Postprandial Hypertriglyceridemia Research Articles

Evaluating the roles of food matrix, lipid micronutrients and bioactives in controlling postprandial hypertriglyceridaemia and inflammation.

Lipids play an important role in human nutrition. Although adequate lipid consumption is necessary for an optimal functioning of the human body, overconsumption of saturated fatty acids can lead to postprandial hypertriglyceridaemia, which triggers the development of atherosclerosis. Important parameters that impact postprandial lipaemia and inflammation are related to the matrix structure and the fat-soluble micronutrient profile of ingested foods/lipids, but the specific effect of these parameters should be further studied, as most of the available studies evaluate their effect at fasting state. This review specifically explores the effects of food structure and fat-soluble micronutrients, from either micronutrient-rich foods or supplements, on postprandial hypertriglyceridaemia and inflammation. The review also highlights the potential of emerging biomarkers such as miRNAs or circulating microvesicles, as an alternative to the widely use biomarkers (e.g. low-density lipoproteins or blood concentration of pro-inflammatory cytokines), to identify inflammation associated with postprandial hypertriglyceridaemia at early stages.

Effect of Alirocumab on postprandial hypertriglyceridemia in subjects with type 2 diabetes: Results from the EUTERPE randomized clinical trial

Effect of Alirocumab on postprandial hypertriglyceridemia in subjects with type 2 diabetes: Results from the EUTERPE randomized clinical trial

Reduced capacity of HDL to acquire free cholesterol from triglyceride-rich lipoproteins is associated with elevated postprandial hypertriglyceridemia

Reduced capacity of HDL to acquire free cholesterol from triglyceride-rich lipoproteins is associated with elevated postprandial hypertriglyceridemia

Reduced Capacity of High-Density Lipoprotein to Acquire Free Cholesterol From Triglyceride-Rich Lipoproteins Is Associated With Elevated Postprandial Hypertriglyceridemia in Healthy Men.

The capacity of high-density lipoprotein cholesterol (HDL) to acquire free cholesterol (FC) from triglyceride-rich lipoproteins during lipoprotein lipase-dependent lipolysis in a process of reverse remnant cholesterol transport, has been proposed as a key biological function of HDL particles that underlies the U-shaped relationship between HDLcholesterol and cardiovascular diseases. Although reverse remnant cholesterol transport has been evaluated in a fasting state, it has never been explored under nonfasting conditions. FC transfer was evaluated in healthy men (n=78) before and throughout the postprandial phase up to 8 hours after consumption of a test meal. Postprandially, the capacity of HDL to acquire FC increased progressively, reaching a maximal mean value of 98.5%±22.5% 6 hours after meal intake (P<0.05). Analysis of the study population according to tertiles of postprandial variation of FC transfer identified subjects exhibiting reduced capacity of HDL to acquire FC (tertile 1), those for whom the capacity of HDL to acquire FC remained unchanged (tertile 2), and subjects characterized by an enhanced FC transfer during the postprandial phase (tertile 3). Across the tertiles, we found an inverse relationship between the maximal postprandial change in FC transfer to HDL and the degree of postprandial triglyceride response. Healthy individuals exhibiting exacerbated postprandial triglyceride response and reduced HDL cholesterol levels feature reduced FC transfer to HDL during the postprandial state. These data suggest that to normalize postprandial triglyceride response, 2 conditions need to be fulfilled: notably elevated FC transfer to HDL in the postprandial phase and increased levels of acceptor HDL particles.

Time-restricted Eating to Improve Metabolic Health: Investigating the Mechanisms Underlying Glycolytic and Lipolytic actions

Time-restricted eating (TRE) is a behavioral intervention approach motivated by the emerging role of circadian rhythms in physiology and metabolism. In this approach, all caloric intake is restricted within a regular interval of less than 12 hours, with no overt attempt to reduce calories. We present a whole-body computational model of TRE that incorporates enzyme and substrate reactions as well as hormonal actions during fasting and postprandial states. The model is divided into seven compartments: brain, heart, skeletal muscle, gastrointestinal tract, liver, adipose tissue, and other tissues. We conducted simulations to test the hypothesis that TRE modulates whole-body glucose balance by improving postprandial hyperglycemia and hypertriglyceridemia, keeping these excursions to a minimum. We simulated different TRE schedules with meals varying in fat and carbohydrate content. Our results highlight the importance of chrono-pharmacological considerations in glycemic control: TRE modulates the interplay between glycogenolysis in the liver, lipolysis in adipose tissue and fatty acid oxidation in other organs to improve glucose control. The alternation of eating and fasting, in particular, could be manipulated to balance blood sugar levels. TRE simulations have also shown beneficial effects on the lipid front, such as lower triglyceride levels and improved lipolytic effciency, meaning the body is better able to use fat stores for fuel. This work was supported by the Canadian Institutes of Health Research (CIHR) and the Natural Sciences and Engineering Research Council of Canada (NSERC) Discovery award. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

SIRT3 rs11246020 Polymorphism Associated Postprandial Triglyceride Dysmetabolism.

Energy metabolism is regulated by SIRT3, no research has been done on the connection between lipid metabolism in the oral fat test and SIRT3 polymorphism. Thus, we conducted a case-control study to investigate the connection between postprandial lipid and SIRT3 polymorphism. 402 non-obese Chinese subjects were enrolled and their postprandial lipid response to oral fat tolerance test (OFTT) was observed to understand the relationship between rs11246020 gene and postprandial triglyceride metabolism. In a binary logic regression model, a protective effect of the T allele of the rs11246020 SIRT3 for postprandial hypertriglyceridemia was shown (OR=0.417, 95% CI = 0.219-0.794, p=0.008). Compared to the CC genotype, individuals with the TT+CT variant of the rs11246020 SIRT3 gene demonstrated significantly lower levels of homeostasis model assessment of insulin resistance (HOMA-IR) (p=0.04), postprandial plasma glucose (PPG) (p=0.037), fasting plasma glucose (FPG) (p=0.02), and 4-hour triglyceridemia (Tg) (p=0.032). The C allele of rs11246020 SIRT3 gene may be a risk factor to increased possibility of postprandial triglyceridemia after an oral fat test, which involved in the mechanism of glucose and insulin metabolism.

Chronic heart failure induces early defenestration of liver sinusoidal endothelial cells (LSECs) in mice.

Chronic heart failure (CHF) is often linked to liver malfunction and systemic endothelial dysfunction. However, whether cardio-hepatic interactions in heart failure involve dysfunction of liver sinusoidal endothelial cells (LSECs) is not known. Here we characterize LSECs phenotype in early and end stages of chronic heart failure in a murine model. Right ventricle (RV) function, features of congestive hepatopathy, and the phenotype of primary LSECs were characterized in Tgαq*44 mice, with cardiomyocyte-specific overexpression of the Gαq protein, at the age of 4- and 12-month representative for early and end-stage phases of CHF, respectively. 4- and 12-month-old Tgαq*44 mice displayed progressive impairment of RV function and alterations in hepatic blood flow velocity resulting in hepatic congestion with elevated GGT and bilirubin plasma levels and decreased albumin concentration without gross liver pathology. LSECs isolated from 4- and 12-month-old Tgαq*44 mice displayed significant loss of fenestrae with impaired functional response to cytochalasin B, significant changes in proteome related to cytoskeleton remodeling, and altered vasoprotective function. However, LSECs barrier function and bioenergetics were largely preserved. In 4- and 12-month-old Tgαq*44 mice, LSECs defenestration was associated with prolonged postprandial hypertriglyceridemia and in 12-month-old Tgαq*44 mice with proteomic changes of hepatocytes indicative of altered lipid metabolism. Tgαq*44 mice displayed right-sided HF and altered hepatic blood flow leading to LSECs dysfunction involving defenestration, shift in eicosanoid profile, and proteomic changes. LSECs dysfunction appears as an early and persistent event in CHF, preceding congestive hepatopathy and contributing to alterations in lipoprotein transport and CHF pathophysiology.

Serum Gamma Glutamyltransferase: A Biomarker for Identifying Postprandial Hypertriglyceridemia.

Elevated serum gamma-glutamyltranspeptidase (GGT) is an independent marker of the activation of systemic inflammation, while conditions associated with elevated triglyceride (TG) levels, such as type 2 diabetes, non-alcoholic fatty liver disease, obesity, and metabolic syndrome, are associated with an increased inflammatory burden. Moreover, serum liver enzymes (GGT, alanine aminotransferase [ALT], aspartate aminotransferase [AST], and alkaline phosphatase [ALP]) are associated with metabolic syndrome and its components, including hypertriglyceridemia. However, the relationship between liver enzymes and postprandial hypertriglyceridemia (PHTG) remains unclear. Therefore, in this study we conducted oral fat tolerance tests (OFTTs) to understand the differences in serum liver enzyme levels among individuals with different lipid tolerance levels and their correlation with PHTG. For the OFTT, we enrolled 202 non-diabetic volunteers whose fasting triglyceride (TG) levels were less than 1.7 mmol/L in this case-control study. The participants were categorized into two groups according to the TG levels at the 0- and 4-h OFTT: a postprandial normal TG (PNTG) group and a PHTG group. Routine fasting serum biochemical indices, liver enzyme (GGT, ALT, AST, and ALP) levels, and 0- and 4-h OFTT lipid levels were assessed. The PHTG group had significantly higher serum GGT and ALT levels and a lower AST/ALT ratio than those in the PNTG group. However, no significant difference was observed in AST and ALP levels compared with the PNTG group. After adjusting for major confounders, logistic regression analysis indicated a significant correlation between serum GGT and PHTG (odds ratio = 1.168, P < 0.001), but not with ALT level, AST level, AST/ALT ratio, and ALP level. The receiver operating characteristic curve analysis demonstrated that the serum GGT level was an effective predictor of PHTG. Serum GGT levels are significantly associated with PHTG risk and serve as an effective biomarker for early identification.

Proteomic Analysis of Human Chylomicron Remnants Isolated by Apolipoprotein B-48 Immunoprecipitation.

Postprandial hypertriglyceridemia (PHTG) is an independent risk factor for coronary heart diseases. PHTG exhibits accumulation of apoB-48 containing chylomicron remnants (CM-Rs) and apoB-100 containing VLDL remnants (VLDL-Rs), which are both known to be atherogenic. However, unlike VLDL-Rs, structural and functional characterization of CM-Rs remains to be elucidated due to challenges in separating CM-Rs from VLDL-Rs. Recently, we successfully isolated CM-Rs and VLDL-Rs utilizing anti-apoB-48 or apoB-100 specific antibodies. This study aimed to characterize the proteome of CM-Rs along with that of VLDL-Rs. Eight healthy subjects were enrolled. Venous blood was drawn 3 hours after high-fat-containing meals. We isolated CM-Rs and VLDL-Rs from sera through combination of ultracentrifugation and immunoprecipitation using apoB-48 or apoB-100 specific antibodies, followed by shotgun proteomic analysis. We identified 42 CM-Rs or VLDL-Rs-associated proteins, including 11 potential newly identified proteins such as platelet basic protein (PPBP) and platelet factor 4, which are chemokines secreted from platelets. ApoA-I, apoA-IV, and clusterin, which are also known as HDL-associated proteins, were significantly more abundant in CM-Rs. Interestingly, apoC-I, which reduces the activity of lipoprotein lipase and eventually inhibits catabolism of remnant proteins, was also more abundant in CM-Rs. Moreover, we identified proteins involved in complement regulation such as complement C3 and vitronectin, and those involved in acute-phase response such as PPBP, serum amyloid A protein 2, and protein S100-A8, in both CM-Rs and VLDL-Rs. We have firstly characterized the proteome of CM-Rs. These findings may provide an explanation for the atherogenic properties of CM-Rs.

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

BackgroundObesity 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. ObjectivesThe objectives of the study were to explore the inflammatory response of postprandial TRLs in white adipocytes and investigate the possible mechanism. MethodsWe 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. ResultsSerum 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-1β, 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. ConclusionsOur results suggest that postprandial hypertriglyceridemia causes chronic inflammation in adipocytes through TRL-induced lysosomal dysfunction and impaired autophagic flux in an mTOR-dependent manner.

Plasma Cytokeratin-18 Fragment Level Reflects the Metabolic Phenotype in Obesity.

There is growing interest in the non-invasive identification and monitoring of the outcome of liver damage in obese patients. Plasma cytokeratin-18 (CK-18) fragment levels correlate with the magnitude of hepatocyte apoptosis and have recently been proposed to independently predict the presence of non-alcoholic steatohepatitis (NASH). The aim of the study was to analyze the associations of CK-18 with obesity and related complications: insulin resistance, impaired lipid metabolism and the secretion of hepatokines, adipokines and pro-inflammatory cytokines. The study involved 151 overweight and obese patients (BMI 25-40), without diabetes, dyslipidemia or apparent liver disease. Liver function was assessed based on alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT) and the fatty liver index (FLI). CK-18 M30 plasma levels, FGF-21, FGF-19 and cytokines were determined by ELISA. CK-18 values >150 U/l were accompanied by high ALT, GGT and FLI, insulin resistance, postprandial hypertriglyceridemia, elevated FGF-21 and MCP-1 and decreased adiponectin. ALT activity was the strongest independent factor influencing high CK-18 plasma levels, even after an adjustment for age, sex and BMI [β coefficient (95%CI): 0.40 (0.19-0.61)]. In conclusion, the applied CK-18 cut-off point at 150 U/l allows to distinguish between two metabolic phenotypes in obesity.

POSTPRANDIAL HYPERTRIGLYCERIDEMIA AS A RISK FACTOR FOR MACROVASCULAR COMPLICATIONS IN TYPE 2 DIABETES MELLITUS

Diabetes mellitus is a common endocrine disorder characterized by chronic hyperglycemia, and disturbances of carbohydrate, fat and protein metabolism. The prevalence of diabetes has been increasing widely in India and worldwide. Diabetes is a cause of signicant mortality and morbidity due to macro and micro vascular complications. Dyslipidemia accompanying type 2 Diabetes plays an important role in pathogenesis of atherosclerotic vascular disease. Post prandial hypertriglyceridemia, irrespective of fasting triglyceride levels, has emerged as a signicant risk factor for symptomatic and asymptomatic macro vascular disease It is a case control study, conducted for a period of 1 year from November 2020 to October 2021, on patients visiting the Out-patient department of NRI institute of Medical Sciences, Sangivalasa, Visakhapatnam. The cases and controls were subjected to clinical and biochemical evaluation to detect presence of macro vascular complications. The cases were subjected to a high fat meal, and plasma triglycerides were measured two and four hours after a fat challenge. It was observed that post prandial hypertriglyceridemia correlated better than fasting triglycerides in patients with macro vascular complications. Persistent and signicant post prandial hypertriglyceridemia was observed in diabetic patients with macro vascular complications; and can be used as a marker for predicting vascular complications in type 2 Diabetes mellitus

Enrichment of Triglyceride-Rich Lipoproteins with Apolipoprotein C-I Is Positively Associated with Their Delayed Plasma Clearance Independently of Other Transferable Apolipoproteins in Postmenopausal Overweight and Obese Women

Background: The role of plasma apolipoprotein (apo) C-I in cardiometabolic risk in humans is unclear. However, in vitro studies showed a dual role for apoC-I, both protective and harmful, depending on the carrier lipoprotein.Objective: We tested the hypothesis that triglyceride (TG)-rich lipoprotein (TRL) apoC-I, not total or HDL apoC-I, is associated with delayed postprandial plasma clearance of TRLs, independently of apoC-II, apoC-III, and apoE.Methods: This cross-sectional study examines the plasma clearance of a 13C-triolein–labeled high-fat meal (68% fat energy) in 20 postmenopausal overweight and obese women [body mass index (in kg/m2) ≥27; aged 45–74 y] as the increment change in area under the 6-h postprandial curves (iAUC6h) of TRL parameters. Lipoproteins were fractionated by fast-protein LC. Transferable apolipoproteins were measured by ELISA. TRL enrichment with apolipoproteins was calculated by dividing their TRL concentrations by TRL apoB. The effects of human apoC-I and apoC-III on the hydrolysis and storage of 3H-triolein–labeled TRLs were tested in 3T3-L1 adipocytes.Results: TRL apoC-I was positively associated with plasma apo B-48 and total and non-HDL TGs, cholesterol, and apoB (r = 0.52–0.97) and negatively with HDL cholesterol (r = −0.52) and LDL diameter (r = −0.91) (P < 0.05). Total and HDL apoC-I were correlated only with total (r = 0.62) and HDL (r = 0.75) cholesterol. Women with high fasting TRL enrichment with apoC-I (99–365 μmol apoC-I/μmol apoB), but not apoC-II, apoC-III, or apoE, had higher iAUC6h for TGs (+195%), 13C-TGs (+319%), and apo B-48 (+186%) than those with low enrichment (14–97 μmol apoC-I/μmol apoB). The 4-h postprandial increase in TRL apoC-I was associated with a 4-h increase in TRL TGs and iAUC6h for TGs, 13C-TGs, and apo B-48 (r = 0.74–0.86, P < 0.001), independently of 4-h changes in TRL apoB, apoC-II, apoC-III, or apoE. ApoC-I and apoC-III inhibited 3H-TRL clearance by adipocytes by >75% (P < 0.001).Conclusions: TRL enrichment with apoC-I is positively associated with postprandial hypertriglyceridemia and remnant accumulation in postmenopausal overweight and obese women, independently of apoC-II, apoC-III, or apoE, which may be due to inhibiting TRL clearance by adipocytes. Reducing TRL apoC-I may ameliorate delayed postprandial plasma clearance of TRLs and associated risks in humans.

The effects of pemafibrate and omega-3 fatty acid ethyl on apoB-48 in dyslipidemic patients treated with statin: A prospective, multicenter, open-label, randomized, parallel group trial in Japan (PROUD48 study).

We compared the lowering effects of pemafibrate and omega-3 fatty acid ethyl on fasting apolipoprotein (apo) B-48 (apoB-48), a marker that reflects postprandial hypertriglyceridemia, which is one of the residual risks for atherosclerotic cardiovascular disease (ASCVD) with statin treatment. This prospective, multicenter, open-label, randomized, parallel group trial was conducted at 4 medical institutions between April 2020 and May 2022. A total of 126 ambulatory patients with dyslipidemia receiving statin treatment for more than 4 weeks, aged 20-79 years with fasting triglyceride (TG) levels of ≥177 mg/dl were randomly assigned to 16-week pemafibrate 0.4 mg per day treatment group (PEMA, n = 63) or omega-3 fatty acid ethyl 4 g per day treatment group (OMEGA-3, n = 63). The primary endpoint was the percentage change in fasting apoB-48 from baseline to week 16. The percentage changes in fasting apoB-48 in PEMA and OMEGA-3 were -50.8% (interquartile range -62.9 to -30.3%) and -17.5% (-38.3 to 15.3%) (P < 0.001), respectively. As the secondary endpoints, the changes in fasting apoB-48 in PEMA and OMEGA-3 were -3.10 μg/ml (-5.63 to -1.87) and -0.90 μg/ml (-2.95 to 0.65) (P < 0.001), respectively. Greater decreases with significant differences in the percentage changes in TG, remnant lipoprotein cholesterol, apoC-III, fasting plasma glucose, alanine aminotransferase, gamma-glutamyl transpeptidase, and alkaline phosphatase were observed in PEMA, compared with OMEGA-3. Greater increases with significant differences in those in high-density lipoprotein (HDL) cholesterol, apoA-I, and apoA-II were observed in PEMA, compared with OMEGA-3. PEMA showed anti-atherosclerotic lipoprotein profiles in gel-permeation high-performance liquid chromatography analyses, compared with OMEGA-3. Although adverse events occurred in 9 of 63 (14.3%) patients in PEMA and 3 of 63 (4.8%) patients in OMEGA-3, no serious adverse events associated with drug were observed in either group. This is the first randomized trial to compare the lowering effects of pemafibrate and omega-3 fatty acid ethyl on fasting apoB-48. We concluded that pemafibrate was superior to omega-3 fatty acid ethyl in lowering effect of fasting apoB-48. Pemafibrate is expected to reduce the residual risk for ASCVD with statin treatment. https://rctportal.niph.go.jp/en, identifier jRCTs071200011.

Abstract 9575: TOTUM-070 Hypocholesterolemic Effect Linked to Intestinal Cholesterol Absorption Inhibition. An in vivo and in vitro Study

TOTUM-070 (T070) is a patented blend of five plant extracts designed to act in combination to prevent hypercholesterolemia. Previous study in dyslipidemic hamster model fed a High Fat High Cholesterol (HFHC) diet for 12 weeks demonstrated that supplementation with T070 at 3,5% to 5% in the diet (n=16 per group) reduced serum non-HDL cholesterol compared to HFHC group (-38%, p&lt;0,001 and -47%, p&lt;0,001, respectively) as well as serum triglyceride levels (-30%, n.s and -46%, p&lt;0,05, respectively). We aimed to decipher the mechanisms of action of T070 both in vivo and in vitro. First, the chemical characterization of T070 by HPLC-UV/MS analyses led to the identification and quantification of 37 biomolecules such as oleuropein, oleanolic acid or chlorogenic acid. Total RNA sequencing analysis of livers from the HFHC and T070 5% supplemented groups highlighted 511 genes with significant different expression level between groups. Among canonical pathways identified, 19 genes implicated in metabolism were differentially regulated with T070. Several functional tests were performed in hamster fed with T070 5% for 12 weeks in comparison to HFHC group (n=14 per group). Dosage of lipoprotein lipase activity ex vivo did not show any difference between groups. Results from hepatic triglyceride production test detected no effect of T070. However, an oral fat tolerance test showed that post-prandial hypertriglyceridemia was significantly reduced by 40% (p&lt;0,01) in T070 group following olive oil gavage compared to the HFHC hamsters. Finally, in vivo intestinal [4- 14 C]-Cholesterol absorption test demonstrated a 12% reduction (n.s) with T070 5% compared to HFHC group. In vitro investigations were assessed on differentiated human enterocyte Caco2 cells. Incubation with T070 at 1g/l for 1h acutely reduced [1,2- 3 H(N)]-cholesterol uptake by 30% in Caco2 cells (p&lt;0.01). Pharmacological inhibition of cholesterol transporter NPC1L1 abolished the effect of T070 on cholesterol uptake. There was no effect of T070 on NPC1L1 protein expression in Caco2 cells, suggesting T070 blocked directly NPC1L1 activity. Altogether, our results demonstrate that hypocholesterolemic effect of T070 is mediated by inhibition of intestinal cholesterol absorption.

Study protocol of the PROUD48 study comparing the effects of pemafibrate and omega-3 fatty acid ethyl esters on ApoB-48 in statin-treated patients with dyslipidaemia: a prospective, multicentre, open-label, randomised, parallel group trial in Japan

IntroductionThis study will compare the lowering effects of pemafibrate and omega-3 fatty acid ethyl esters on fasting apolipoprotein B-48 (apoB-48), a surrogate marker reflecting postprandial hypertriglyceridaemia, which is a residual...

Observational study of post prandial hypertriglyceridemia is a reliable predictor for coronary artery disease

Introduction: Hypertriglyceridemia is recognized as a high-risk factor for coronary artery disease. It remains unclear whether fasting or postprandial hypertriglyceridemia is more informative for predicting the risk of coronary artery disease. Recent studies recommended postprandial Hypertriglyceridemia as a useful predictor of cardiovascular disease risk. This study was conducted to find the correlation between postprandial Hypertriglyceridemia in patients with coronary artery disease. Materials and Methods: This was an observational study on 100 patients diagnosed with coronary artery disease from 14/10/2017 to 10/09/2018. In patients diagnosed with coronary artery disease based on ECG changes or TMT, changes were included in the study. Fasting lipid profile, FBS, and 2-hour postprandial Triglyceride were done. All statistical data were analyzed using frequency, percentages, and ratios. A chi-square test is used to study the associations among different variables. Results: Among the 100 cases included in the study, 68 were males, and 32 were females. Postprandial Hypertriglyceridemia was found in 71% of patients, 48% had high BMI, 80% of Patients had high Waist Hip ratio, and 64 % of patients had diabetes mellitus. There is a statistically significant correlation between postprandial Triglyceride and coronary artery disease with a relative risk of 1.45.

Association postprandial hypertriglyceridemia, carotid intima-media thickness and body mass index in patients with coronary artery disease combined with nonalcoholic liver steatosis

Background and Aims : To estimate the frequency of postprandial hypertriglyceridemia (PPG), carotid intima-media thickness and body mass index (BMI) in patients with coronary artery disease (CHD) combined with nonalcoholic liver steatosis (NALS).

Observational study of post prandial hypertriglyceridemia is a reliable predictor for coronary artery disease

Introduction: Hypertriglyceridemia is recognized as a high-risk factor for coronary artery disease. It remains unclear whether fasting or postprandial hypertriglyceridemia is more informative for predicting the risk of coronary artery disease. Recent studies recommended postprandial Hypertriglyceridemia as a useful predictor of cardiovascular disease risk. This study was conducted to find the correlation between postprandial Hypertriglyceridemia in patients with coronary artery disease. Materials and Methods: This was an observational study on 100 patients diagnosed with coronary artery disease from 14/10/2017 to 10/09/2018. In patients diagnosed with coronary artery disease based on ECG changes or TMT, changes were included in the study. Fasting lipid profile, FBS, and 2-hour postprandial Triglyceride were done. All statistical data were analyzed using frequency, percentages, and ratios. A chi-square test is used to study the associations among different variables. Results: Among the 100 cases included in the study, 68 were males, and 32 were females. Postprandial Hypertriglyceridemia was found in 71% of patients, 48% had high BMI, 80% of Patients had high Waist Hip ratio, and 64 % of patients had diabetes mellitus. There is a statistically significant correlation between postprandial Triglyceride and coronary artery disease with a relative risk of 1.45.

Correlation of fasting and postprandial triglyceride levels and carotid artery intimal medial thickness in type 2 diabetic patients

Background: Although the prevalence of both type 1 and type 2 diabetes mellitus is increasing worldwide, the prevalence of type 2 DM is rising more rapidly, because of sedentary lifestyle, increasing obesity and increased life expectancy. Objectives: To study correlation between fasting and postprandial triglyceride levels and Carotid artery intimal medial thickness (CIMT) in Type 2 Diabetic Patients. Material and Methods: This cross sectional observation study was done in Department of General Medicine, Mysore Medical College and Research Institute, Mysore, Karnataka, India during January 2019 to June 2020. Sample size was 50 and Simple Random sampling method was used. Results: The mean carotid IMT of subjects with postprandial triglycerides &lt; 200 with normal fasting triglyceride was 0.92±0.33. The mean carotid IMT of subjects with postprandial triglyceride 200-299 with normal fasting triglyceride was 1.52±0.57. The mean carotid IMT of subjects with postprandial triglycerides ≥300 with normal fasting triglycerides was 1.66±0.45. Conclusion: postprandial hypertriglyceridemia, despite normal fasting triglyceride levels, may be an independent risk factor for early atherosclerosis in type 2 diabetes. Hence evaluating not only for FTG but also PPTG level during clinical assessment of patients with type 2 diabetes is important.