Effect of acute dietary alteration upon intestinal lipid synthesis

The specific activities of three enzymes engaged in complex lipid synthesis, diglyceride acyltransferase, cholinephosphotransferase, and lysolecithin acyltransferase were studied in intestinal mucosa of hamsters fed either saline, hydrolyzed casein, or corn oil for 9 1/2 hr. In the most proximal intestine, saline feeding was associated with a reduced specific activity in villous tips with all three enzymes studied when compared with the two caloric supplemented groups. In the most distal intestine, oil feeding increased the activity of lysolecithin acyltransferase and choline phosphotransferase twofold as compared to casein fed hamsters; diglyceride acyltransferase was increased one- and one-half-fold. The response of lysolecithin acyltransferase and diglyceride acyltransferase to fat feeding was incomplete when compared to hamsters fed a fat supplemented diet for 7 days, suggesting that their pattern of response to dietary substrate was similar to the disaccharidases. By contrast, the response of cholinephosphotransferase to fat feeding was complete at 24 hr, suggesting that it responds in a manner similar to the glycolytic enzymes.     

Formation of lymph chylomicron phosphatidylcholines in the rat during the absorption of safflower oil or triolein

The chylomicron phosphatidylcholines from rats fed safflower oil or triolein were isolated and separated into four different fractions according to the degree of unsaturation. Fraction 1, which was rich in palmitic, stearic and oleic acid, was a minor fraction (7.6–11.6 mole%) during the absorption of safflower oil, but was quantitatively important (27–51 mole%) after triolein feeding when significant amounts of dioleoylphosphatidylcholine were present. Fraction 2, which was a major fraction in all the experiments, contained linoleic acid in combination with a saturated or monounsaturated fatty acid. The third fraction contained mainly linoleic acid and was present only after safflower oil feeding. This indicates that dilinoleoyl-phosphatidylcholine is formed in the intestine after ingestion of linoleic acid. Fraction 4, which was rich in arachidonic acid and saturated fatty acids, accounted for 15–20 mole% of the chylomicron phosphatidylcholines with both kinds of fat meals. Incorporation of³H-choline indicated that the dilinoleoyl- and dioleoyl-phosphatidylcholines were formed by synthesis de novo while the majority of the rem aining phosphatidylcholines originated partly from acylated biliary lysolecithins and partly from the existing pool of mucosal phospholipids not formed during active fat absorption.     

Chylomicron Formation and Secretion is Required for Lipid-Stimulated Release of Incretins GLP-1 and GIP

Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretins produced in the intestine that play a central role in glucose metabolism and insulin secretion. Circulating concentrations of GLP-1 and GIP are low and can be difficult to assay in rodents. These studies utilized the novel intestinal lymph fistula model we have established to investigate the mechanism of lipid-stimulated incretin secretion. Peak concentrations of GLP-1 and GIP following an enteral lipid stimulus (Liposyn) were significantly higher in intestinal lymph than portal venous plasma. To determine whether lipid-stimulated incretin secretion was related to chylomicron formation Pluronic L-81 (L-81), a surfactant inhibiting chylomicron synthesis, was given concurrently with Liposyn. The presence of L-81 almost completely abolished the increase in lymph triglyceride seen with Liposyn alone (P < 0.001). Inhibition of chylomicron formation with L-81 reduced GLP-1 secretion into lymph compared to Liposyn stimulation alone (P = 0.034). The effect of L-81 relative to Liposyn alone had an even greater effect on GIP secretion, which was completely abolished (P = 0.004). These findings of a dramatic effect of L-81 on lymph levels of GLP-1 and GIP support a strong link between intestinal lipid absorption and incretin secretion. The relative difference in the effect of L-81 on the two incretins provides further support that nutrient-stimulation of GIP and GLP-1 is via distinct mechanisms.     

Prolonged Chronic Consumption of a High Fat with Sucrose Diet Alters the Morphology of the Small Intestine

(1) The high-fat diet (HFD) of western countries has dramatic effect on the health of several organs, including the digestive tract, leading to the accumulation of fats that can also trigger a chronic inflammatory process, such as that which occurs in non-alcohol steatohepatitis. The effects of a HFD on the small intestine, the organ involved in the absorption of this class of nutrients, are still poorly investigated. (2) To address this aspect, we administered a combined HFD with sucrose (HFD w/Suc, fat: 58% Kcal) regimen (18 months) to mice and investigated the morphological and molecular changes that occurred in the wall of proximal tract of the small intestine compared to the intestine of mice fed with a standard diet (SD) (fat: 18% Kcal). (3) We found an accumulation of lipid droplets in the mucosa of HFD w/Suc-fed mice that led to a disarrangement of mucosa architecture. Furthermore, we assessed the expression of several key players involved in lipid metabolism and inflammation, such as perilipin, leptin, leptin receptor, PI3K, p-mTOR, p-Akt, and TNF-α. All these molecules were increased in HFD mice compared to the SD group. We also evaluated anti-inflammatory molecules like adiponectin, adiponectin receptor, and PPAR-γ, and observed their significant reduction in the HFD w/Suc group compared to the control. Our data are in line with the knowledge that improper eating habits present a primary harmful assault on the bowel and the entire body’s health. (4) These results represent a promising starting point for future studies, helping to better understand the complex and not fully elucidated spectrum of intestinal alterations induced by the overconsumption of fat.     

Carbohydrate content of apolipoprotein B-48 from rat chylomicrons of varying density

Monosaccharide composition was determined in apolipoprotein B-48 (apoB) of chylomicrons of rat mesenteric lymph. Chylomicrons were separated into three fractions based on density. Triglyceride and apolipoprotein content were determined in each. ApoB was isolated and quantified using precipitation with isopropanol. Chylomicrons were collected in lymph under normal conditions, and with Poloxalene 2930 when chylomicron secretion was inhibited. Most of the triglyceride was carried in the least dense fraction, while the highest apoB content was in the most dense fraction under normal conditions. Mannose and galactosamine contents of apoB were similar in all fractions while contents of both glucosamine and galactose were highest in the least dense fraction. When chylomicron secretion was inhibited by Poloxalene, the amount of triglyceride recovered in the least dense fraction was significantly reduced. Despite the inhibition of lipid transport in the least dense fraction of chylomicrons by Poloxalene, there was little change in apoB recoveries and in the relative content of various monosaccharides in the apoB from each of the three fractions as compared to results obtained during lipid absorption under normal conditions. In conclusion, carbohydrate composition of apoB of chylomicrons is heterogeneous and varies with chylomicron density.     

Distribution among tissues of intravenously administered sucrose octaoleate

The distribution of [¹⁴C]oleate label in rat tissues in the 6 hr after intravenous administration of sucrose octa-[¹⁴C]oleate (7.5 mg; SuO₈) was compared with that observed after administration of [¹⁴C]triolein. The [¹⁴C]-oleate label, whether injected as triolein emulsion, or as chylomicrons obtained from donor animals, rapidly cleared from the serum; only 10% or less remained in the serum 15 min after injection. Labeled SuO₈ disappeared less rapidly from the serum; about one-third of the dose was present after 15 min, and after 120 min 14% remained. In the liver, there was an initial greater accumulation of fatty acid label when and emulsion of either triolein or SuO₈ was given rather than the chylomicrons. The octaester continued to accumulate in the liver throughout the 6 hr of study, and 78% of the initial dose was present at that time. By contrast, although one-third of the triolein, as of SuO₈, was found in the liver shortly after injection, levels subsequently decreased; at 6 hr, 12% of the label remained associated with that organ. A small portion, up to 8% of the acid label, whether administered as chylomicrons or as a triolein emulsion, was found in the epididymal fat pads. Smaller amounts, usually 1% or less, of the [¹⁴C]oleate label were found in fat pads following the injection of labeled SuO₈. In a separate study, the levels of acid label in the liver and spleen were monitored for 21 days following the intravenous administration of [¹⁴C]SuO₈. There was an initial accumulation of approximately half of the injected lipid label in the liver and one-quarter in the spleen. By day 21, the level in the liver had decreased to one-third of that administered, while the level in spleen remained at one-quarter.     

Effects of dietary triglyceride on the properties and lipid composition of plasma lipoproteins: Acute experiments in rats fed safflower oil

Male rats were administered 1.5 ml safflower oil by gastric intubation 0, 4, and 8 hr after a 16 hr fast. Plasma, liver, and adipose tissue were collected 16 hr after the last fatty meal. Rats fasted for 16 hr served as controls. Following fat feeding, the fatty acid composition of the very low density lipoprotein, triglyceride, and hepatic triglyceride were similar, as were the percentages of 18:2 in the very low density lipoprotein and hepatic cholesteryl esters. The phospholipids of liver and plasma lipoproteins were similar in the control groups, except that more 16:0 was present in the plasma lipoproteins. After fat feeding, the plasma lipoproein phospholipids were enriched with 18:2 more than were the hepatic phospholipids. Furthermore, the percentage of 18:2 in phospholipid was much less than in triglyceride or cholesteryl esters. Clearly, esterified lipids of liver and plasma lipoproteins (very low density lipoprotein, low density lipoprotein, and high density lipoprotein), and to a lesser extent, adipose tissue, were enriched with 18:2 derived from dietary triglyceride fatty acid even 16 hr after the terminal meal. A major proportion of the very low density lipoprotein isolated by ultracentrifugation in zonal rotors from plasma of fat fed animals had a faster rate-zonal mobility than did the very low density lipoprotein isolated from plasma of control animals. The very low density lipoprotein isolated from plasma of fat fed rats contained fewer moles of phospholipids, cholesterol, and cholesteryl esters, relative to triglyceride than did the very low density lipoprotein from plasma of animals not receiving safflower oil. The molar ratio triglyceride:phospholipid:cholesterol:cholesterol esters in the very low denity lipoprotein was 100:42.0:22.1:44.5 in the control group and 100:35.4:17.8:19.5 in the fat fed animals. It is postulated that an important biochemical mechanism by which dietary triglyceride fatty acids consumed by the animal over a long period of time alter plasma concentrations of triglyceride, phospholipids, and cholesterol esters is the directive influence of plasma free fatty acid, derived from dietary triglyceride, on the secretion of very low density lipoprotein lipids by the liver.     

Measurement of human chylomicron triglyceride clearance with a labeled commercial lipid emulsion

Human chylomicron triglyceride (TG) kinetics has been difficult to determine directly owing to technical limitations. This report describes a new method for studying chylomicron metabolism. Healthy volunteers (n=10) sipped a drink providing 175 mg fat·kg⁻¹·h⁻¹ for 7.5 h to produce a steady-state chylomicronemia. A commercial 10% intravenous lipid emulsion was labeled with [³H]triolein, purified by high-performance liquid chromatography, and sterilized. A trace amount of labeled emulsion was injected intravenously 30 min before (i.e., in the fasting state) and 5, 6, and 7 h after sipping began (i.e., triplicate determinations in the fed state). Chylomicron half-lives were calculated from the monoexponential decay curves, and apparent distribution volumes were estimated by back-extrapolation to time zero. Plasma and estimated chylomicron TG concentrations increased from 89±13 and 0.8±0.3 to 263±43 and 91±39 mg/dL (mean±SEM), respectively, with feeding. Tracer-determined chylomicron TG half-lives were 5.34±0.58 and 6.51±0.58 min during the fasting and fed states, respectively (P<0.01). The apparent distribution volume during the fasting state was 24% greater than plasma volume (4515±308 vs. 3630±78 mL, P<0.02), consistent with significant margination of lipid emulsion particles to endothelial binding sites. Margination was reduced during the fed state, suggesting that native chylomicrons competed with lipid emulsion particles for endothelial lipoprotein lipase. The results indicate that a radiolabeled commercial lipid emulsion is metabolized in a fashion similar to native chylomicron TG, and thus can be used to study chylomicron TG kinetics.     

Effect of high doses of synthetic estrogen on lipid metabolism in castrated male rats

The mechanism by which high doses of estrogen influences lipid metabolism was studied with a microtubular blocking agent. Castrated male rats received oral injection daily for 14 days of 3 mg hexestrol in olive oil, or oil alone as controls. About half of the animals in each group were injected intraperitoneally with 4 mg/100 g body weight colchicine 3 hr before they were killed. Hexestrol treatment caused an accumulation of esterified cholesterol in the liver while it decreased those in serum. Triglyceride concentrations slightly decreased in the liver but were unaffected in serum. On polyacrylamide-gel disc electrophoresis, the peaks of high density lipoproteins (HDL) and low density lipoproteins (LDL) were decreased remarkably. Electron microsopic examination of hepatocytes revealed electron-lucent lipid droplets in the cytoplasm. After a colchicine treatment of the control animals, concentrations of esterified cholesterol and triglycerides markedly increased in the liver, while those in serum decreased. Electron microscopic examination of hepatocytes revealed numerous secretory vesicles filled with nascent VLDL. In hexestrol-treated animals, the colchicine treatment was associated with marked decreases in serumesterified cholesterol and triglyceride as seen in the controls. However, there were no further increases of esterified cholesterol in the liver, and the increase of triglycerides was slight. Electron microscopic examination showed less secretory droplets than in the controls. These data suggest that very low density lipoproteins (VLDL) synthesis in the liver of hexestrol treated rats was inhibited. An accumulation of esterified cholesterol with a marked decrease in serum could not be accounted for by the inhibition of lipoproteins secretion, but rather by their enhanced entry into the liver.     

Lipid absorption in the young of protein-deficient rats

The effect of reduced protein in the diet during pregnancy on the subsequent absorption of triolein and of oleic acid which were infused into the intestine of the young was studied. Pregnant rats were fed diets containing either 24% or 4% casein as the sole source of protein. Control and prenatally protein-deprived (PPD) young were studied at birth, before and after suckling, and at 4, 8, and 12 days. Both body weight and the weight and length of intestine were reduced in PPD young. Uptake of triolein from the lumen and retention in enterocytes increased on suckling in newborn control pups, but the amount transferred from or metabolized by the cells did not change. In suckled PPD young, transfer of triolein increased through the enterocyte as well. Unsuckled PPD pups had reduced absorption and retention per enterocyte, per g body weight, per cm gut, and in total. In intestines of control and PPD suckled newborn and postnatal pups, absorption per cell did not differ. Blood lipid levels were increased markedly between 0 and 4 days and tended to decrease to newborn levels by 12 days in both diet groups. Oleic acid absorption in newborn and 12-day PPD pups were reduced in total, per g body weight and per cm of gut. The individual enterocytes were shown to be equally capable of absorption and transfer of triolein and oleic acid. Differences in absorption are related primarily to the numbers of absorptive cells.     

Release of chylomicrons by isolated cells of rat intestinal mucosa

Fat-laden mucosal cells were isolated by flotation from fed male rats after digesting scrapings of washed jejunum with collagenase in bicarbonate buffer. About 50–60 million cells were obtained per preparation, which were 95–100% viable as assessed by Trypan Blue. The isolated cells were capable of effective incorporation of labeled fatty acids and glucose into triglycerides and phospholipids, and of labeled leucine and glucosamine into the protein envelope of the released chylomicrons. The secretion of the labeled protein paralleled the release of the labeled fat, both of which were linear with the concentration of the albumin in the incubation mixture. About 80% of the total fat of the cell was released as chylomicrons within 30 min when incubated in the presence of albumin-bicarbonate buffer. Injection of puromycin 24 hr prior to harvesting of cells led to a complete inhibition of chylomicron release. Addition of puromycin to the incubation medium gave 50–80% inhibition of release. No inhibition of release of chylomicrons resulted from a treatment with ethionine. The released chylomicrons were separated from the cells by Millipore filtration. Presented in part at the AOCS Meeting, Chicago, September 1970.     

Distribution of glycosphingolipids and ceramide of rat small intestinal mucosa

Previous studies have suggested that glycosphingolipids may be involved in a number of physiological functions of the small intestinal mucosa. Regional variations in many of these processes exist along the length of this organ. In the present studies, the glycosphingolipid and ceramide composition of the proximal, middle and distal thirds of the rat small intestine were characterized and compared. Mono- and trihexosylceramide were the major neutral glycolipids and hematoside (GM₃), the principal ganglioside of this organ. Monohexosylceramide was the major glycolipid of the proximal segment, whereas trihexosylceramide predominated in the distal segments. The total content of neutral glycolipids, ceramide and gangliosides as well as the content of the individual glycosphingolipids and ceramide were highest in the distal segment, intermediate in the middle and lowest in the proximal segment. Additionally, regional variations were noted in the fatty acid composition of the major glycosphingolipids. These differences in the composition of glycolipids and ceramide along the length of the intestine may be responsible, at least partially, for the regional functional specialization seen in this organ.     

Raman Study on Lipid Droplets in Hepatic Cells Co-Cultured with Fatty Acids

The purpose of the present study was to investigate molecular compositions of lipid droplets changing in live hepatic cells stimulated with major fatty acids in the human body, i.e., palmitic, stearic, oleic, and linoleic acids. HepG2 cells were used as the model hepatic cells. Morphological changes of lipid droplets were observed by optical microscopy and transmission electron microscopy (TEM) during co-cultivation with fatty acids up to 5 days. The compositional changes in the fatty chains included in the lipid droplets were analyzed via Raman spectroscopy and chemometrics. The growth curves of the cells indicated that palmitic, stearic, and linoleic acids induced cell death in HepG2 cells, but oleic acid did not. Microscopic observations suggested that the rates of fat accumulation were high for oleic and linoleic acids, but low for palmitic and stearic acids. Raman analysis indicated that linoleic fatty chains taken into the cells are modified into oleic fatty chains. These results suggest that the signaling pathway of cell death is independent of fat stimulations. Moreover, these results suggest that hepatic cells have a high affinity for linoleic acid, but linoleic acid induces cell death in these cells. This may be one of the causes of inflammation in nonalcoholic fatty liver disease (NAFLD).     

A comparative study of the lipids of chylomicron membrane and fat core and of the lymph serum of dogs

Thoracic lymph was collected from 13 dogs fed corn oil and butterfat. The chylomicrons were isolated by centrifugation. The lipid composition of the fat core and the membrane of the chylomicron was compared to that of the surrounding lymph serum. The fat cores contained 90–96% triglyceride, 0.7–1.9% free cholesterol, 0.2–0.5% steryl ester, 0.9–3.5% free fatty acid and 1.4–6.1% diglyceride, but no phospholipid. The lipids of the membranes contained 58–75% phospholipid, 20–35% triglyceride, 2–5% free cholesterol, 1–2% free fatty acid, and 2–3% diglyceride, but little or no steryl ester. The membrane phospholipids were made up of 70–90% lecithin, 5–20% phosphatidyl ethanolamine, and 1–3% each of lysolecithin and sphingomyelin. The lymph serum contained 24–47% of total lipid as phospholipid, of which 70–92% was lecithin; the phosphatidyl ethanolamine, lysolecithin and sphingomyelin also present contributed 1–10% each. The neutral lipids of the lymph serum contained 49–75% triglyceride, 2–15% free cholesterol, 6–23% esterified cholesterol, 10–33% free fatty acid and 1–6% diglyceride. Alterations in dietary fat, or plant sterol supplementation led to lesser changes in the lipids of the chylomicron membranes than in the lipids of any other lymph fraction. The least variation was seen in the phospholipids. Taken in part from a PhD Thesis submitted by T. C. Huang to Queen's University, Kingston, Canada, in April 1965. Presented at the AOCS 56th Spring Meeting, Houston, May 1965.     

Effect of fructose on rat lipids

Young and mature albino rats were fed Purina chow with and without fructose in the drinking water, and the lipid contents in the serum and livers were determined. Fructose elevated the serum triglyceride and caused an accumulation after 24 hr of liver triglyceride in fed but not fasted mature rats. In young male rats, the liver triglyceride was increased initially but was not found after 10 days. Serum phospholipids were increased in young and mature rats; the content and specific activity of the high density (HD)-lipoproteins being increased in young rats. In vivo incorporation of labeled acetate into liver cholesterol was reduced. Results suggest that fructose or triglyceride metabolism, or both, in rats differ with age.     

Hypolipidemic activity of the surfactants aminimides,and their effects on lipid metabolism of rodents

A series of short chain fatty acid derivatives of aminimides were shown to possess hypolipidemic activity in rats and mice. Most of the agents tested lowered both serum cholesterol and triglyceride levels by at least 30% in mice and were effective in hyperlipidemic induced mice. 1,1-Dimethyl-1-(2-hydroxypropyl)-amine mersitimide lowered serum cholesterol levels 41% and serum triglyceride levels 56% at 20 mg/kg/day I.P. after 16 days. The same agent was active orally when administered to rats with a 38% reduction in serum cholesterol and a 52% reduction in serum triglycerides after 14 days. The agents inhibited liver acetyl CoA synthetase, ATP dependent citrate lyase and phosphatidate phosphohydrolase activities in vitro and in vivo. Reduction of cholesterol, triglycerides, neutral lipids and phospholipid levels were noted in the livers of mice treated for 16 days. In rat studies, cholesterol, triglyceride and phospholipid levels were reduced in liver, small intestine and the feces after two weeks' dosing. The cholesterol content was reduced in the very low density lipoprotein (VLDL) and low density lipoprotein (LDL) fractions but elevated in the high density lipoproteins (HDL). Triglyceride levels were lowered in the VLDL, and neutral lipid levels were reduced in the chylomicron and VLDL fractions.     

The behavior of glyceride-fatty acid mixtures in bile salt solution: Studies by gel filtration

Bile salt lipid emulsions were prepared which simulated the emulsified oil-micellar phase system of the small intestinal content during fat digestion. Application of such emulsions to gel columns prepared and eluted with 6 mM sodium taurodeoxycholate separated an emulsion phase and a micellar phase. The distribution of lipid solutes into the two phases under these conditions was measured. Micellar dimensions were larger as lipid concentrations were increased. Inclusion of multiple lipid classes resulted in larger micellar particles. Monoglyceride and fatty acids were eluted completely in the micellar phase under these conditions. Minimal measurable amounts of triolein were recovered in micellar solution. This was confirmed by extraction, chromatographic separation and quantitative analysis. As diolein concentration was increased, less was recovered in the micellar phase. When monoglyceride was added, more diolein entered the micellar phase. Addition of triglyceride enhanced the distribution of diolein into the emulsion phase.     

Metformin Inhibits Lipid Droplets Fusion and Growth via Reduction in Cidec and Its Regulatory Factors in Rat Adipose-Derived Stem Cells

Metformin is still being investigated due to its potential use as a therapeutic agent for managing overweight or obesity. However, the underlying mechanisms are not fully understood. Inhibiting the adipogenesis of adipocyte precursors may be a new therapeutic opportunity for obesity treatments. It is still not fully elucidated whether adipogenesis is also involved in the weight loss mechanisms by metformin. We therefore used adipose-derived stem cells (ADSCs) from inguinal and epididymal fat pads to investigate the effects and mechanisms of metformin on adipogenesis in vitro. Our results demonstrate the similar effect of metformin inhibition on lipid accumulation, lipid droplets fusion, and growth in adipose-derived stem cells from epididymal fat pads (Epi-ADSCs) and adipose-derived stem cells from inguinal fat pads (Ing-ADSCs) cultures. We identified that cell death-inducing DFFA-like effector c (Cidec), Perilipin1, and ras-related protein 8a (Rab8a) expression increased ADSCs differentiation. In addition, we found that metformin inhibits lipid droplets fusion and growth by decreasing the expression of Cidec, Perilipin1, and Rab8a. Activation of AMPK pathway signaling in part involves metformin inhibition on Cidec, Perilipin1, and Rab8a expression. Collectively, our study reveals that metformin inhibits lipid storage, fusion, and growth of lipid droplets via reduction in Cidec and its regulatory factors in ADSCs cultures. Our study supports the development of clinical trials on metformin-based therapy for patients with overweight and obesity.     

Aroma Release from Solid Droplet Emulsions: Effect of Lipid Type

Aroma compounds partition between the different phases of a food emulsion and the headspace but only those in the headspace are perceived. Phase transitions in the lipid droplets profoundly affect the position of the partitioning equilibria and hence headspace aroma concentration. The release of four volatile aroma compounds (ethyl butanoate, pentanoate, heptanoate and octanoate) from eicosane, hydrogenated palm fat or Salatrim^® emulsions stabilized with sodium caseinate were investigated as a function of fat crystallization, particle size and droplet concentration. For all compounds, the headspace aroma concentration in equilibrium with solid droplet emulsions was significantly higher than that in equilibrium with liquid droplet emulsions. The partitioning of volatile aroma compounds from emulsion does not depend on the type of liquid lipid, however, the interactions between solid lipid droplets and aroma compounds are significantly influenced by the nature of the crystalline fat. Notably, partitioning into the headspace was much lower for solid triglyceride droplet emulsions than for solid alkane emulsions. It was proposed that both residual liquid lipid in solid triglycerides and aroma co-crystallization with solid lipid could be responsible for higher aroma absorption by solid triglycerides.     

Delayed Metabolism of Postprandial Triglyceride-Rich Lipoproteins in Subjects with Echolucent Carotid Plaques

Subjects with echolucent carotid plaques have an increased risk of ischemic cerebrovascular events independent of degree of stenosis. Low plasma lipoprotein lipase (LPL) activity promotes a proatherogenic lipid profile, and delayed chylomicron clearance is a risk factor for atherosclerosis. This study was conducted to determine plasma LPL activity and postprandial metabolism of triglycerides in relation to carotid plaque morphology. Plaque echogenicity was assessed by B-mode ultrasound and analysis of the grey scale median (GSM). Echolucent plaques were defined as GSM ≤ 63 (the median) and echogenic plaques as GSM > 63, and 57 subjects with carotid plaques and 38 subjects without carotid plaques were recruited. Blood samples were collected before and at 2-h interval for 8 h after a standard high fat meal. LPL activity and mass was determined before and after heparin administration. Postheparin LPL activity was decreased in subjects with echolucent plaques compared to subjects with echogenic plaques (P = 0.06) and to controls (P = 0.04). Plaque echogenicity increased linearly with increasing levels of postheparin LPL activity (P = 0.02) and mass (P = 0.03). Subjects with echolucent plaques had delayed postprandial clearance of chylomicron triglycerides compared to controls (P = 0.04). Low postheparin LPL activity due to attenuated mobilization of LPL from capillary endothelium may play an important role in the formation of echolucent plaques by modulation of postprandial lipids and subsequent fat accumulation in the arterial wall.