilon 4 alleles are closely related to moderate-severe hypertriglyceridemia-associated recurrent acute pancreatitis.