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Fast Food

Fasting

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Fasting

Hypertriglyceridemia positively associated with morbidity of coronary heart disease (CD), postprandial (non-fasting) hypertriglyceridaemia also correlates with the risk status for CHD, which is related to the increase in chylomicron (CM)-remnant lipoproteins, produced from the intestine. CM-remnant particles, as well as oxidized low density lipoprotein (LDL) or very low density lipoprotein (VLDL) remnants, are highly atherogenic and act by enhancing systemic inflammation, platelet activation, coagulation, thrombus formation, and macrophage foam cell formation. Cholesterol levels of remnant lipoproteins significantly correlate with small, dense LDL, impaired glucose tolerance (IGT) and CHD prevalence. We have developed an assay of apolipoprotein(apo)B-48 levels to evaluate the accumulation of CM remnants. Fasting apoB-48 level correlate with the morbidity of postprandial hypertriglyceridemia, obesity, type III hyperlipoproteinaemia, the metabolic syndrome, hypothyroidism, chronic kidney disease, and IGT. Fasting apoB-48 levels also correlate with carotid intima-media thickening and CHD prevalence, and high apoB-48 level are a significant predictor of CHD risk independent of the fasting TG level. Diet interventions, such as dietary fibers, polyphenols, medium-chain fatty acids, diacylglycerol, and long-chain n-3 polyunsaturated fatty acids (PUFA), ameliorate postprandial hypertriglyceridemia; drugs for dyslipidemia (n-3 PUFA, statins, fibrates or ezetimibe) and drugs for diabetes concerning incretins (dipeptidyl-peptidase IV inhibitor or glucagon like peptide-1 analogue) may improve postprandial hypertriglyceridemia. Since the accumulation of CM remnants correlates to impaired lipid and glucose metabolism and atherosclerotic cardiovascular events, further studies are required to investigate the characteristics, physiological activities, and functions of CM remnants for the development of new interventions to reduce atherogenicity.

  1. Fasting and Postprandial Hypertriglyceridemia

In Japan, the morbidity and mortality of atherosclerotic cardiovascular diseases (ASCVD), including coronary heart disease (CHD) and stroke has gradually increased for recent decades. An intensive intervention against hypercholesterolemia or hyper low-density lipoprotein (LDL)-cholesterolemia using statins has improved the primary and secondary prevention of CHD events, however, the complete suppression of CHD events has not yet been accomplished. Recently, the importance of controlling “residual risk factors” for CHD has been emphasized; hypertriglyceridemia (≧150 mg/dL) and hypo high-density lipoprotein(HDL)-cholesterolemia (<40 mg/dL) have both been investigated in basic and clinical research settings to determine a possible method for the prevention of ASCVD (1,2). As fasting triglyceride (TG) levels at the registration increased (<100, 100-149, 150-199, 200-499, and ≥500 mg/dL) the age- and sex-adjusted hazard ratio (HR) for adjusted all-cause mortality worsened (1.06, 1.16, 1.29, and 1.28 compared with <100 mg/dL, respectively)(3). A systematic review and meta-analysis of 35 observational studies reveals that fasting hypertriglyceridemia was significantly associated with cardiovascular death (odds ratios (OR) 1.80; 95% confidence interval (CI) 1.31-2.49), cardiovascular events (OR, 1.37; 95% CI, 1.23-1.53) and myocardial infarction (OR, 1.31; 95% CI, 1.15-1.49)(4). Moreover, on a background of statin treatment after ACS, fasting triglycerides were related to risk of CHD death, nonfatal myocardial infarction, stroke, and unstable angina in models adjusted for classic CHD risk factors (5). The Japan Atherosclerosis Society Guidelines 2012 suggested that if a subject with hypertriglyceridemia (fasting TG level ≥150 mg/dL) is defined as high risk for ASCVD (especially CHD) by an annual medical checkup, he or she should be encouraged to receive secondary checkups and medical intervention (6). However, fasting TG levels may be varied by the lipid content and the consumption time of the patient’s meal, fasting TG level is not always positively correlated with the atherogenicity. Slightly elevated TG levels that are observed in patients with impaired glucose tolerance (IGT) or the metabolic syndrome (MetS) are highly atherogenic while the severely high TG levels that are observed in patients with primary chylomicronemia or lipoprotein lipase (LPL) deficiency are rarely atherogenic. Therefore, the measurement of the fasting TG level is insufficient for evaluating individual ASCVD risks; the exact analysis of impaired lipoprotein metabolism as the background has been requested.

In contrast, many studies have revealed that postprandial (non-fasting) hypertriglyceridemia is likely to reflect the risk for ASCVD. Iso et al. showed the positive correlation between the incidence of CHD (myocardial infarctions, angina pectoris events, and sudden cardiac deaths) and non-fasting TG levels in a 15.5-year prospective observation; the multivariate relative risk of CHD associated with a 1 mmol/L increase in TG level was 1.29 (95% CI: 1.09-1.53; p <0.01) for men and 1.42 (1.15-1.75; p <0.01) for women independent of total cholesterol levels (7). Nordestgaard et al. also showed that non-fasting TG levels correlated with the morbidity of CHD (8) and ischemic stroke (9) in a prospective cohort study (Copenhagen City Heart Study). However, there has been no standardized reference value for postprandial TG levels to define postprandial hypertriglyceridemia as a risk factor for ASCVD events. In 2016, the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine published a joint consensus statement recommending the routine use of non-fasting blood samples for assessing plasma lipid profiles (10), based on the epidemiological data that there was no clinically significant difference between LDL-C and non-HDL-C levels in both the fasting and the postprandial state. As maximal mean changes in TG levels at 1-6 h after habitual meals were stable (+26 mg/dL), they suggested that the cut-off for abnormal postprandial TG levels should be >2 mmol/L (175 mg/dL) and pointed out the usefulness of measuring non-fasting lipid levels in usual clinical settings (10). For the future, the cut-off value of non-fasting TG level based upon the prospective study in a larger population is strongly recommended for the purpose of evaluating ASCVD risks with high sensitivity.

  1. Metabolism of Remnant Lipoproteins

In patients with hypertriglyceridemia, the TG-rich lipoproteins (TRLs) are mainly increased during the fasting and the postprandial state. TRLs are metabolized in the exogenous and endogenous pathways. The exogenous pathway distributes the lipids that are absorbed by the intestine after a meal to the peripheral tissue using chylomicron (CM) particles during postprandial state. In the intestines, CM particles are synthesized by apoB-48, apoA-1, TG, and cholesterol ester (CE) in enterocytes during the fasting state; expanded by lipid-enriched foods; and secreted into the intestinal lymphatic trunks (11,12). TGs that are contained in CM particles are released into the bloodstream with apoC-2 and apoE and are metabolized by apoC-2 activated LPLs. CM particles are referred to smaller CM remnant particles that are rich in CE and less in TG that CM. The liver takes up CM remnant particles, predominantly via the LDL receptor with apoE acting as the ligand or by LDL receptor-related proteins (LRP1) with the cooperation of heparan sulfate proteoglycans (HSPG) (13,14,15). On the other hand, the endogenous pathway distributes the lipids that are stored in the liver to the peripheral tissues by very low-density lipoproteins (VLDL) during fasting states. An VLDL particle is synthesized with apoB-100, TG, and CE in hepatocytes and produced throughout the day; they are then metabolized into smaller VLDL remnants and intermediate-density lipoproteins (IDL) by LPL and further metabolized to LDLs by hepatic lipase. LDLs are absorbed by the liver or peripheral tissues. The apoB gene encodes both apoB-48 and apoB-100 proteins. One apoB-48 protein is contained within one CM particle up to the liver uptake, one apoB-100 protein is also contained within one VLDL particle up to the liver uptake. ApoB-100 protein consists of 4563 amino acids and apoB48 protein is generated when a stop codon (UAA) at residue 2153 is created by RNA editing of apobec-1 protein (16).

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