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1Latest Papers from Table of Contents or Articles in PressP. Zanoni ; S. A. Khetarpal ; D. B. Larach ; W. F. Hancock-Cerutti ; J. S. Millar ; M. Cuchel ; S. DerOhannessian ; A. Kontush ; P. Surendran ; D. Saleheen ; S. Trompet ; J. W. Jukema ; A. De Craen ; P. Deloukas ; N. Sattar ; I. Ford ; C. Packard ; A. Majumder ; D. S. Alam ; E. Di Angelantonio ; G. Abecasis ; R. Chowdhury ; J. Erdmann ; B. G. Nordestgaard ; S. F. Nielsen ; A. Tybjaerg-Hansen ; R. F. Schmidt ; K. Kuulasmaa ; D. J. Liu ; M. Perola ; S. Blankenberg ; V. Salomaa ; S. Mannisto ; P. Amouyel ; D. Arveiler ; J. Ferrieres ; M. Muller-Nurasyid ; M. Ferrario ; F. Kee ; C. J. Willer ; N. Samani ; H. Schunkert ; A. S. Butterworth ; J. M. Howson ; G. M. Peloso ; N. O. Stitziel ; J. Danesh ; S. Kathiresan ; D. J. Rader
American Association for the Advancement of Science (AAAS)
Published 2016Staff ViewPublication Date: 2016-03-12Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: Aged ; Amino Acid Substitution ; Animals ; Cholesterol, HDL/*blood ; Coronary Disease/*blood/*genetics ; DNA Mutational Analysis ; Female ; Genetic Variation ; Heterozygote ; Homozygote ; Humans ; Leucine/genetics ; Male ; Mice ; Middle Aged ; Proline/genetics ; Protein Processing, Post-Translational ; Risk ; Scavenger Receptors, Class B/*genetics/metabolismPublished by: -
2Articles: DFG German National LicensesStaff View
ISSN: 1432-0428Keywords: Keywords Atherosclerosis ; C-peptide ; diabetes mellitus ; hepatic lipase ; hyperinsulinaemia ; insulin ; insulin antibodies ; intermediate density lipoprotein ; lipoprotein lipase ; postprandial triglycerides.Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary To examine the hypothesis that hyperinsulinaemia promotes atherosclerosis, cholesterol-fed rabbits were injected subcutaneously with 6 IU of human insulin (n = 16) or placebo (n = 20) daily for 24 weeks; injection of insulin resulted in hyperinsulinaemia for up to 16 h after injection. Compared to placebo rabbits, insulin-treated rabbits had higher levels of insulin antibodies in plasma, similar levels of intermediate density, low density and high density lipoprotein cholesterol and similar activities of hepatic and lipoprotein lipase in post-heparin plasma, but lower levels of plasma C-peptide, blood glucose, postprandial plasma triglycerides, plasma cholesterol and very low density lipoprotein cholesterol. On univariate analysis, with and without adjustment for differences in plasma cholesterol levels between the two groups, there were no significant differences in extent or severity of atherosclerosis between insulin and placebo rabbits. Furthermore, after combining the results from all the rabbits to examine plasma insulin levels and the other variables mentioned above as predictors of atherosclerosis severity, plasma insulin level was not a predictor, on univariate or multiple linear regression analysis; the first ranked independent predictors were postprandial intermediate density lipoprotein cholesterol in the arch, and postprandial plasma triglyceride in both the thoracic and abdominal aorta. These results suggest that exogenous hyperinsulinaemia does not promote atherogenesis in cholesterol-fed rabbits, but that postprandial levels of intermediate density lipoprotein cholesterol or plasma triglycerides may be involved in atherogenesis. [Diabetologia (1997) 40: 512–520]Type of Medium: Electronic ResourceURL: -
3Articles: DFG German National LicensesStaff View
ISSN: 1573-7284Keywords: Lipoprotein lipase deficiency ; Familial combined hyperlipidemia ; Dysbetalipoproteinemia ; The St. Thomas' Hospital rabbit strain ; Atherosclerosis ; Lipoprotein permeabilitySource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract In humans with the lipoprotein lipase deficiency disorder large amounts of chylomicrons and large very low-density lipoprotein (VLDL) accumulate in plasma. In spite of this, atherosclerosis does not seem to develop at an accelerated rate, suggesting that these lipoproteins do not promote atherogenesis. In humans with dysbetalipoproteinemia remnant lipoproteins (intermediate density lipoprotein (IDL) plus B-VLDL) accumulate in plasma and these particles may therefore be the factor causing accelerated atherosclerosis in this disorder. Epidemiological studies in humans suggest that IDL or remnant lipoproteins are predictors of the severity or progression of atherosclerosis. Similar studies in the St. Thomas' Hospital rabbit strain, an animal model with genetically elevated plasma levels of VLDL, IDL and low-density lipoprotein (LDL), showed that IDL or remnant lipoproteins were better predictors of the extent of atherosclerosis than were LDL or VLDL. Studies of lipoprotein/arterial wall interactions have demonstrated that the larger the lipoprotein particle, the lower the influx into intima. Very large VLDL and chylomicrons do not seem to enter intima. Although high-density lipoprotein (HDL) enters intima faster than other lipoproteins, the small HDL particles seem to penetrate the entire arterial wall and leave via lymphatics and vasa vasorum in the outer media and adventitia. In contrast, LDL, and possibly also IDL and smaller VLDL, may only leave the intima via the lumen of the artery. In conclusion, a substantial body of evidence suggests that remnant lipoproteins (IDL and smaller VLDL) share with LDL the potential for promoting atherosclerosis, whereas very large VLDL and chylomicrons do not seem to have this effect.Type of Medium: Electronic ResourceURL: