Non-fasting Triglyceride Research Articles

Comparison of fasting and non-fasting lipid profile in healthy adult population

Lipid profile is done in fasting blood specimen commonly, the reasons being: 1. Triglycerides remain elevated for several hours in postprandial state, 2. Reference range are established for fasting serum lipid profile.This study was proposed to compare the lipid profiles obtained in fasting and non-fasting conditions. If a reliable correlation between fasting and non-fasting lipid profile will be obtained, assay for lipids in non-fasting state may be adopted for clinical evaluation. This might help in reducing the difficulties faced in obtaining the sample in fasting state. This was a cross-sectional study, conducted from October 2011 to October 2013. Total of 200 subjects were included in the study. Two Samples were collected from each individual, one sample after 8-12 hours fasting and second sample in non-fasting state (random sample). Total cholesterol, Triglycerides, HDL-cholesterol were analyzed by standard methods and, LDL-cholesterol was calculated using Friedewald’s formula. Significant increase was observed in non-fasting Triglyceride and VLDL-C as compared to fasting samples in total population, but we observed significant difference in total cholesterol and LDL-C in total population. Significant reduction was observed in HDL-C in non-fasting state as compared to fasting state. Positive correlation was observed between fasting and non-fasting total cholesterol triglyceride, VLDL-C, HDL-C and LDL-C in the total population. Non-fasting sample can be used to measure Total cholesterol and HDL-C. Non-fasting sample can be used to measure triglyceride, VLDL-C and LDL-C provided reference intervals are established in non-fasting state for the same in larger population.

Fasting Versus Non-Fasting in Assessing Lipid Profile and Complete Blood Picture

Coronary Heart Disease (CHD) is the world’s leading cause of death and represents a serious global health problem. The general recommendations to operators in the prevention of CHD should include complete lipid profile testing, that is Total Cholesterol(TC), Total Triglycerides(TG), High Density Lipoprotein (HDL), Low Density Lipoprotein (LDL) and Very Low Density Lipoprotein (VLDL). Recent recommendations have supported non-fasting lipid assessment. On the other hand, classification of dyslipidemias was derived in fasting samples, and cohort studies and clinical trials have performed fasting assessments.The aim of this study was to evaluate fasting versus non-fasting in measuring lipid profile & complete blood picture.A total of 80 female were divided into four groups of 20 female each. The 1st three groups were fasting for 4, 6,14 hours respectively and the 4th group was non-fasting. Blood samples were taken from these females for biochemical & hematological investigations.The lipid profile parameters were measured using Synchron CX4 clinical system Beckman Coulter Inc., Brea, CA. Complete Blood Picture was measured by using automated hematological analyzers BC-3000 plus (Hamburg, Germany). Statistical analysis was carried out using SPSS( Statistical Package for Social Sciences) number 22.Biochemically, for TC,TG & VLDL, it was found that fasting 6 , 14 hours gave significant differences (P< 0.05) when compared with non-fasting group while there were non-significant results for the mean level of HDL & LDL between groups . Regarding hematological assessment, there were non-significant differences between groups in measuring Hemoglobin, Red blood cells, White blood cells, Platelet counts.Since non-fasting may weaken the accuracy in diagnosing some forms of hyperlipidemia, we proposed that laboratories & organizations should also offer measurement of fasting triglycerides according to clinical situations , as in the case of very high non-fasting triglyceride concentration

Preliminary establishment of reference interval for non-fasting serum triglycerides among healthy middle-aged and elderly people in some communities Beijing

Objective To establish the reference interval of serum triglyceride (TG) for 4 hours after meal in healthy middle and old people of Beijing community, and to provide the diagnostic basis for the judgment of dyslipidemia after meal. Methods Selected 369 elderly people from January to October 2018 in the health examination of Guang′anmen Hospital of the Chinese Academy of Traditional Chinese Medicine. The subjects collected fasting venous blood samples in the morning the next day after fasting for 12 hours, then ate a standard breakfast that conformed to the local dietary habits, and collected venous blood samples again 4 hours after eating. Serum TG levels were measured 4 h after meal using AU5822 fully automatic biochemical analyzer and matching reagents. The comparison of postprandial TG between different age and sex groups was statistically significant using the nonparametric test of two independent samples, and the comparison between postprandial and fasting TG using the nonparametric test of two paired samples with P<0.05 as the difference. The 95% confidence interval was calculated using a nonparametric method according to the relevant requirements of the CLSI EP28-A3c file, and the reference interval was expressed as P2.5, P97.5. Results The median 4-hour post-prandial TG of the middle-aged and elderly aged 45-59 years and those aged ≥ 60 years at health checkups were 1.65 (1.25, 2.13) mmol/L and 1.58 (1.25, 2.00) mmol/L, there was no significant difference between the two groups (Z=-1.040, P>0.05). There was no statistical difference between males 1.69 (1.22, 2.31) mmol/L and females 1.63 (1.26, 2.12) mmol/L at 4 hours postprandial TG levels in the 45-59 year-old group (Z=-0.179, P>0.05),there was also no statistical difference between 1.64 (1.22, 2.06) mmol/L for men and 1.53 (1.28, 1.99) mmol/L for women aged 60 years or older (Z=-0.256, P>0.05).Compared with the median fasting TG of 1.05 (0.87, 1.29) mmol/L, the median serum TG of 1.61 (1.25, 2.09) mmol/L at 4 hours after meal was significantly increased (Z=-16.449, P<0.01). The difference between postprandial and fasting was 0.52 (0.30, 0.85) mmol/L.The reference range of serum TG at 4 hours after meal was 0.82 to 3.02 mmol/L. Conclusion In this study, the reference range of serum triglycerides for 4 hours after meal was established in some healthy elderly population groups in Beijing. Key words: Non-fasting serum Triglyceride; Healthy population; Middle-aged and elderly people; Reference range

Fasting and Non-Fasting Triglycerides and Risk of Cardiovascular Events in Diabetic Patients Under Statin Therapy.

Few data specifically investigate associations between fasting/non-fasting triglycerides (TG) and cardiovascular (CV) events under statin therapy among Japanese diabetic patients.Methods and Results:We recruited 4,988 participants with diabetes from the EMPATHY study. Median follow-up was 3 years. We evaluated associations between serum fasting/non-fasting TG and first CV events in Cox-regression hazard models adjusted by classical risk factors. CV events were defined as (1) major adverse cardiac events (MACE) including myocardial infarction, stroke, or cardiac death; and (2) CV diseases (CVD) including myocardial infarction, unstable angina, ischemic stroke, or large artery disease or peripheral arterial disease. Fasting as well as non-fasting TG were associated with MACE (adjusted hazard ratio [HR]: 1.017 per 10 mg/dL; 95% confidence interval [CI]: 1.000-1.037; P=0.046, adjusted HR: 1.028 per 10 mg/dL; 95% CI: 1.006-1.050; P=0.0091) and CVD (adjusted HR: 1.024 per 10 mg/dL; 95% CI: 1.011-1.038; P=4.4×10-3, adjusted HR: 1.028 per 10 mg/dL; 95% CI: 1.010-1.046; P=4.9×10-3). Comparing the top quartile with the bottom quartile of non-fasting TG, adjusted HR significantly increased 5.18 (95% CI: 1.38-18.3, P=0.014) for MACE, and 2.40 (95% CI: 1.11-4.75, P=0.021) for CVD, while adjusted HR did not change when divided into quartile of fasting TG. Non-fasting TG could be considered as a substitute for fasting TG as a risk stratification for future CV events among Japanese diabetic patients.

Genomics of hypertriglyceridemia.

With regard to heritability of phenotypes, the serum triglyceride level is considered to be highly heritable, with approximately 50% of its variability estimated to derive from parents. Thus, approximately 50% could be modifiable via environmental factors, including lifestyle and medications. Lipoproteins are definitive risk factors for atherosclerotic cardiovascular disease (ASCVD); among these, low-density lipoprotein (LDL) particles have been established as a causal factor for the development of ASCVD. Recently, triglyceride-rich lipoproteins have emerged as additional lipoproteins, which should be considered as residual targets for ASCVD risk reduction by LDL-lowering therapies. Compared with LDL particles, triglyceride-rich lipoproteins are significantly increased in the postprandial state, making it difficult to assess their clinical relevance. However, numerous pieces of evidence suggest that fasting and non-fasting triglycerides are associated with ASCVD. In addition, a recent meta-analysis of a Mendelian randomization study suggests that consideration of apolipoprotein B (APOB) might be better than considering LDL and triglyceride-rich lipoproteins separately. In this review, we examine (1) how triglyceride levels are determined by genetics, (2) lessons from extreme cases exhibiting severe hypertriglyceridemia, and (3) why triglycerides are important, by highlighting clinical and genetic evidence of their associations with ASCVD risk.

Postprandial dyslipidemia in insulin resistant states in adolescent populations.

Obesity and the metabolic syndrome are becoming increasingly prevalent not only in adults, but also in adolescents. The metabolic syndrome, a complex cluster of metabolic abnormalities, increases one's risk of developing type 2 diabetes and cardiovascular disease (CVD). Dyslipidemia, a key component of the metabolic syndrome, is highly associated with insulin resistance and contributes to increased CVD risk. Dyslipidemia has traditionally been assessed using a fasting lipid profile [i.e. fasting triglycerides, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C)]. However, the postprandial state predominates over the course of a day and non-fasting triglycerides independently predict CVD risk. In insulin resistant states, the intestine overproduces triglyceride-rich lipoprotein (TRL) particles, termed chylomicrons (CMs), following ingestion of a fat-containing meal, as well as in the fasting state. Along with elevated hepatic TRLs (i.e. very-low density lipoproteins), CMs contribute to remnant lipoprotein accumulation, small dense LDL particles, and reduced HDL-C, which collectively increase CVD risk. Given the early genesis of atherosclerosis and physiological metabolic changes during adolescence, studying postprandial dyslipidemia in the adolescent population is an important area of study. Postprandial dyslipidemia in the pediatric population poses a significant public health concern, warranting a better understanding of its pathogenesis and association with insulin resistance and CVD. This review discusses the metabolic syndrome, focusing on the link between insulin resistance, postprandial dyslipidemia, and CVD risk. Furthermore, the clinical significance and functional assessment of postprandial dyslipidemia, specifically in the adolescent population, is discussed in more detail.

Postprandial Hypertriglyceridaemia Revisited in the Era of Non-Fasting Lipid Profile Testing: A 2019 Expert Panel Statement, Main Text.

Residual vascular risk exists despite the aggressive lowering of Low-Density Lipoprotein Cholesterol (LDL-C). A contributor to this residual risk may be elevated fasting, or non-fasting, levels of Triglyceride (TG)-rich lipoproteins. Therefore, there is a need to establish whethe a standardised Oral Fat Tolerance Test (OFTT) can improve atherosclerotic Cardiovascular (CV) Disease (ASCVD) risk prediction in addition to a fasting or non-fasting lipid profile. An expert panel considered the role of postprandial hypertriglyceridaemia (as represented by an OFTT) in predicting ASCVD. The panel updated its 2011 statement by considering new studies and various patient categories. The recommendations are based on expert opinion since no strict endpoint trials have been performed. Individuals with fasting TG concentration <1 mmol/L (89 mg/dL) commonly do not have an abnormal response to an OFTT. In contrast, those with fasting TG concentration ≥2 mmol/L (175 mg/dL) or nonfasting ≥2.3 mmol/L (200 mg/dL) will usually have an abnormal response. We recommend considering postprandial hypertriglyceridaemia testing when fasting TG concentrations and non-fasting TG concentrations are 1-2 mmol/L (89-175 mg/dL) and 1.3-2.3 mmol/L (115-200 mg/dL), respectively as an additional investigation for metabolic risk prediction along with other risk factors (obesity, current tobacco abuse, metabolic syndrome, hypertension, and diabetes mellitus). The panel proposes that an abnormal TG response to an OFTT (consisting of 75 g fat, 25 g carbohydrate and 10 g proteins) is >2.5 mmol/L (220 mg/dL). Postprandial hypertriglyceridaemia is an emerging factor that may contribute to residual CV risk. This possibility requires further research. A standardised OFTT will allow comparisons between investigational studies. We acknowledge that the OFTT will be mainly used for research to further clarify the role of TG in relation to CV risk. For routine practice, there is a considerable support for the use of a single non-fasting sample.

Reduced Postprandial Serum Triglyceride After a Meal Prepared Using an Airfryer: A Randomized Crossover Trial (P08-103-19)

ObjectivesElevated circulating non-fasting triglyceride (TG) or postprandial triglyceride (ppTG) is as an independent contributor to risk for coronary heart disease. We hypothesized that a commonly consumed fried meal (including French fries and chicken nuggets) prepared by airfrying would result in a significantly lower ppTG response than the same meal prepared using a conventional deep fat frying approach. MethodsWe conducted a randomized crossover trial to evaluate the effect of airfryer cooking compared to conventional deep fat frying preparation in young healthy male (n = 10) and female subjects (n = 6). A 7-day washout period was included between meal test days. All study participants were blinded to the method of meal preparation. ResultsThe airfryer resulted in a significantly lower postprandial triglyceride response compared to deep fat frying of the same meal (P < 0.001). Glucose, insulin, and free fatty acid response differences were not found. Self-reported satiety did not differ after the meals. Furthermore, air-frying did not influence circulating inflammatory biomarkers, cholesterol, or apolipoproteins. ConclusionsAir frying of common fried meals results in lower postprandial triglyceride excursions in young healthy volunteers in the absence of any effects on satiety. Air-frying represents a useful and practical method to reduce meal fat content in line with current dietary recommendations on triglyceride management and general healthy eating. Funding SourcesThis research was funded by Philips Research China, Philips (China) Investment Co., Ltd., Shanghai, China. Supporting Tables, Images and/or Graphs▪▪▪

SUN-167 Quetiapine-Induced Hypertriglyceridemia and Hyperglycemia Presenting as Simultaneous Diabetic Ketoacidosis and Acute Pancreatitis

Background: Quetiapine-induced metabolic emergencies such as diabetic ketoacidosis (DKA) and acute pancreatitis (AP) are rare. We describe a case of new-onset hypertriglyceridemia (HTG) and diabetes mellitus (DM) following the initiation of quetiapine, presenting as concurrent new-onset DKA and AP. Clinical Case: A 34 year-old male with bipolar disorder and schizophrenia presented with three days of epigastric pain, nausea, and vomiting. He had no prior history of DM or dyslipidemia (DLD). He reported long-standing use of divalproex, benztropine, and haloperidol. He had started quetiapine three months prior, at which time glycosylated hemoglobin A1c (HgbA1c) was 5.7% and non-fasting triglyceride (TG) level was 266 (range 30-150 mg/dL). He was a smoker, but denied alcohol or drug use. On admission, he was hypertensive, tachycardic, and febrile with significant abdominal pain. His blood glucose was 522 (range 55-110 mg/dL) with an anion gap of 27 (range 5-17), venous pH of 7.18 (range 7.33-7.43), bicarbonate of 7 (range 23-31 mEq/L), and serum creatinine of 1.8 (0.6-1.4 mg/dL). He also had an elevated serum lipase of 317 (range 5-55 U/L), TG of 2436 (range 30-150 mg/dL), and computed tomography confirmed peri-pancreatic edema consistent with AP. Thyroid function tests were normal. Abdominal ultrasound was negative for cholelithiasis. He was treated with aggressive intravenous (IV) hydration and IV insulin, and later transitioned to subcutaneous (SQ) insulin after resolution of DKA. Quetiapine was stopped and he was discharged on haloperidol, benztropine, fenofibrate, and SQ insulin. Due to improving BG levels, insulin was gradually tapered over the next few weeks and subsequently discontinued. HgbA1c obtained three months later was 5.7% (off insulin) and fasting TG level was 212 mg/dL. Discussion: Second generation antipsychotics (SGAs), particularly olanzapine and clozapine, are known to cause metabolic abnormalities such as weight gain, hyperglycemia, and hyperlipidemia. Although quetiapine is described to have low risk for development of diabetes or lipid abnormalities, it can cause life-threatening complications like DKA and AP. While DKA has been reported in many case series, AP is exceedingly rare. There are fewer than ten reported cases with or without HTG following quetiapine use, usually within the first year of drug initiation. Since many of these patients do not have pre-existing DLD or DM, it is important for providers and patients to be aware of the risk of developing these life-threatening complications, even with a relatively safe SGA. Current guidelines recognize the importance of laboratory monitoring for early detection of metabolic disturbances in patients taking SGAs; however, recommendations regarding frequency of monitoring remain variable. Updated surveillance parameters are needed to facilitate the prevention of such metabolic emergencies.

Triglycerides and triglyceride-rich lipoproteins in the development and progression of atherosclerosis.

In this review, we intend to show the heterogenicity of the triglyceride group, including the triglyceride-rich lipoproteins and its subparticles, apolipoproteins, and its role in atherogenesis through epidemiological and genetic studies, observing the association of these various components and subclasses with subclinical atherosclerosis and cardiovascular events. Also, we reevaluated the moment of blood collection for the triglyceride measurement and its repercussion in atherosclerosis. Finally, we present the current scenario and new insights about the pharmacologic treatment of hypertriglyceridemia. Recent studies have been observed, a correlation between cardiovascular disease and triglyceride components (as apolipoproteins A-V, C-I, C-III) as well as proteins involved in the metabolism pathway, such as the angiopoietin-like proteins. Also, the triglyceride-rich lipoproteins, also known as remnants, were recently associated with atherogenesis. Another important topic addressed is about nonfasting triglyceride level, which has been postulated as a better predictor of cardiovascular events than fasting collection. Regarding hypertriglyceridemia treatment, the drug therapy was updated, as the omega-3 polyunsaturated fatty acids were tested in primary prevention as eicosapentaenoic acid and docosahexaenoic acid combination resulted in no benefit, whereas the administration of icosapent ethyl in secondary prevention and high-risk patients showed a robust decrease of the cardiovascular outcomes.

Low-Grade Inflammation in the Association between Mild-to-Moderate Hypertriglyceridemia and Risk of Acute Pancreatitis: A Study of More Than 115000 Individuals from the General Population.

How mild-to-moderate hypertriglyceridemia (2-10 mmol/L; 177-886 mg/dL) potentially causes acute pancreatitis is unknown; however, cellular studies indicate that inflammation might be a driver of disease progression. We tested the hypotheses that (a) mild-to-moderate hypertriglyceridemia is associated with low-grade inflammation and that (b) the association between mild-to-moderate hypertriglyceridemia and risk of acute pancreatitis depends on low-grade inflammation. From the Copenhagen General Population Study and the Copenhagen City Heart Study, 117865 men and women 20-100+ years of age with measurements of nonfasting plasma triglycerides at baseline were followed prospectively for development of acute pancreatitis. After multivariable adjustment, a 1 mmol/L (89 mg/dL) higher nonfasting triglyceride concentration was associated with 17% (95% CI, 16%-18%, P = 3 × 10-17) higher plasma C-reactive protein (CRP) and a 4.2% (4.0%-4.4%, P = 6 × 10-17) higher blood leukocyte count. Higher concentrations of nonfasting triglycerides were associated almost linearly with higher risk of acute pancreatitis (P for trend = 5 × 10-6), with hazard ratios of 1.5 (95% CI, 0.9-2.5), 2.0 (95% CI, 1.1-3.6), 2.2 (95% CI, 1.0-4.7), 4.2 (95% CI, 1.6-11.5), and 7.7 (95% CI, 3.0-19.8) in individuals with nonfasting triglycerides of 1.00-1.99 mmol/L (89-176 mg/dL; 46% of the population), 2.00-2.99 mmol/L (177-265 mg/dL; 17%), 3.00-3.99 mmol/L (266-353 mg/dL; 6%), 4.00-4.99 mmol/L (354-442 mg/dL; 2%), and ≥5mmol/L(443 mg/dL; 2%), respectively, vs individuals with <1 mmol/L (89 mg/dL; 27%). The association with risk of acute pancreatitis appeared more pronounced in individuals with CRP of ≥1.39 mg/L (P for trend = 0.001) and leukocytes of ≥7 × 109/L (P = 2 × 10-4) than in those with CRP <1.39 mg/L (P = 0.03) and leukocytes <7 × 109/L (P = 0.04); however, there was no formal evidence of statistical interaction (P = 0.38 for CRP and P = 0.41 for leukocytes). Mild-to-moderate hypertriglyceridemia is associated with low-grade inflammation and higher risk of acute pancreatitis. The association between mild-to-moderate hypertriglyceridemia and risk of acute pancreatitis is possibly partly mediated by low-grade inflammation.

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

BackgroundOverweight is always accompanied by hypertriglyceridemia (HTG), but the change in non-fasting triglyceride (TG) concentration in overweight subjects without postprandial hypertriglyceridemia was unknown. MethodsConcentrations 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. ResultsOW 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. ConclusionsOverweight 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.

How to Design Economic Predictive Laboratory Panel Evaluating Acute Ischemic Stroke Outcome

Background: acute ischemic stroke (AIS) remains the third cause of death and disability, and acute phase responses, both increasing international normalized ratio (INR) and activated partial thromboplastin time (APTT) are associated with worse outcome. Erythrocyte sedimentation rate (ESR) serves as severity marker, and non-fasting triglycerides (TG) indicates remnants of chylomicrons and very low density lipoproteins potentially pro-inflammatory. Aims: to design predictive economic panel evaluating AIS. Patients and methods: 100(AIS) patients were included, clinically evaluated by Scandinavian Stroke Scale (SSS) and Modified Rankin Score (MRS), subjected to complete blood count (CBC) on Cell-Dyne3700, manual ESR, INR and APTT on SYSMEX-CA1500, serum uric acid (SUA), serum albumin and non-fasting (TG) on Beckman Coulter AU480. Statistical analysis: STATA intercooled version 9.2. Results: odd ratio (OR), confidence interval (CI) of (MRS) in correlation to WBCs count in quartile (Q)3, 4 (OR 8.14, CI 2.29 - 8.90, significant P = 0.01; and OD13.5, CI 3.39 - 53.68, high significant P = 0.001 respectively), to APTT in Q3 (OD 4.15, CI 1.09 - 15.82, P = 0.04), SUA in Q3 (OD 0.19, CI 0.05 - 0.68, P = 0.01), TG in Q3,4 (OD 0.24 CI 0.06 - 0.88, P = 0.03; and OD 0.09, CI 0.02 - 0.34 P = 0.001 respectively) and serum albumin in Q3(OD 0.13, CI 0.04 - 0.51, P = 0.003), insignificant correlations to ESR, INR and platelets. Conclusion: according to (MRS), the economic predictive panel should be included WBCs, APTT, SUA, and non-fasting TG with serum albumin as prognostic tool evaluating functional disability in AIS.

2-Acyl-3-carboxyl-tetrahydroisoquinoline Derivatives: Mixed-Type PTP1B Inhibitors without PPARγ Activation.

A novel series of 2-acyl-3-carboxyl-tetrahydroisoquinoline derivatives were synthesized and biologically evaluated. Among them, (S)-2-{(E)-3-furan-2-ylacryloyl}-7-[(2E,4E)-5-(2,4,6-trifluorophenyl)penta-2,4-dienyloxy]-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid (compound 17u) was identified as a potent protein tyrosine phosphatase 1B (PTP1B) inhibitor without peroxisome proliferator-activated receptor (PPAR) γ activation: PTP1B inhibition IC50=0.19 µM and PPARγ ΕC50>10 µM. Compound 17u exhibited mixed-type inhibition for PTP1B, and this mode of inhibition was rationalized by computational ligand docking into the catalytic and allosteric sites of PTP1B. Compound 17u also showed high oral absorption at 10 mg/kg (per os (p.o.), Cmax=4.67 µM) in rats, significantly reduced non-fasting plasma glucose and triglyceride levels with no side effects at 30 mg/kg/d (p.o.) for 4 weeks, and attenuated elevations in plasma glucose levels in the oral glucose tolerance test performed 24 h after its final administration in db/db mice. In conclusion, the substituted 2-acyl-3-carboxyl-tetrahydroisoquinoline is a novel scaffold of mixed-type PTP1B inhibitors without PPARγ activation, and compound 17u has potential as an efficacious and safe anti-diabetic drug as well as a useful tool for investigations on the physiological and pathophysiological effects of mixed-type PTP1B inhibition.

Fasting versus Non-fasting Lipid profile in the clinical practice

There are pros and cons doing fasting and random non-fasting lipid profile test. However, when we consider cardio vascular risk, non-fasting lipid test more reliable than fasting test. In current practice, using fasting lipid profile was challenged in 2007 by two studies that showed that random non-fasting triglyceride (TG) could be superior than fasting TG in predicting risk of cardiovascular risk. Postprandial concentrations of triglyceride were higher than fasting. However, levels of non-fasting triglycerides are better at predicting future cardiovascular events than levels of fasting triglycerides. Random non-fasting lipid test is not a new phenomenon, it already practicing in Denmark since 2009. Moreover, NICE guidelines have recommended non-fasting test in the primary prevention setting since 2014. As the major shift in newer guidelines reflects the changing focus of risk assessment from LDL to non-HDL cholesterol (apolipoprotein B) as a better predictor of cardiovascular risk, indirectly tell us non-fasting lipid level superior than fasting lipid. The aim of the review is to compare both fasting and non-fasting measurements in our clinical practice.

The Effect of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors on Nonfasting Remnant Cholesterol in a Real World Population.

Background Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors have demonstrated significant effects on low-density lipoprotein (LDL) cholesterol and nonhigh density lipoprotein (HDL) cholesterol. To date, there have been limited reports on the effect of PCSK9 inhibitors on remnant cholesterol. Objectives Assess the effect of PCSK9 inhibitors on nonfasting remnant cholesterol in a real world population. Identify whether pretreatment triglyceride levels are associated with PCSK9 inhibition success as indicated by changes in remnant cholesterol levels. Methods Patients in our adult lipid clinic (n = 109) receiving PCSK9 inhibition for atherosclerotic cardiovascular disease or familial hypercholesterolemia who had available pre- and post-PCSK9 inhibition standard nonfasting lipid data were, retrospectively, selected for data analysis. Remnant cholesterol was the difference between non-HDL and LDL cholesterol. LDL cholesterol was measured directly and calculated from Friedewald and Martin/Hopkins methods. Data were analyzed using repeated measures ANOVA and multivariable linear regression for differential effects on remnant and LDL cholesterol based upon pretreatment nonfasting triglyceride levels. Results Remnant cholesterol as well as total, LDL, non-HDL cholesterol, and triglycerides decreased significantly (P<0.001) after PCSK9 inhibition. Patients with higher pretreatment triglyceride levels showed greater decrease in remnant cholesterol after PCSK9 inhibition (P<0.001) than those with lower pretreatment triglycerides. Conclusions In patients receiving PCSK9 inhibitors, remnant cholesterol as determined from nonfasting blood was reduced in proportion to pretreatment triglycerides.

Mild hyperbaric oxygen inhibits the growth-related decline in skeletal muscle oxidative capacity and prevents hyperglycemia in rats with type 2 diabetes mellitus.

Humans and animals with type 2 diabetes mellitus (T2DM) exhibit low skeletal muscle oxidative capacity and impaired glucose metabolism. The aim of the present study was to investigate the effects of exposure to mild hyperbaric oxygen on these changes in obese rats with T2DM. Five-week-old non-diabetic Long-Evans Tokushima Otsuka (LETO) and diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats were divided into normobaric (LETO-NB and OLETF-NB) and mild hyperbaric oxygen (LETO-MHO and OLETF-MHO) groups. The LETO-MHO and OLETF-MHO groups received 1266 hPa with 36% oxygen for 3 h daily for 22 weeks. Fasting and non-fasting blood glucose, HbA1c, and triglyceride levels were lower in the OLETF-MHO group than in the OLETF-NB group (P < 0.05). In the soleus muscle, peroxisome proliferator-activated receptor δ/β (Pparδ/β), Pparγ, and PPARγ coactivator-1α (Pgc-1α) mRNA levels were lower in the OLETF-NB group than in all other groups (P < 0.05), whereas myogenin (Myog) and myogenic factor 5 (Myf5) mRNA levels were higher in the OLETF-MHO group than in the LETO-NB and OLETF-NB groups (P < 0.05). The soleus muscles in the OLETF-NB group contained only low-oxidative Type I fibers, whereas those in all other groups contained high-oxidative Type IIA and Type IIC fibers in addition to Type I fibers. Exposure to mild hyperbaric oxygen inhibits the decline in skeletal muscle oxidative capacity and prevents the hyperglycemia associated with T2DM. Pgc-1α, Myog, and Myf5 mRNA levels appear to be closely associated with skeletal muscle oxidative capacity in rats with T2DM.

Abstract P093: Correlates of Vascular Health in Children and Adolescents With Dyslipidemia

Introduction: Impaired vascular function and structure has been associated with cardiovascular risk factors such as elevated levels of Low Density Lipoprotein cholesterol (LDL-C) and triglycerides, depressed High Density Lipoprotein cholesterol (HDL-C), elevated blood pressure (BP) and body mass index (BMI) in children and young adults. These changes can result in premature coronary artery disease. The degree to which these measures predict vascular damage in children and adolescents is less clear. Hypothesis: We hypothesized that commonly used clinical and laboratory measures will predict vascular health as assessed by measures of carotid artery intima-media thickness (CIMT), pulse wave velocity (PWV), and augmentation index (Aix) in at risk youth. Methods: Children and adolescents with dyslipidemia (n=120, 13.1 ± 1.9 years old, 49% female (59 of 120)) were recruited from a pediatric preventive cardiology clinic. Non-fasting total cholesterol, HDL cholesterol, and triglycerides were obtained prior to the clinic visit. LDL-C and non-HDL-C were calculated with the Martin equation. Remnant particles were calculated as: total cholesterol minus (HDL-C + LDL-C). BP, height, weight, and waist circumference (WC) were measured at the clinic visit. WC was measured 2cm above the iliac crest by a single observer. Tobacco smoke exposure history was obtained using a parent questionnaire. PWV and Aix were measured using a SphygmoCor XCEL combined oscillometric and tonometric device. CIMT was measured via B mode ultrasound on the far wall of the left and right common carotid arteries using a semi-automated edge detection software. Multiple linear regression with backwards selection was used to identify the strongest predictors of CIMT, PWV, and normalized Aix. Results: Age (β=0.26; p=0.002), systolic BP (β=0.16; p=0.04), waist-to-height ratio (β=0.24; p=0.01), hemoglobin A1c (β=0.18; p=0.01) and presence of hypertriglyceridemic waist (defined as triglycerides ≥110mg/dL and WC ≥90 percentile) (β=0.28; p=0.006) were the strongest predictors of PWV (R2=0.353). Diastolic BP (β=0.21; p=0.01), waist-to-height percentile (β=0.22; p=0.01), and remnant particles (β=0.21; p=0.01) were the strongest predictors of normalized Aix (R2=0.175). Age (β=0.19; p=0.03), and systolic BP (β=0.28; p=0.002) were the strongest predictors of CIMT (R2=0.138). Triglycerides, history of tobacco smoke exposure, total cholesterol, LDL-C, HDL-C, and non-HDL-C were not predictive of CIMT, PWV, or normalized Aix. Conclusion: BP consistently predicted was the most common predictor of CIMT, PWV, and Aix in children and adolescents with dyslipidemia. Waist-to-height ratio/percentile was also a reliable predictor in both PWV and Aix. BP and abdominal obesity management should be a focus in this at risk population.

Abstract P227: Circulating and Dietary Linoleic Acid and Prevalent Diabetes in Post-Myocardial Infarction Patients

Background: Circulating linoleic acid 18:2n-6 (LA) has been considered to reflect LA intake, but its utility as a dietary biomarker could be affected by metabolism. Objective: To study the associations of plasma and dietary LA with T2D prevalence in drug-treated patients with a history of myocardial infarction (MI). Methods: Cross-sectional analysis of baseline data in 4,072 Dutch post-MI patients of the Alpha Omega Cohort. Circulating LA (as % of total fatty acids) was assessed in plasma cholesterol esters (CE) in the total cohort and in plasma phospholipids (PL) in a random subset of 833 patients. LA intake was assessed by a 203-item validated food frequency questionnaire. Prevalence ratios of T2D and associations with metabolic parameters were estimated in plasma and dietary LA quintiles using multivariable generalized linear models adjusted for demographic, lifestyle and dietary factors. Results: Patients were on average 69 years old, 79% was male and 77% were overweight or obese. Most patients used statins (86%), antihypertensive drugs (90%) and antiplatelet drugs (84%). A total of 813 patients (20%) had T2D. Mean LA intake (±SD) was 5.7±2.2 energy%, and circulating LA was 49.9±5.0% in CE and 18.7±3.0% in PL. Spearman’s correlations of dietary LA with circulating LA in CE and PL were 0.16 and 0.10, respectively. Higher plasma LA, but not dietary LA, was significantly associated with a lower diabetes prevalence (Table 1). BMI (β= -0.07, p&lt;0.001), log non-fasting triglycerides (β= -0.01, p&lt;0.001), log non-fasting glucose (β= -0.01, p&lt;0.001), and log alcohol intake (β= -0.03, p&lt;0.001) were significantly associated with circulating LA in plasma CE. Similar associations were found for LA in plasma PL. Dietary LA was not significantly associated with T2D prevalence and metabolic parameters (all p&gt;0.05). Conclusions: Circulating LA may reflect both LA intake and metabolic state in drug-treated post-MI patients. This bears restrictions for its use as a biomarker of dietary LA intake in epidemiological studies.

Fasting or Non-fasting Lipids for Atherosclerotic Cardiovascular Disease Risk Assessment and Treatment?

Dyslipidemia is a major modifiable risk factor for atherosclerotic cardiovascular disease (ASCVD); however, lipid testing for risk assessment and treatment surveillance has been underutilized. Several factors likely account for this, including the common practice of measuring lipid levels in the fasting state, which often necessitates that patients return for an additional visit. In this review, we evaluate potential advantages and cautions associated with measuring lipids in the non-fasting state. There is similar performance with the use of either fasting or non-fasting total cholesterol and HDL cholesterol in ASCVD risk assessment. Observational studies demonstrate that in comparison to fasting levels, non-fasting triglycerides are approximately 20% higher on average, although the magnitude of difference is subject to substantial inter-patient variability. Higher triglycerides can lead to the under-estimation of low-density lipoprotein cholesterol (LDL-C) by approximately 10mg/dL or more when calculated using the Friedewald equation. This is especially clinically relevant at low LDL-C levels, although a novel validated algorithm for LDL-C estimation largely overcomes this limitation. Non-fasting lipid assessment is reasonable in many clinical circumstances given that ASCVD risk prediction is similar using fasting or non-fasting lipid values and because LDL-C can be accurately estimated using modern methods. Allowing the option for non-fasting lipid assessment can reduce a barrier to lipid testing and can facilitate a more convenient assessment of ASCVD risk with the ultimate potential effect of reducing the global burden of ASCVD. However, certain patients such as those with severe hypertriglyceridemias or high-risk patients being treated to low LDL-C levels may still need fasting lipid panels performed for precise diagnosis and to standardize therapeutic monitoring.