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Assessment of postprandial triglycerides in clinical practice: Validation in a general population and coronary heart disease patients.
Perez-Martinez P, Alcala-Diaz JF, Kabagambe EK, Garcia-Rios A, Tsai MY, Delgado-Lista J, Kolovou G, Straka RJ, Gomez-Delgado F, Hopkins PN, Marin C, Borecki I, Yubero-Serrano EM, Hixson JE, Camargo A, Province MA, Lopez-Moreno J, Rodriguez-Cantalejo F, Tinahones FJ, Mikhailidis DP, Perez-Jimenez F, Arnett DK, Ordovas JM, Lopez-Miranda J
(2016) J Clin Lipidol 10: 1163-71
MeSH Terms: Adult, Age Factors, Aged, Coronary Artery Disease, Dietary Fats, Female, Humans, Hyperlipidemias, Logistic Models, Male, Middle Aged, Odds Ratio, Postprandial Period, Prevalence, Triglycerides
Show Abstract · Added September 30, 2016
BACKGROUND - Previous studies have suggested that for clinical purposes, subjects with fasting triglycerides (TGs) between 89-180 mg/dl (1-2 mmol/l) would benefit from postprandial TGs testing.
OBJECTIVE - To determine the postprandial TG response in 2 independent studies and validate who should benefit diagnostically from an oral-fat tolerance test (OFTT) in clinical practice.
METHODS - A population of 1002 patients with coronary heart disease (CHD) from the CORDIOPREV clinical trial and 1115 white US subjects from the GOLDN study underwent OFTTs. Subjects were classified into 3 groups according to fasting cut points of TGs to predict the usefulness of OFTT: (1) TG < 89 mg/dl (<1 mmol/l); (2) TG, 89-180 mg/dl (1-2 mmol/l); and (3) TG > 180 mg/dl (>2 mmol/l). Postprandial TG concentration at any point > 220 mg/dl (>2.5 mmol/l) has been pre-established as an undesirable postprandial response.
RESULTS - Of the total, 49% patients with CHD and 42% from the general population showed an undesirable response after the OFTT. The prevalence of undesirable postprandial TG in the CORDIOPREV clinical trial was 12.8, 50.3, and 89.7%, in group 1, 2, and 3, respectively (P < .001) and 11.2, 58.1, and 97.5% in group 1, 2, and 3, respectively (P < .001) in the GOLDN study.
CONCLUSIONS - These two studies validate the predictive values reported in a previous consensus. Moreover, the findings of the CORDIOPREV and GOLDN studies show that an OFTT is useful to identify postprandial hyperlipidemia in subjects with fasting TG between 1-2 mmol/l (89-180 mg/dL), because approximately half of them have hidden postprandial hyperlipidemia, which may influence treatment. An OFTT does not provide additional information regarding postprandial hyperlipidemia in subjects with low TG (<1 mmol/l, <89 mg/dL) or increased TG (>2 mmol/l, >180 mg/dl).
Copyright © 2016 National Lipid Association. Published by Elsevier Inc. All rights reserved.
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15 MeSH Terms
Noninvasive biomagnetic detection of intestinal slow wave dysrhythmias in chronic mesenteric ischemia.
Somarajan S, Muszynski ND, Cheng LK, Bradshaw LA, Naslund TC, Richards WO
(2015) Am J Physiol Gastrointest Liver Physiol 309: G52-8
MeSH Terms: Chronic Disease, Eating, Electrodiagnosis, Electromyography, Gastrointestinal Motility, Humans, Jejunum, Magnetometry, Mesenteric Ischemia, Postprandial Period, Predictive Value of Tests, Time Factors
Show Abstract · Added April 26, 2016
Chronic mesenteric ischemia (CMI) is a challenging clinical problem that is difficult to diagnose noninvasively. Diagnosis early in the disease process would enable life-saving early surgical intervention. Previous studies established that superconducting quantum interference device (SQUID) magnetometers detect the slow wave changes in the magnetoenterogram (MENG) noninvasively following induction of mesenteric ischemia in animal models. The purpose of this study was to assess functional physiological changes in the intestinal slow wave MENG of patients with chronic mesenteric ischemia. Pre- and postoperative studies were conducted on CMI patients using MENG and intraoperative recordings using invasive serosal electromyograms (EMG). Our preoperative MENG recordings showed that patients with CMI exhibited a significant decrease in intestinal slow wave frequency from 8.9 ± 0.3 cpm preprandial to 7.4 ± 0.1 cpm postprandial (P < 0.01) that was not observed in postoperative recordings (9.3 ± 0.2 cpm preprandial and 9.4 ± 0.4 cpm postprandial, P = 0.86). Intraoperative recording detected multiple frequencies from the ischemic portion of jejunum before revascularization, whereas normal serosal intestinal slow wave frequencies were observed after revascularization. The preoperative MENG data also showed signals with multiple frequencies suggestive of uncoupling and intestinal ischemia similar to intraoperative serosal EMG. Our results showed that multichannel MENG can identify intestinal slow wave dysrhythmias in CMI patients.
Copyright © 2015 the American Physiological Society.
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12 MeSH Terms
Apolipoprotein A-V deficiency enhances chylomicron production in lymph fistula mice.
Zhang LS, Xu M, Yang Q, Ryan RO, Howles P, Tso P
(2015) Am J Physiol Gastrointest Liver Physiol 308: G634-42
MeSH Terms: Administration, Oral, Animals, Apolipoprotein A-V, Apolipoproteins, Cholesterol, Chylomicrons, Disease Models, Animal, Duodenum, Fistula, Intestinal Absorption, Lymph, Lymphatic Diseases, Lymphatic System, Male, Mice, Inbred C57BL, Mice, Knockout, Postprandial Period, Time Factors, Triolein, Up-Regulation
Show Abstract · Added August 24, 2015
Apolipoprotein A-V (apoA-V), a liver-synthesized apolipoprotein discovered in 2001, strongly modulates fasting plasma triglycerides (TG). Little is reported on the effect of apoA-V on postprandial plasma TG, an independent predictor for atherosclerosis. Overexpressing apoA-V in mice suppresses postprandial TG, but mechanisms focus on increased lipolysis or clearance of remnant particles. Unknown is whether apoA-V suppresses the absorption of dietary lipids by the gut. This study examines how apoA-V deficiency affects the steady-state absorption and lymphatic transport of dietary lipids in chow-fed mice. Using apoA-V knockout (KO, n = 8) and wild-type (WT, n = 8) lymph fistula mice, we analyzed the uptake and lymphatic transport of lipids during a continuous infusion of an emulsion containing [(3)H]triolein and [(14)C]cholesterol. ApoA-V KO mice showed a twofold increase in (3)H (P < 0.001) and a threefold increase in (14)C (P < 0.001) transport into the lymph compared with WT. The increased lymphatic transport was accompanied by a twofold reduction (P < 0.05) in mucosal (3)H, suggesting that apoA-V KO mice more rapidly secreted [(3)H]TG out of the mucosa into the lymph. ApoA-V KO mice also produced chylomicrons more rapidly than WT (P < 0.05), as measured by the transit time of [(14)C]oleic acid from the intestinal lumen to lymph. Interestingly, apoA-V KO mice produced a steadily increasing number of chylomicron particles over time, as measured by lymphatic apoB output. The data suggest that apoA-V suppresses the production of chylomicrons, playing a previously unknown role in lipid metabolism that may contribute to the postprandial hypertriglyceridemia associated with apoA-V deficiency.
Copyright © 2015 the American Physiological Society.
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20 MeSH Terms
Effect of the glucagon-like peptide-1 receptor agonist lixisenatide on postprandial hepatic glucose metabolism in the conscious dog.
Moore MC, Werner U, Smith MS, Farmer TD, Cherrington AD
(2013) Am J Physiol Endocrinol Metab 305: E1473-82
MeSH Terms: Acetaminophen, Animals, Consciousness, Dogs, Female, Gastric Emptying, Glucagon, Glucagon-Like Peptide-1 Receptor, Glucose, Hypoglycemic Agents, Insulin, Liver, Male, Peptides, Postprandial Period, Receptors, Glucagon
Show Abstract · Added June 2, 2014
The impact of the GLP-1 receptor agonist lixisenatide on postprandial glucose disposition was examined in conscious dogs to identify mechanisms for its improvement of meal tolerance in humans and examine the tissue disposition of meal-derived carbohydrate. Catheterization for measurement of hepatic balance occurred ≈16 days before study. After being fasted overnight, dogs received a subcutaneous injection of 1.5 μg/kg lixisenatide or vehicle (saline, control; n = 6/group). Thirty minutes later, they received an oral meal feeding (93.4 kJ; 19% protein, 71% glucose polymers, and 10% lipid). Acetaminophen was included in the meal in four control and five lixisenatide dogs for assessment of gastric emptying. Observations continued for 510 min; absorption was incomplete in lixisenatide at that point. The plasma acetaminophen area under the curve (AUC) in lixisenatide was 65% of that in control (P < 0.05). Absorption of the meal began within 15 min in control but was delayed until ≈30-45 min in lixisenatide. Lixisenatide reduced (P < 0.05) the postprandial arterial glucose AUC ≈54% and insulin AUC ≈44%. Net hepatic glucose uptake did not differ significantly between groups. Nonhepatic glucose uptake tended to be reduced by lixisenatide (6,151 ± 4,321 and 10,541 ± 1,854 μmol·kg(-1)·510 min(-1) in lixisenatide and control, respectively; P = 0.09), but adjusted (for glucose and insulin concentrations) values did not differ (18.9 ± 3.8 and 19.6 ± 7.9 l·kg(-1)·pmol(-1)·l(-1), lixisenatide and control, respectively; P = 0.94). Thus, lixisenatide delays gastric emptying, allowing more efficient disposal of the carbohydrate in the feeding without increasing liver glucose disposal. Lixisenatide could prove to be a valuable adjunct in treatment of postprandial hyperglycemia in impaired glucose tolerance or type 2 diabetes.
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16 MeSH Terms
The association between LRP-1 variants and chylomicron uptake after a high fat meal.
Frazier-Wood AC, Kabagambe EK, Wojczynski MK, Borecki IB, Tiwari HK, Smith CE, Ordovas JM, Arnett DK
(2013) Nutr Metab Cardiovasc Dis 23: 1154-8
MeSH Terms: Adult, Alleles, Chylomicrons, Diet, High-Fat, Dietary Fats, Female, Genetic Association Studies, Humans, Intestinal Absorption, Linkage Disequilibrium, Low Density Lipoprotein Receptor-Related Protein-1, Magnetic Resonance Spectroscopy, Male, Meals, Middle Aged, Minnesota, Oligonucleotide Array Sequence Analysis, Polymorphism, Single Nucleotide, Postprandial Period, Utah
Show Abstract · Added May 19, 2014
BACKGROUND AND AIMS - In vitro studies suggest that low density lipoprotein receptor-related protein 1 (LRP1) plays a role in the secondary uptake of chylomicrons. In addition, in vivo studies using LRP-1 knockout mice show these animals exhibit delayed chylomicron clearance. Whether this is true in humans is unknown. We aimed to determine whether genetic variants in LRP-1 are associated with postprandial chylomicron uptake in humans given an oral fat challenge.
METHODS AND RESULTS - As many as 817 men and women (mean age +/- standard deviation = 48.4 +/- 16.4 years) forming the study population for the Genetics of Lipid Lowering Drugs Network (GOLDN) study ingested an oral fat load of 700 kilocalories per m² of body surface area at 83% fat, after an 8-h fast. Chylomicrons were measured by nuclear resonance spectroscopy (NMR) at fasting, and 3.5 and 6 h after the meal. 26 Single nucleotide polymorphisms (SNPs) in the LRP-1 gene were genotyped on the Affymetrix 6.0 array. Chylomicrons were, as expected, zero at fasting. Mixed linear models adjusted for age, sex, study site and pedigree tested for associations between LRP-1 SNPs and changes in chylomicron concentrations 3.5-6 h. A gene-based test across all 26 SNPs was conducted which corrected for the linkage disequilibrium (LD) between SNPs. 11 LRP-1 SNPs were significantly associated with the change in chylomicron concentration correction for multiple testing (Q < 0.05). The subsequent gene-based test, was also significant (P = 0.01).
CONCLUSION - These results require replication but strongly indicate the role of LRP1 in postprandial lipoprotein uptake and/or clearance.
Copyright © 2013 Elsevier B.V. All rights reserved.
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20 MeSH Terms
Energy expenditure in obese children with pseudohypoparathyroidism type 1a.
Shoemaker AH, Lomenick JP, Saville BR, Wang W, Buchowski MS, Cone RD
(2013) Int J Obes (Lond) 37: 1147-53
MeSH Terms: Absorptiometry, Photon, Adolescent, Age of Onset, Basal Metabolism, Blood Glucose, Body Composition, Calorimetry, Indirect, Child, Disease Susceptibility, Energy Metabolism, Female, Glycated Hemoglobin A, Humans, Insulin, Pediatric Obesity, Phenotype, Polymorphism, Single Nucleotide, Postprandial Period, Pseudohypoparathyroidism, Rest, Thermogenesis, United States, Weight Gain
Show Abstract · Added December 10, 2013
CONTEXT - Patients with pseudohypoparathyroidism type 1a (PHP-1a) develop early-onset obesity. The abnormality in energy expenditure and/or energy intake responsible for this weight gain is unknown.
OBJECTIVE - The aim of this study was to evaluate energy expenditure in children with PHP-1a compared with obese controls.
PATIENTS - We studied 6 obese females with PHP-1a and 17 obese female controls. Patients were recruited from a single academic center.
MEASUREMENTS - Resting energy expenditure (REE) and thermogenic effect of a high fat meal were measured using whole room indirect calorimetry. Body composition was assessed using whole body dual energy x-ray absorptiometry. Fasting glucose, insulin, and hemoglobin A1C were measured.
RESULTS - Children with PHP-1a had decreased REE compared with obese controls (P<0.01). After adjustment for fat-free mass, the PHP-1a group's REE was 346.4 kcals day(-1) less than obese controls (95% CI (-585.5--106.9), P<0.01). The thermogenic effect of food (TEF), expressed as percent increase in postprandial energy expenditure over REE, was lower in PHP-1a patients than obese controls, but did not reach statistical significance (absolute reduction of 5.9%, 95% CI (-12.2-0.3%), P=0.06).
CONCLUSIONS - Our data indicate that children with PHP-1a have decreased REE compared with the obese controls, and that may contribute to the development of obesity in these children. These patients may also have abnormal diet-induced thermogenesis in response to a high-fat meal. Understanding the causes of obesity in PHP-1a may allow for targeted nutritional or pharmacologic treatments in the future.
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23 MeSH Terms
Hepatic glucose metabolism in late pregnancy: normal versus high-fat and -fructose diet.
Coate KC, Smith MS, Shiota M, Irimia JM, Roach PJ, Farmer B, Williams PE, Moore MC
(2013) Diabetes 62: 753-61
MeSH Terms: Animals, Diabetes, Gestational, Diet, High-Fat, Disease Models, Animal, Dogs, Down-Regulation, Female, Fructose, Glucokinase, Glucose, Glucose Intolerance, Glycogen Phosphorylase, Liver Form, Glycogen Synthase, Hyperglycemia, Insulin Resistance, Liver, Liver Glycogen, Maternal Nutritional Physiological Phenomena, Postprandial Period, Pregnancy
Show Abstract · Added June 2, 2014
Net hepatic glucose uptake (NHGU) is an important contributor to postprandial glycemic control. We hypothesized that NHGU is reduced during normal pregnancy and in a pregnant diet-induced model of impaired glucose intolerance/gestational diabetes mellitus (IGT/GDM). Dogs (n = 7 per group) that were nonpregnant (N), normal pregnant (P), or pregnant with IGT/GDM (pregnant dogs fed a high-fat and -fructose diet [P-HFF]) underwent a hyperinsulinemic-hyperglycemic clamp with intraportal glucose infusion. Clamp period insulin, glucagon, and glucose concentrations and hepatic glucose loads did not differ among groups. The N dogs reached near-maximal NHGU rates within 30 min; mean ± SEM NHGU was 105 ± 9 µmol·100 g liver⁻¹·min⁻¹. The P and P-HFF dogs reached maximal NHGU in 90-120 min; their NHGU was blunted (68 ± 9 and 16 ± 17 µmol·100 g liver⁻¹·min⁻¹, respectively). Hepatic glycogen synthesis was reduced 20% in P versus N and 40% in P-HFF versus P dogs. This was associated with a reduction (>70%) in glycogen synthase activity in P-HFF versus P and increased glycogen phosphorylase (GP) activity in both P (1.7-fold greater than N) and P-HFF (1.8-fold greater than P) dogs. Thus, NHGU under conditions mimicking the postprandial state is delayed and suppressed in normal pregnancy, with concomitant reduction in glycogen storage. NHGU is further blunted in IGT/GDM. This likely contributes to postprandial hyperglycemia during pregnancy, with potential adverse outcomes for the fetus and mother.
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20 MeSH Terms
Portal glucose delivery stimulates muscle but not liver protein metabolism.
Kraft G, Coate KC, Dardevet D, Farmer B, Donahue EP, Williams PE, Cherrington AD, Moore MC
(2012) Am J Physiol Endocrinol Metab 303: E1202-11
MeSH Terms: Amino Acid Transport System ASC, Amino Acids, Animals, Dogs, Enteral Nutrition, Glucose, Infusions, Intravenous, Large Neutral Amino Acid-Transporter 1, Liver, Male, Muscle, Skeletal, Phosphorylation, Portal Vein, Postprandial Period, Protein Biosynthesis, Ribosomal Protein S6 Kinases, 70-kDa
Show Abstract · Added December 5, 2013
Portal vein glucose delivery (the portal glucose signal) stimulates glucose uptake and glycogen storage by the liver, whereas portal amino acid (AA) delivery (the portal AA signal) induces an increase in protein synthesis by the liver. During a meal, both signals coexist and may interact. In this study, we compared the protein synthesis rates in the liver and muscle in response to portal or peripheral glucose infusion during intraportal infusion of a complete AA mixture. Dogs were surgically prepared with hepatic sampling catheters and flow probes. After a 42-h fast, they underwent a 3-h hyperinsulinemic (4× basal) hyperglucagonemic (3× basal) hyperglycemic (≈160 mg/dl) hyperaminoacidemic (hepatic load 1.5× basal; delivered intraportally) clamp (postprandial conditions). Glucose was infused either via a peripheral (PeG; n = 7) or the portal vein (PoG; n = 8). Protein synthesis was assessed with a primed, continuous [(14)C]leucine infusion. Net hepatic glucose uptake was stimulated by portal glucose infusion (+1 mg·kg(-1)·min(-1), P < 0.05) as expected, but hepatic fractional AA extraction and hepatic protein synthesis did not differ between groups. There was a lower arterial AA concentration in the PoG group (-19%, P < 0.05) and a significant stimulation (+30%) of muscle protein synthesis associated with increased expression of LAT1 and ASCT2 AA transporters and p70S6 phosphorylation. Concomitant portal glucose and AA delivery enhances skeletal muscle protein synthesis compared with peripheral glucose and portal AA delivery. These data suggest that enteral nutrition support may have an advantage over parenteral nutrition in stimulating muscle protein synthesis.
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16 MeSH Terms
Regulation of hepatic glucose uptake and storage in vivo.
Moore MC, Coate KC, Winnick JJ, An Z, Cherrington AD
(2012) Adv Nutr 3: 286-94
MeSH Terms: AMP-Activated Protein Kinases, Animals, Biological Transport, Blood Glucose, Fructose, Glucose, Glycogen, Humans, Insulin, Liver, Models, Animal, Portal Vein, Postprandial Period
Show Abstract · Added December 5, 2013
In the postprandial state, the liver takes up and stores glucose to minimize the fluctuation of glycemia. Elevated insulin concentrations, an increase in the load of glucose reaching the liver, and the oral/enteral/portal vein route of glucose delivery (compared with the peripheral intravenous route) are factors that increase the rate of net hepatic glucose uptake (NHGU). The entry of glucose into the portal vein stimulates a portal glucose signal that not only enhances NHGU but concomitantly reduces muscle glucose uptake to ensure appropriate partitioning of a glucose load. This coordinated regulation of glucose uptake is likely neurally mediated, at least in part, because it is not observed after total hepatic denervation. Moreover, there is evidence that both the sympathetic and the nitrergic innervation of the liver exert a tonic repression of NHGU that is relieved under feeding conditions. Further, the energy sensor 5'AMP-activated protein kinase appears to be involved in regulation of NHGU and glycogen storage. Consumption of a high-fat and high-fructose diet impairs NHGU and glycogen storage in association with a reduction in glucokinase protein and activity. An understanding of the impact of nutrients themselves and the route of nutrient delivery on liver carbohydrate metabolism is fundamental to the development of therapies for impaired postprandial glucoregulation.
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13 MeSH Terms
High-fat meal effect on LDL, HDL, and VLDL particle size and number in the Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN): an interventional study.
Wojczynski MK, Glasser SP, Oberman A, Kabagambe EK, Hopkins PN, Tsai MY, Straka RJ, Ordovas JM, Arnett DK
(2011) Lipids Health Dis 10: 181
MeSH Terms: Adult, Aged, Cardiovascular Diseases, Cholesterol, VLDL, Cohort Studies, Dietary Fats, Family Health, Female, Humans, Hypertriglyceridemia, Lipoproteins, HDL, Lipoproteins, IDL, Lipoproteins, LDL, Lipoproteins, VLDL, Magnetic Resonance Spectroscopy, Male, Middle Aged, Particle Size, Postprandial Period, Risk Factors, Sex Characteristics, Triglycerides, United States
Show Abstract · Added April 23, 2015
BACKGROUND - Postprandial lipemia (PPL) is likely a risk factor for cardiovascular disease but these changes have not been well described and characterized in a large cohort. We assessed acute changes in the size and concentration of total and subclasses of LDL, HDL, and VLDL particles in response to a high-fat meal. Participants (n = 1048) from the Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) Study who ingested a high-fat meal were included in this analysis. Lipids were measured at 0 hr (fasting), 3.5 hr, and 6 hr after a standardized fat meal. Particle size distributions were determined using nuclear magnetic resonance spectroscopy. Analyses were stratified by baseline triglycerides (normal vs. elevated) and gender. The effect of PPL on changes in lipoprotein subclasses was assessed using repeated measures ANOVA.
RESULTS - Postprandially, LDL-C, HDL-C, VLDL-C, and triglycerides increased regardless of baseline triglyceride status, with the largest increases in VLDL-C and TG; however, those with elevated triglycerides demonstrated larger magnitude of response. Total LDL particle number decreased over the 6-hour time interval, mostly from a decrease in the number of small LDL particles. Similarly, total VLDL particle number decreased due to reductions in medium and small VLDL particles. Large VLDL particles and chylomicrons demonstrated the largest increase in concentration. HDL particles demonstrated minimal overall changes in total particle number.
CONCLUSIONS - We have characterized the changes in LDL and VLDL particle number, and their subclass patterns following a high-fat meal.
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23 MeSH Terms