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The time dependence of the liking of foodstuffs was investigated in a study with 25 subjects, consisting of three parts: (1) on day one, a sensory specific satiety study, which was extended until 125 min after consumption; (2) on days two to seven, a repeated in home taste and evaluation study; (3) on day eight, a second sensory specific satiety study as in 1. In parts 1 and 3, subjects were asked to eat either cheese biscuits or pears in light syrup to satiety. The change in liking of both foodstuffs, after eating one of the two foodstuffs to satiety, was followed during 125 min. In part 2, the same subjects were asked to taste and evaluate each product at home, every day for six days. In the sensory specific satiety studies (parts 1 and 3) a significant decrease in liking was observed for the product eaten to satiety, as long as 125 min after consuming that product to satiety. For both products contrast effects were observed: the liking of the uneaten product increased after eating the other product to satiety, while liking of the eaten product decreased. This contrast effect lasted longer after eating cheese biscuits to satiety, than after eating pears to satiety. In the in home taste and evaluation study, a significant and linear decrease in liking was observed for both products during six days. There was a significant effect (p < 0.05) of eating cheese biscuits to satiety in the sensory specific satiety study on day 1, on the liking ratings of the in home consumption study. No such effect was observed for the pears. The results indicate that sensory specific satiety is relatively strong for more than 2 h after consumption and can have effects on liking ratings for more than 24 h. These effects were different for the products tested. Based on these results, we suggest that combining eating a product to satiety and in home evaluation over several days, could possibly be useful as an accelerated method to predict changes in liking upon repeated consumption. © 2004 Elsevier Ltd. All rights reserved.

1. The present study investigated the acute and chronic effect of dinner with alcoholic beverages on serum nitric oxide (NO) metabolites, namely nitrate and nitrite (NOx), in 11 healthy, non-smoking middle-aged men. 2. In a randomized, diet-controlled, cross-over trial, subjects consumed dinner with four glasses of red wine, beer, spirits (Dutch gin) or sparkling mineral water (control) for 3 weeks. At the end of each 3 week period, serum NOx concentrations were measured just before and 1, 5 and 13 h after dinner. 3. Serum NOx concentrations were approximately 50% higher 1 and 5 h after dinner with any beverage compared with just before dinner (P = 0.0001). At 1 h after dinner, the serum NOx concentration was approximately 11% lower after dinner with alcoholic beverages compared with concentrations observed after dinner with water (P = 0.01). The fasted serum NOx concentration (13 h after dinner) was similar to the preprandial concentration and there were no differences in serum NOx concentrations between the alcoholic beverages. 4. Food intake acutely and transiently increased serum NOx concentrations, an effect that was slightly attenuated if combined with alcoholic beverages. Chronic moderate alcohol consumption had no effect on serum NOx concentration.

The increasing prevalence in many countries of people with overweight and obesity is undoubtedly one of the biggest threats to public health. Dietary proteins, because of their positive effects on satiation/ satiety, may help to reduce energy intake and promote a healthy body composition with less body fat. Several mechanisms have been put forward to explain why proteins, as compared to fats and carbohydrates, enhance satiation. These are diet-induced thermogenesis, increased post-prandial concentration of plasma amino acids and effects on gut hormones, playing a role in the brain gut axis. In this paper these mechanisms are discussed and the significance of whey proteins for weight management is evaluated. It is concluded that replacement of either fat or carbohydrates by whey proteins can be helpful in reduction of energy intake. To what extent whey proteins offer a specific advantage in this regard as compared to other dietary proteins, should be investigated in more detail. Copyright © 2006 by New Century Health Publishers, LLC.

Chemicals/CAS: Carotenoids, 36-88-4; Chylomicrons

The vagal nerve and gut hormones CCK and GLP-1 play important roles in the control of food intake. However, it is not clear to what extent CCK and GLP-1 increase satiation by stimulating receptors located on abdominal vagal nerve endings or via receptors located elsewhere. This study aimed to further explore the relative contribution of the abdominal vagal nerve in mediating the satiating effects of endogenous CCK and GLP-1. Total subdiaphragmatic vagotomy or sham operation was combined with administration of CCK1 and GLP-1 receptor antagonists devazepide and exendin (9-39) in 12 pigs, applying an unbalanced Latin Square within-subject design. Furthermore, effects of vagotomy on preprandial and postprandial acetaminophen absorption, glucose, insulin, GLP-1 and CCK plasma concentrations were investigated.Ad libitum liquid meal intake (mean±SEM) was similar in sham and vagotomized pigs (4180±435 and 3760±810g/meal). Intake increased by about 20% after blockade of CCK1 receptors, independently of the abdominal vagal nerve. Food intake did not increase after blockade of GLP-1 receptors. Blockade of CCK1 and GLP-1 receptors increased circulating CCK and GLP-1 concentrations in sham pigs only, suggesting the existence of a vagal reflex mechanism in the regulation of plasma CCK1 and GLP-1 concentrations. Vagotomy decreased acetaminophen absorption and changed glucose, insulin, CCK and GLP-1 concentrations indicating a delay in gastric emptying. Our data show that at liquid feeding, satiation is decreased effectively by pharmacological blockade of CCK1 receptors. We conclude that regulation of liquid meal intake appears to be primarily regulated by CCK1 receptors not located on abdominal vagal nerve endings. Chemicals/CAS: cholecystokinin, 9011-97-6, 93443-27-7; devazepide, 103420-77-5; glucagon like peptide 1, 89750-14-1; glucose, 50-99-7, 84778-64-3; insulin, 9004-10-8; paracetamol, 103-90-2

Background: A high plasma total homocysteine (tHcy) concentration is a risk factor for cardiovascular disease. The increase in tHcy induced by methionine, the sole dietary precursor of homocysteine, might be modulated by other amino acids present in dietary proteins. Objectives: Our objectives were to compare the postprandial effect of free and dietary methionine on plasma tHcy concentrations and to investigate whether serine and cystine modify the effect of free methionine on tHcy. Design: We conducted a randomized crossover trial in 24 healthy men. Each subject ingested 4 meals on separate days, which were separated by 1 wk. tHcy concentrations were measured in the fasting state and at 2, 4, 6, 8, 10, and 24 h after meal ingestion. The meals were 1) a low-protein meal fortified with 30 mg methionine/kg body wt (reference, denoted by "Met"), 2) meal 1 additionally fortified with 60.6 mg serine/kg body wt (MetSer), 3) meal 1 additionally fortified with 12.3 mg cystine/kg body wt (MetCys), and 4) a protein-rich meal containing 30 mg methionine, 60.6 mg serine, and 12.3 mg cystine per kg body wt (Protein). Results: The mean (±SD) fasting tHcy concentration was 9.1 ± 2.7 μmol/L. Mean peak tHcy concentrations were 17.9 ± 4.5, 14.3 ± 3.3, 14.8 ± 3.9, and 11.2 ± 3.1 μmol/L after Met, MetSer, MetCys, and Protein, respectively. Compared with the mean 24-h area under the tHcy-by-time curve after Met, the mean curves after MetSer, MetCys, and Protein were 37%, 32%, and 77% smaller, respectively (all P < 0.0005). Conclusions: Dietary methionine increases tHcy much less than does free methionine. Serine and cystine attenuate the tHcy-raising effect of free methionine. Thus, dietary proteins with a high content of serine or cystine relative to methionine may lead to lower postprandial tHcy responses. © 2004 American Society for Clinical Nutrition.

Distension and chemosensitization of the stomach are insufficient to induce a ghrelin response, suggesting that postgastric feedback is required. This postgastric feedback may be regulated through insulin. We investigated the relation between gastric emptying rate and the postprandial ghrelin response as well as the role of insulin and other hormones possibly mediating this response. Fifteen healthy men [BMI 21.6 kg/m2 (SD 1.9), age 20.5 yr (SD 2.5)] were studied in a single-blind, crossover design. Subjects received two treatments separated by 1 wk: 1) a dairy breakfast in combination with a 3-h intravenous infusion of glucagon-like peptide-1 (GLP-1), which delays gastric emptying, and 2) a dairy breakfast in combination with a 3-h intravenous infusion of saline. Blood samples were drawn before breakfast and during the infusion. Postprandial ghrelin (total) responses were lower following the saline infusion compared with the GLP-1 infusion (P < 0.05). Acetaminophen concentrations, an indirect measurement of gastric emptying rate, were inversely correlated with total ghrelin concentrations (saline r = -0.76; 95% CI = -0.90, -0.49, GLP-1 r = -0.47; 95% CI = -0.76, -0.04). Ghrelin concentrations were only weakly correlated with insulin concentrations (saline r = -0.36; 95% CI = -0.69, 0.09; GLP- 1 r = -0.42; 95% CI = -0.73, 0.03), but strongly inversely correlated with GIP concentrations (saline r = -0.74; 95% CI= -0.89, -0.45; GLP-1 r = -0.63; 95% CI = -0.84, -0.27). In conclusion, our results support the hypothesis that ghrelin requires postgastric feedback, which may not be regulated through insulin. Conversely, our data suggest a role of glucose-dependent insulinotropic polypeptide in ghrelin secretion. Copyright © 2006 the American Physiological Society.

Background: A high plasma concentration of total homocysteine (tHcy) is associated with increased risk of cardiovascular disease. A high protein intake and hence a high intake of methionine-the sole dietary precursor of homocysteine-may raise plasma tHcy concentrations. Objectives: We studied whether high intake of protein increases plasma concentrations of tHcy in the fasting state and throughout the day. Design: We conducted a randomized, dietary controlled, crossover trial in 20 healthy men aged 18-44 y. For 8 d, men consumed a controlled low-protein diet enriched with either a protein supplement [high-protein diet (21% of energy as protein)] or an isocaloric amount of short-chain glucose polymers [low-protein diet (9% of energy as protein)]. After a 13-d washout period, treatments were reversed. On days 1 and 8 of each treatment period, blood was sampled before breakfast (fasting) and throughout the day. Results: Fasting tHcy concentrations did not differ significantly after the 1-wk high-protein and the 1-wk low-protein diets. The high-protein diet resulted in a significantly higher area under the 24-h homocysteine-by-time curves compared with the low-protein diet, both on day 1 (difference: 45.1 h · μmol/L; 95% CI: 35.3, 54.8 h · μmol/L; P < 0.0001) and on day 8 (difference: 24.7 h · μmol/L; 95% CI: 15.0, 34.5 h · μmol/L; P < 0.0001). Conclusions: A high-protein diet increases tHcy concentrations throughout the day but does not increase fasting tHcy concentrations. As previously shown, the extent of the tHcy increase is modified by the amino acid composition of the protein diet. The clinical relevance of this finding depends on whether high concentrations of tHcy-particularly postprandially-cause cardiovascular disease. © 2005 American Society for Clinical Nutrition.

The VLDL receptor (VLDLr) is involved in tissue delivery of VLDL-triglyceride (TG)-derived FFA by facilitating the expression of lipoprotein lipase (LPL). However, vldlr-/- mice do not show altered plasma lipoprotein levels, despite reduced LPL expression. Because LPL activity is crucial in postprandial lipid metabolism, we investigated whether the VLDLr plays a role in chylomicron clearance. Fed plasma TG levels of vldlr -/- mice were 2.5-fold increased compared with those of vldlr +/+ littermates (1.20 ± 0.37 mM vs. 0.47 ± 0.18 mM; P < 0.001). Strikingly, an intragastric fat load led to a 9-fold increased postprandial TG response in vldlr-/- compared with vldlr +/+ mice (226 ± 188 mM/h vs. 25 ± 11 mM/h; P < 0.05). Accordingly, the plasma clearance of [3H]TG-labeled protein-free chylomicron-mimicking emulsion particles was delayed in vldlr -/- compared with vldlr+/+ mice (half-life of 12.0 ± 2.6 min vs. 5.5 ± 0.9 min; P < 0.05), with a 60% decreased uptake of label into adipose tissue (P < 0.05). VLDLr deficiency did not affect the plasma half-life and adipose tissue uptake of albumin-complexed [14C]FFA, indicating that the VLDLr facilitates postprandial LPL-mediated TG hydrolysis rather than mediating FFA uptake. We conclude that the VLDLr plays a major role in the metabolism of postprandial lipoproteins by enhancing LPL-mediated TG hydrolysis. Chemicals / CAS: carbon 14, 14762-75-5; lipoprotein lipase, 83137-80-8, 9004-02-8; Albumins; Chylomicrons; Fatty Acids, Nonesterified; Lipoprotein Lipase, EC 3.1.1.34; Receptors, LDL; Triglycerides; VLDL receptor

Previous studies have shown that overexpression of human apolipoprotein C-I (apoC-I) results in moderate hypercholesterolemia and severe hypertriglyceridemia in mice in the presence and absence of apoE. We assessed whether physiological endogenous apoC-I levels are sufficient to modulate plasma lipid levels independently of effects of apoE on lipid metabolism by comparing apolipoprotein E gene-deficient/apolipoprotein C-I gene-deficient (apoe -/-apoc1-/-), apoe-/-apoc +/-, and apoe-/-apoc1+/+ mice. The presence of the apoC-I gene-dose-dependently increased plasma cholesterol (+45%; P < 0.001) and triglycerides (TGs) (+137%; P < 0.001), both specific for VLDL. Whereas apoC-I did not affect intestinal [3H]TG absorption, it increased the production rate of hepatic VLDL-TG (+35%; P < 0.05) and VLDL-[ 35S]apoB (+39%; P < 0.01). In addition, apoC-I increased the postprandial TG response to an intragastric olive oil load (+120%; P < 0.05) and decreased the uptake of [3H]TG-derived FFAs from intravenously administered VLDL-like emulsion particles by gonadal and perirenal white adipose tissue (WAT) (-34% and -25%, respectively; P < 0.05). As LPL is the main enzyme involved in the clearance of TG-derived FFAs by WAT, and total postheparin plasma LPL levels were unaffected, these data demonstrate that endogenous apoC-I suffices to attenuate the lipolytic activity of LPL. Thus, we conclude that endogenous plasma apoC-I increases VLDL-total cholesterol and VLDL-TG dose-dependently in apoe-/- mice, resulting from increased VLDL particle production and LPL inhibition. Copyright © 2006 by the American Society for Biochemistry and Molecular Biology, Inc. Chemicals / CAS: cholesterol, 57-88-5; heparin, 37187-54-5, 8057-48-5, 8065-01-8, 9005-48-5; lipid, 66455-18-3; lipoprotein lipase, 83137-80-8, 9004-02-8; olive oil, 8001-25-0; Apolipoprotein C-I; Apolipoproteins C; Apolipoproteins E; Cholesterol, 57-88-5; Lipase, EC 3.1.1.3; Lipoprotein Lipase, EC 3.1.1.34; Lipoproteins, VLDL

The function of scavenger receptor class B type I (SR-BI) in mediating the selective uptake of high density lipoprotein (HDL) cholesterol esters is well established. However, the potential role of SR-BI in chylomicron and chylomicron remnant metabolism is largely unknown. In the present investigation, we report that the cell association of 160 nm-sized triglyceride-rich chylomicron-like emulsion particles to freshly isolated hepatocytes from SR-BI-deficient mice is greatly reduced (>70%), as compared with wild-type littermate mice. Competition experiments show that the association of emulsion particles with isolated hepatocytes is efficiently competed for (>70%) by the well established SR-BI ligands, HDL and oxidized low density lipoprotein (LDL), whereas LDL is ineffective. Upon injection into SR-BI-deficient mice the hepatic association of emulsion particles is markedly decreased (∼80%) as compared with wild-type mice. The relevance of these findings for in vivo chylomicron (remnant) metabolism was further evaluated by studying the effect of SR-BI deficiency on the intragastric fat load-induced postprandial triglyceride response. The postprandial triglyceride response is 2-fold higher in SR-BI-deficient mice as compared with wild-type littermates (area-under-the-curve 39.6 ± 1.2 versus 21.1 ± 3.6; p < 0.005), with a 4-fold increased accumulation of chylomicron (remnant)-associated triglycerides in plasma at 6 h after intragastric fat load. We conclude that SR-BI is important in facilitating chylomicron (remnant) metabolism and might function as an initial recognition site for chylomicron remnants whereby the subsequent internalization can be exerted by additional receptor systems like the LDL receptor and LDL receptor-related protein. Chemicals / CAS: Antigens, CD36; Chylomicron Remnants; Chylomicrons; Emulsions; Receptors, Immunologic; Receptors, Scavenger; Scavenger Receptors, Class B; Triglycerides

Appetite suppressants may be one strategy in the fight against obesity. This study evaluated whether Korean pine nut free fatty acids (FFA) and triglycerides (TG) work as an appetite suppressant. Korean pine nut FFA were evaluated in STC-1 cell culture for their ability to increase cholecystokinin (CCK-8) secretion vs. several other dietary fatty acids from Italian stone pine nut fatty acids, oleic acid, linoleic acid, alpha-linolenic acid, and capric acid used as a control. At 50 μM concentration, Korean pine nut FFA produced the greatest amount of CCK-8 release (493 pg/ml) relative to the other fatty acids and control (46 pg/ml). A randomized, placebo-controlled, double-blind cross-over trial including 18 overweight post-menopausal women was performed. Subjects received capsules with 3 g Korean pine (Pinus koraiensis) nut FFA, 3 g pine nut TG or 3 g placebo (olive oil) in combination with a light breakfast. At 0, 30, 60, 90, 120, 180 and 240 minutes the gut hormones cholecystokinin (CCK-8), glucagon like peptide-1 (GLP-1), peptide YY (PYY) and ghrelin, and appetite sensations were measured. A wash-out period of one week separated each intervention day. CCK-8 was higher 30 min after pine nut FFA and 60 min after pine nut TG when compared to placebo (p < 0.01). GLP-1 was higher 60 min after pine nut FFA compared to placebo (p < 0.01). Over a period of 4 hours the total amount of plasma CCK-8 was 60% higher after pine nut FFA and 22% higher after pine nut TG than after placebo (p < 0.01). For GLP-1 this difference was 25% after pine nut FFA (P < 0.05). Ghrelin and PYY levels were not different between groups. The appetite sensation "prospective food intake" was 36% lower after pine nut FFA relative to placebo (P < 0.05). This study suggests that Korean pine nut may work as an appetite suppressant through an increasing effect on satiety hormones and a reduced prospective food intake. © 2008 Pasman et al; licensee BioMed Central Ltd.

Background: The most satiating macronutrient appears to be dietary protein. Few studies have investigated the effects of dietary protein on ghrelin secretion in humans. Objective: This study was designed to investigate whether a high-protein (HP) breakfast is more satiating than a high-carbohydrate breakfast (HC) through suppression of postprandial ghrelin concentrations or through other physiologic processes. Design: Fifteen healthy men were studied in a single-blind, crossover design. Blood samples and subjective measures of satiety were assessed frequently for 3 h after the consumption of 2 isocaloric breakfasts that differed in their protein and carbohydrate content (58.1% of energy from protein and 14.1% of energy from carbohydrate compared with19.3% of energy from protein and 47.3% of energy from carbohydrate). The gastric emptying rate was indirectly assessed with the acetaminophen absorption test. Results: The HP breakfast decreased postprandial ghrelin secretion more than did the HC breakfast (P < 0.01). Ghrelin concentrations were correlated with glucose-dependent insulinotropic polypeptide (r = -0.65; 95% CI: -0.85, -0.29) and glucagon concentrations (r = -0.47; 95% CI: -0.75, -0.03). Compared with the HC breakfast, the HP breakfast increased glucagon (P < 0.0001) and cholecystokinin (P < 0.01), tended to increase glucose-dependent insulinotropic polypeptide (P = 0.07) and glucagon-like peptide 1 (P = 0.10), and decreased the gastric emptying rate (P < 0.0001). Appetite ratings were not significantly different between the 2 treatments, and the HP breakfast did not significantly affect ad libitum energy intake. Conclusions: The HP breakfast decreased postprandial ghrelin concentrations more strongly over time than did the HC breakfast. High associations between ghrelin and glucose-dependent insulinotropic polypeptide and glucagon suggest that stimulation of these peptides may mediate the postprandial ghrelin response. The HP breakfast also reduced gastric emptying, probably through increased secretion of cholecystokinin and glucagon-like peptide 1. © 2006 American Society for Nutrition.

Background: Ghrelin plays an important role in the regulation of food intake. Little is known about how ghrelin concentrations are modified by dietary factors. Objective: We examined the effects of both amount and type of carbohydrate on ghrelin concentrations and all correlations among the variables ghrelin, glucose, insulin, leptin, and all 4 subjective measures of appetite. Design: Twenty healthy nonobese men were studied in a double-blind, randomized, crossover design. Subjective measures of appetite and concentrations of ghrelin, glucose, insulin, and leptin were frequently assessed for 4 h after liquid breakfast meals differing in energy content and carbohydrate structure-ie, water, low-calorie (LC) meal, high-calorie simple carbohydrate (HC-SC) meal, and high-calorie complex carbohydrate (HC-CC) meal. Results: Ghrelin concentrations decreased after the HC-SC breakfast by 41%, after the HC-CC breakfast by 33%, and after the LC breakfast by 24%. No significant differences in ghrelin concentration among the 3 breakfasts were observed until 120 min. Ghrelin concentrations were correlated with subjective measures of hunger (r = 0.51) and fullness (r = -0.44). The percentage decrease in ghrelin between 0 and 30 min was inversely correlated with the percentage increases in insulin (r = -0.76) and glucose (r= -0.79) but not with changes in leptin (r = 0.10). The percentage changes in ghrelin concentrations between 30 and 180 min were correlated with the percentage changes in insulin (r= -0.53) and leptin (r= -0.47) but not with changes in glucose (r = 0.22). Conclusion: The results support the hypothesis that ghrelin requires postgastric feedback, which may be regulated through insulin. © 2005 American Society for Clinical Nutrition.

Bile acids (BA) are signaling molecules with a wide range of biological effects, also identified among the most responsive plasma metabolites in the postprandial state. We here describe this response to different dietary challenges and report on key determinants linked to its interindividual variability. Healthy men and women (n = 72, 62 ± 8 yr, mean ± SE) were enrolled into a 12-wk weight loss intervention. All subjects underwent an oral glucose tolerance test and a mixed-meal tolerance test before and after the intervention. BA were quantified in plasma by liquid chromatography-tandem mass spectrometry combined with whole genome exome sequencing and fecal microbiota profiling. Considering the average response of all 72 subjects, no effect of the successful weight loss intervention was found on plasma BA profiles. Fasting and postprandial BA profiles revealed high interindividual variability, and three main patterns in postprandial BA response were identified using multivariate analysis. Although the women enrolled were postmeno-pausal, effects of sex difference in BA response were evident. Exome data revealed the contribution of preselected genes to the observed interindividual variability. In particular, a variant in the SLCO1A2 gene, encoding the small intestinal BA transporter organic anion-transporting polypeptide-1A2 (OATP1A2), was associated with delayed postprandial BA increases. Fecal microbiota analysis did not reveal evidence for a significant influence of bacterial diversity and/or composition on plasma BA profiles. The analysis of plasma BA profiles in response to two different dietary challenges revealed a high interindividual variability, which was mainly determined by genetics and sex difference of host with minimal effects of the microbiota. NEW & NOTEWORTHY Considering the average response of all 72 subjects, no effect of the successful weight loss intervention was found on plasma bile acid (BA) profiles. Despite high interindividual variability, three main patterns in postprandial BA response were identified using multivariate analysis. A variant in the SLCO1A2 gene, encoding the small intestinal BA transporter organic anion-transporting polypeptide-1A2 (OATP1A2), was associated with delayed postprandial BA increases in response to both the oral glucose tolerance test and the mixed-meal tolerance test. © 2017, American Physiological Society. All rights reserved. Chemicals/CAS: chenodeoxycholic acid, 474-25-9; cholic acid, 32500-01-9, 361-09-1, 81-25-4; deoxycholic acid, 83-44-3; glycine, 56-40-6, 6000-43-7, 6000-44-8; glycochenodeoxycholic acid, 640-79-9; glycocholic acid, 475-31-0; glycodeoxycholic acid, 16409-34-0, 360-65-6; taurine, 107-35-7; taurochenodeoxycholic acid, 516-35-8; taurocholic acid, 145-42-6, 59005-70-8, 81-24-3; taurodeoxycholic acid, 1180-95-6, 516-50-7; tauroursodeoxycholic acid, 14605-22-2; ursodeoxycholic acid, 128-13-2, 2898-95-5; Bile Acids and Salts

Objective - The use of the HIV protease inhibitor ritonavir (RTV) is frequently associated with hypertriglyceridemia and lipodystrophy. The aim of our study was to determine the mechanism underlying the observed hypertriglyceridemia. Methods and Results - Feeding female APOE*3-Leiden transgenic mice a Western-type diet supplemented with RTV (35 mg/kg per day) for 2 weeks resulted in a 2-fold increase in fasting plasma triglyceride (TG) levels, which was specific for very low-density lipoprotein (VLDL). RTV did not change the hepatic VLDL-TG production. Instead, RTV did increase the postprandial TG response to an oral fat load (area under the curve, 25.5±12.1 versus 13.8±6.8 mmol/L per hour in controls; P<0.05). Likewise, RTV hampered the plasma clearance of intravenously injected glycerol tri[3H]oleate-labeled VLDL-like emulsion particles (half time, 19.3±10.5 versus 5.0±1.3 minutes in controls; P<0.05) associated with a decrease of 44% in plasma lipoprotein lipase activity. Accordingly, RTV decreased the uptake of TG-derived fatty acids (FAs) into adipose tissue, as well as the uptake of albumin-bound FA. Conclusions - We conclude that RTV causes hypertriglyceridemia via decreased lipoprotein lipase-mediated clearance of VLDL-TG. In addition, RTV specifically impairs the uptake of FA in adipose tissue, which may contribute to the lipodystrophy that is frequently observed in HIV-infected subjects on antiretroviral therapy. © 2005 American Heart Association, Inc. Chemicals / CAS: lipoprotein lipase, 83137-80-8, 9004-02-8; proteinase inhibitor, 37205-61-1; ritonavir, 155213-67-5; triolein, 122-32-7; heparin, 37187-54-5, 8057-48-5, 8065-01-8, 9005-48-5; tritium, 10028-17-8; Anticoagulants; apolipoprotein E3 (Leidein); Apolipoprotein E3; Apolipoproteins E; Cholesterol, VLDL; Emulsions; Fatty Acids; Heparin, 9005-49-6; HIV Protease Inhibitors; Lipoprotein Lipase, EC 3.1.1.34; Ritonavir; Triglycerides; Triolein, 122-32-7; Tritium, 10028-17-8