Search results for "Apolipoprotein B-48"

showing 5 items of 5 documents

Characterization of a mutant form of human apolipoprotein B (Thr26_Tyr27del) associated with familial hypobetalipoproteinemia

2016

We have previously identified a deletion mutant of human apoB [apoB (Thr26_Tyr27del)] in a subject with primary hypobetalipoproteinemia. The present study determined the effect of Thr26_Tyr27del mutation on apoB secretion using transfected McA-RH7777 cells. Transient or stable transfection of apoB-48 containing the Thr26_Tyr27del mutation showed drastically reduced secretion of the mutant as compared to wild-type apoB-48. No lipoproteins containing the mutant apoB-48 were secreted into the medium. Incubation of transfected cells in a lipid-rich medium in the presence of cycloheximide showed rapid turnover of cell-associated mutant apoB-48 as compared to that of wild-type apoB-48. Immunofluo…

0301 basic medicineSettore MED/09 - Medicina InternaTime FactorsApolipoprotein B-48 secretionApolipoprotein BMutantDNA Mutational AnalysisApolipoprotein B mutation Apolipoprotein B-48 secretion Hypobetalipoproteinemia Proteasomal degradation030204 cardiovascular system & hematologymedicine.disease_causeEndoplasmic ReticulumHypobetalipoproteinemiaschemistry.chemical_compound0302 clinical medicineProteasomal degradationProteolysiSequence DeletionMutationbiologyMedicine (all)TransfectionProteasome InhibitorPhenotypeBiochemistryApolipoprotein B-100lipids (amino acids peptides and proteins)Proteasome InhibitorsHumanHeterozygoteProteasome Endopeptidase ComplexTime FactorCycloheximideTransfectiondigestive systemCell LineDNA Mutational Analysi03 medical and health sciencesmedicineHumansSecretionGenetic Predisposition to DiseaseMolecular BiologyEndoplasmic reticulumnutritional and metabolic diseasesCell Biologymedicine.diseaseMolecular biology030104 developmental biologychemistryProteolysisbiology.proteinHypobetalipoproteinemiaApolipoprotein B mutationApolipoprotein B-48Hypobetalipoproteinemia
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Normal intestinal dietary fat and cholesterol absorption, intestinal apolipoprotein B (ApoB) mRNA levels, and ApoB-48 synthesis in a hypobetalipoprot…

1997

Abstract The purpose of this study was to characterize intestinal apolipoprotein B (apoB) metabolism in subjects with familial hypobetalipoproteinemia (FHBL), where segregation analysis supports linkage to the apoB gene but no apoB truncations are present. We investigated cholesterol and fat absorption, intestinal apoB mRNA synthesis and editing, as well as apoB-48 synthesis. Plasma triglycerides (TG) and retinyl palmitate in the chylomicron fractions were analyzed after 12 hours of fasting and then repeatedly for 14 hours after ingestion of a vitamin A—containing high-fat meal. Cholesterol absorption was assessed using a dual stable-isotope method. Mean peak times and concentrations and ar…

AdultMaleVitaminmedicine.medical_specialtyApolipoprotein BEndocrinology Diabetes and Metabolismdigestive systemAbsorptionCholesterol DietaryHypobetalipoproteinemiasEatingchemistry.chemical_compoundEndocrinologyInternal medicineRetinyl palmitatemedicineHumansRNA MessengerIntestinal MucosaHypoalphalipoproteinemiaAgedApolipoproteins BMethioninebiologyCholesterolnutritional and metabolic diseasesNuclease protection assayMiddle Agedmedicine.diseaseDietary FatsLipidsEndocrinologychemistrybiology.proteinFemalelipids (amino acids peptides and proteins)RNA EditingApolipoprotein B-48ChylomicronMetabolism
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Luminal Lipid Regulates CD36 Levels and Downstream Signaling to Stimulate Chylomicron Synthesis

2011

International audience; The membrane glycoprotein CD36 binds nanomolar concentrations of long chain fatty acids (LCFA) and is highly expressed on the luminal surface of enterocytes. CD36 deficiency reduces chylomicron production through unknown mechanisms. In this report, we provide novel insights into some of the underlying mechanisms. Our in vivo data demonstrate that CD36 gene deletion in mice does not affect LCFA uptake and subsequent esterification into triglycerides by the intestinal mucosa exposed to the micellar LCFA concentrations prevailing in the intestine. In rodents, the CD36 protein disappears early from the luminal side of intestinal villi during the postprandial period, but …

CD36 AntigensMaleMTPCD36[SDV]Life Sciences [q-bio]BiochemistryMicrosomal triglyceride transfer proteinMice0302 clinical medicineIntestinal mucosaCricetinaeChylomicronsLipoproteinHypertriglyceridemiaMice Knockout0303 health sciencesMitogen-Activated Protein Kinase 3biologyPostprandial PeriodLipid-binding ProteinIntestineApoB48ERKmedicine.anatomical_structurePostprandialBiochemistrylipids (amino acids peptides and proteins)Apolipoprotein B-48MAP Kinase Signaling SystemEnterocyteCHO CellsChylomicron03 medical and health sciencesCricetulusparasitic diseasesmedicineAnimalsRats WistarMolecular Biology030304 developmental biologyUbiquitinationLipid absorptionLipid metabolismCell BiologyLipid MetabolismRatsEnterocytesMetabolismbiology.proteinApolipoprotein B-48CD36[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryChylomicron
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Liraglutide Reduces Postprandial Hyperlipidemia by Increasing ApoB48 (Apolipoprotein B48) Catabolism and by Reducing ApoB48 Production in Patients Wi…

2018

Objective— Treatment with liraglutide, a GLP-1 (glucagon-like peptide-1) agonist, has been shown to reduce postprandial lipidemia, an important feature of diabetic dyslipidemia. However, the underlying mechanisms for this effect remain unknown. This prompted us to study the effect of liraglutide on the metabolism of ApoB48 (apolipoprotein B48). Approach and Results— We performed an in vivo kinetic study with stable isotopes (D 8 -valine) in the fed state in 10 patients with type 2 diabetes mellitus before treatment and 6 months after the initiation of treatment with liraglutide (1.2 mg/d). We also evaluated, in mice, the effect of a 1-week liraglutide treatment on postload triglycerides an…

MaleApolipoprotein B-48Agonistmedicine.medical_specialtymedicine.drug_classhyperlipidemiasGene Expression030209 endocrinology & metabolism030204 cardiovascular system & hematologypatients03 medical and health sciences0302 clinical medicineInternal medicineDiabetes mellitusChylomicronsHyperlipidemiaAnimalsHumansMedicineDiacylglycerol O-AcyltransferaseProspective StudiesTriglycerides[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismMice Inbred BALB Cliraglutidebusiness.industryLiraglutideCatabolismType 2 Diabetes Mellitus[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismPostprandial Periodmedicine.diseaseLipoprotein LipaseJejunumEndocrinologyPostprandialAdipose TissueDiabetes Mellitus Type 2kineticsdiabetes mellitusFemaleApolipoprotein B-48Carrier ProteinsCardiology and Cardiovascular Medicinebusinessmedicine.drug
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Induction of body weight loss through RNAi-knockdown of APOBEC1 gene expression in transgenic rabbits

2014

In the search of new strategies to fight against obesity, we targeted a gene pathway involved in energy uptake. We have thus investigated the APOB mRNA editing protein (APOBEC1) gene pathway that is involved in fat absorption in the intestine. The APOB gene encodes two proteins, APOB100 and APOB48, via the editing of a single nucleotide in the APOB mRNA by the APOBEC1 enzyme. The APOB48 protein is mandatory for the synthesis of chylomicrons by intestinal cells to transport dietary lipids and cholesterol. We produced transgenic rabbits expressing permanently and ubiquitously a small hairpin RNA targeting the rabbit APOBEC1 mRNA. These rabbits exhibited a moderately but significantly reduced …

perte de poidsobesityApolipoprotein BAgricultural BiotechnologyGene Expressionlcsh:MedicinetransgenesisSmall hairpin RNAAnimals Genetically Modified0302 clinical medicinesirnaRNA interferenceGene expressionGene Knockdown TechniquesBiologie de la reproductionMedicine and Health SciencesTransgenesIntestinal MucosaRNA Small Interferinglcsh:Science[SDV.BDD]Life Sciences [q-bio]/Development Biology2. Zero hunger0303 health sciencesGene knockdownReproductive BiologyMultidisciplinarybiologyGenetically Modified OrganismsBiologie du développementapobec1; obesity; editing apob; apob100; apob48; chylomicron; intestine; rabbit; sirna; transgenesis; knockdownchylomicronknockdownAgricultureInherited Metabolic DisordersDevelopment BiologyobésitéCholesterolPhenotypeTransgenic Engineering[ SDV.BDLR ] Life Sciences [q-bio]/Reproductive BiologyLiverapobapob48Gene Knockdown Techniquesanimal transgéniqueRNA Interferencelipids (amino acids peptides and proteins)RabbitsGenetic EngineeringResearch ArticleBiotechnologyexpression géniqueTransgeneAPOBEC-1 DeaminaseMolecular Sequence DatarabbitDiet High-Fat03 medical and health sciencesintestinCytidine DeaminaseWeight Loss[SDV.BDD] Life Sciences [q-bio]/Development BiologyAnimalsHumanslapinRNA Messenger[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyintestineTriglycerides[SDV.BDLR] Life Sciences [q-bio]/Reproductive Biology030304 developmental biologyapobec1Base SequenceGenetically Modified AnimalsAPOBEC1editinglcsh:RBiology and Life Sciences[SDV.BDLR]Life Sciences [q-bio]/Reproductive BiologyMolecular biologyapob100DyslipidemiaMetabolic Disordersbiology.proteinlcsh:QRNA EditingApolipoprotein B-48030217 neurology & neurosurgery
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