The objective of this study was to estimate postprandial hypertriglycemia by a newly designed oral fat-loading test. Twenty-three healthy normolipidemic volunteers were orally administered a test meal consisting of a mixture of Telmeal 2.0  and 20 g of saltfree butter after fasting for 12 h. To measure the levels of total cholesterol (T-Cho), triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C), remnant-like particlecholesterol (RLP-C), lipoprotein (a) [Lp (a)], free fatty acid, apolipoproteins (Apos), plasma glucose (PG), immunoreactive insulin (IRI), and high-sensitivity C-reactive protein (hs-CRP), venous blood samples were collected before the meal and at each hour until 9 h after fat-loading. The levels of both TG and RLP-C were drastically elevated at 2 h after fat-loading and these levels remained high until 4 h ( p < 0.01). A significant correlation between TG and RLP-C was also observed at 2, 3 and 4 h, and the values of the correlation coefficients (r) were 0.837, 0.838, and 0.908, respectively. In contrast, the levels of T-Cho, HDL-C, Lp (a), Apos, PG, and hs-CRP did not change. Furthermore, there were no gastrointestinal symptoms during or after the study. These results strongly suggested that this newly designed fat-loading test was very useful for evaluating postprandial hypertriglycemia, including remnant concentrations. IntroductionMultiple epidemiological and clinical studies have established that dyslipidemia, e.g., increased total cholesterol (T-Cho), particularly low-density lipoprotein-cholesterol (LDL-C), and decreased high-density lipoproteincholesterol (HDL-C), is the most crucial factor in the pathogenesis of atherosclerosis, including coronary heart disease (CHD) and subsequent sudden death (1-5). In contrast, although some investigators have reported that moderately elevated fasting triglycerides (TG) increased coronary events (6-9), the independent role of TG in the contribution of CHD has been controversial, since the fasting level of TG is inversely related to that of HDL-C in lipid metabolism (10). Most studies on the relationship between atherosclerosis and lipids have been based on fasting lipid levels.Recently, however, some prospective studies have clearly shown the potential importance of postprandial hypertriglycemia in the etiology of CHD even after adjusting for HDL-C using multivariate analyses (11,12 A Newly Designed Oral Fat-loading Test TG level could predict the incidence of CHD, even in Japanese subjects who showed a decreased level of T-Cho, followed over a 15.5-year period (11). Talmud et al. have also suggested that the combined evaluation of apolipoprotein (Apo) B with nonfasting TG could provide useful diagnostic criteria for CHD risk (12). In addition, considerable evidence supports the view that postprandial hypertriglycemia is associated with insulin resistance, its concomitant compensatory hyperinsulinemia, and obesity (13,14).In contrast, although several investigators have tried and reported fat-loading tests to examine postprandial hypertrigl...

The localization of creatine kinase (CK) M in canine myocardium was immunocytochemically studied by a direct immunoperoxidase method. Specific antiserum against CK-M was produced in rabbits immunized with canine CK-MM. An anti-CK-M Fab'-horseradish peroxidase conjugate was prepared by the maleimide method. Frozen sections prepared from fixed canine myocardium were stained with the conjugate and observed by light and electron microscopy. In light microscopy of longitudinal sections, CK-M showed a cross-striated pattern consisting of distinct broad and narrow brown bands. Immunoelectron microscopy revealed that the regions of the broad and narrow brown bands corresponded to the A-band and the Z-line, respectively. Most CK-M in the A-band was associated with the thick fibers, and a small amount of CK-M was found in the M-line. These findings suggest that ATP regeneration from the ADP produced by myosin ATPase is related to the participation of this CK associated with the thick fibers rather than that of the M-line-bound CK. Creatine kinase M was also found in the sarcolemmal membrane, the membranes of the sarcoplasmic reticulum, and the mitochondrial outer and inner membranes. This report provides new information for understanding the physiological role of the phosphorylcreatine shuttle in the myocardial energy transport system.

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To clarify the changes in creatine kinase M localization along with the progress of myocardial ischemia, immunoelectron microscopic studies were performed using rabbit anti-canine creatine kinase M Fab'-horseradish peroxidase conjugate in 21 dogs. Myocardial ischemia was induced by occlusion of the left anterior descending coronary artery for 15 (n = 5), 30 (n = 5), 60 (n = 5), or 180 (n = 4) minutes. Two dogs were used as normal controls. As we have already demonstrated, most creatine kinase M in normal myocardial cells was localized over the entire A band in association with the thick filament, suggesting that creatine kinase in this region (A-band creatine kinase) was the enzyme coupled with myosin ATPase. After 15 minutes of ischemia, creatine kinase M showed only minimal changes in its location, indicating that A-band creatine kinase still has the ability to couple with myosin ATPase (reversible injury). However, after 30 minutes of ischemia, A-band creatine kinase diffused markedly to the I band (transitional phase), and after 60 minutes of ischemia, it leaked out to extracellular spaces (irreversible injury). After 180 minutes of ischemia, most A-band creatine kinase disappeared from the myocardial cells (coagulation necrosis). These features of creatine kinase M localization seemed to reflect each stage of ischemic cell injury. We conclude that myocardial ischemia results in a dissociation of creatine kinase molecules from the thick filament, which leads the energy transport system to destruction.

Amylase activity detected in thyroid extracts was significantly higher than that of normal sera. A starch film technique revealed the existence of amylase activity in the follicular lumen and on the follicular epithelia. By electrophoretic analysis of thyroid extracts, 4 bands of amylase activity were observed, one being of the same mobility as parotid and the other 3 more anodic. Amylase extracted from the thyroid appeared in the same position as pancreatic or parotid amylase on Sephadex G75 gel filtration. The possibility is discussed that the thyroid may synthesize amylase of salivary type, which is secreted from the follicular epithelia into the follicular lumen, where it may be transformed into anionic forms.