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Marja-Riitta Taskinen declares associations with the following companies: Kowa, Novartis, Solvay, Merck Sharpe & Dohme. ...doi:10.1016/j.atherosclerosissup.2012.06.001 pmid:22818818 fatcat:hebqmm6ap5euzd75wzangkdxta
Elevations in plasma triglyceride are the result of overproduction and impaired clearance of triglyceride-rich lipoproteins-very low-density lipoproteins (VLDL) and chylomicrons. Hypertriglyceridemia is characterized by an accumulation in the circulation of large VLDL-VLDL1-and its lipolytic products, and throughout the VLDL-LDL delipidation cascade perturbations occur that give rise to increased concentrations of remnant lipoproteins and small, dense low-density lipoprotein (LDL). The elevateddoi:10.3389/fendo.2020.00252 pmid:32477261 pmcid:PMC7239992 fatcat:6wqggma23vg4nksvju2siz6dz4
more »... risk of atherosclerotic cardiovascular disease in hypertriglyceridemia is believed to result from the exposure of the artery wall to these aberrant lipoprotein species. Key regulators of the metabolism of triglyceride-rich lipoproteins have been identified and a number of these are targets for pharmacological intervention. However, a clear picture is yet to emerge as to how to relate triglyceride lowering to reduced risk of atherosclerosis.
Taskinen, J. Bor en / Atherosclerosis 239 (2015) 483e495 ...doi:10.1016/j.atherosclerosis.2015.01.039 pmid:25706066 fatcat:3un6ogsuubgo5ishrxbiaz56vi
Nonalcoholic fatty liver disease (NAFLD) is a chronic condition characterized by fat accumulation combined with low-grade inflammation in the liver. A large body of clinical and experimental data shows that increased flux of free fatty acids from increased visceral adipose tissue and de novo lipogenesis can lead to NAFLD and insulin resistance. Thus, individuals with obesity, insulin resistance, and dyslipidaemia are at the greatest risk of developing NAFLD. Conversely, NAFLD is a phenotype ofdoi:10.1111/obr.12820 pmid:30589487 fatcat:4jliyadljfcghdw3qis5ummuc4
more »... ardiometabolic syndrome. Notably, researchers have discovered a close association between NAFLD and impaired glucose metabolism and focused on the role of NAFLD in the development of type 2 diabetes. Moreover, recent studies provide substantial evidence for an association between NAFLD and atherosclerosis and cardiometabolic disorders. Even if NAFLD can progress into severe liver disorders including nonalcoholic steatohepatitis (NASH) and cirrhosis, the majority of subjects with NAFLD die from cardiovascular disease eventually. In this review, we propose a potential pathological link between NAFLD/NASH and cardiometabolic syndrome. The potential factors that can play a pivotal role in this link, such as inflammation, insulin resistance, alteration in lipid metabolism, oxidative stress, genetic predisposition, and gut microbiota are discussed.
1104 ROVAMO ET AL. on experimental hypotrophy in the rat. 111. Plasma insulin and glucagon. Biol Neonate 29362 29. Angervall L. Karlsson K, Martinsson A 1981 Effects on rat fetuses of intrauterine injections of insulin. Diabetologia 20:558 30. Susa JB. McCormick KL. Widness JA, Singer DB, Oh W, Adamsons K, Schwartz R 1979 Chronic hyperinsulinaemia in the fetal rhesus monkey. Effects on fetal growth and composition diabetes. Diabetes 28:1058 31. Hill DJ. Milner RDG 1980 Increased somatomedin anddoi:10.1203/00006450-198411000-00010 pmid:6393024 fatcat:4ckd4lsrdvhvfbfgcdllezqpuq
more »... cartilage metabolic activity in rabbit fetuses injected with insulin in utero. Diabetologia 19:143 32. Spencer GSG. Hill DJ. Garsson GJ, McDonald AA, Colenbrander B 1983 Somatomedin activity and growth hormone levels in body fluids of the fetal pig: effect of chronic hyperinsulinaemia. J Endocrinol 96:107 33. Daughaday WH. Philips LS. Mueller MC 1976 The effects of insulin and growth hormone on the release of somatomedin by the isolated rat liver. Endocrinology 98: 12 14 34. Binoux M. Lassarde C. Hardovin N 1982 Somatomedin production by rat liver in organ culture. 111. Studies on the release of insulin-like growth factor and its carrier protein measured by radioligand assays. Effects of growth hormone, insulin and cortisol. Acta Endocrinol 99:422 35. Ktorza A. Nurjhan N. Girard JR. Picon L 1983 Hyperglycaemia induced by glucose infusion in the unrestrained pregnant rat: effect on body weight and lipid synthesis in post-mature fetuses. Diabetologia 24: 128 36. Heinze E, Nguyan Thi C, Vetter U. Fussganger RD 1982 Interrelationship of insulin and somatomedin activity in fetal rats. Biol Neonate 41:240 37. De Prins FA. Van Assche FA. Milner RDG 1983 C-peptide levels in amniotic fluid in experimental fetal growth retardation. Biol Neonate 43: 18 1 003 1-3998/84/18 1 1 -1 104$02.00/0 PEDIATRIC RESEARCH
Taskinen. Determinants of low HDL levels in familial combined hyperlipidemia. J. Lipid Res. 2003. 44: 1536-1544. ...doi:10.1194/jlr.m300069-jlr200 pmid:12777471 fatcat:uce5aktwtvbutnnifvsj2zdtga
We have previously shown that lipoprotein lipase (LPL) activity of tissues is an important determinant not only of plasma VLDL levels but also of HDL-cholesterol. Studies were designed to investigate whether the serum lipoprotein alterations in uncontrolled insulin-deficient diabetes can be accounted for by changes in LPL activity of tissues. The heparin-releasable LPL activity was determined from biopsy samples of adipose tissue and skeletal muscle in 16 patients with newly detected untreateddoi:10.1007/bf01236268 pmid:231535 fatcat:6vpccuir7rgflienohge6hajsi
more »... nsulin-deficient diabetes and in 16 age-, sex-and body weight-matched healthy control subjects. Repeat assays were carried out after the patients had been on insulin treatment for an average of two weeks and when the diabetes was well controlled. When untreated the patients had increased concentrations of triglycerides and cholesterol in whole serum and in VLDL and LDL while the HDL cholesterol level was lower than that of controls (p < 0.01). The cholesterol/triglyceride ratio in each of the three lipoproteins was similar in patients and controls. While untreated the diabetic patients had significantly reduced mean LPL activity both in adipose tissue (average 34% of control mean, p < 0.001) and in skeletal muscle (average 45% of control mean, p < 0.05). In the whole group HDL-cholesterol was positively correlated with adipose tissue LPL activity (r = + 0.58, p < 0.001) while log serum total triglyceride and log VLDL-triglyceride showed significant negative correlations with LPL activity of both adipose tissue and skeletal muscle. After initiation of insulin treatment the LPL activity increased significantly (p < 0.01) in both tissues but was still subnormal after 2 weeks. At the same time the VLDL and LDL concentrations had returned to normal while the ItDL-cholesterol remained low. The results suggest that the increase of VLDL and LDL triglyceride and the decrease of HDL-cholesterol present in uncontrolled insulin-deficient diabetes are, at least partly, accounted for by decreased LPL activity of tissues. The restoration of tissue LPL and of serum HDL-eholesterol by insulin are relatively slow processes. The results are consistent with the hypothesis that HDL-cholesterol concentration is dependent on the efficiency of removal of triglyceride-rich lipoproteins from the circulation.
Context Mathematical models may help the analysis of biological systems by providing estimates of otherwise un-measurable quantities such as concentrations and fluxes. The variability in such systems makes it difficult to translate individual characteristics to group behavior. Mixed effects models offer a tool to simultaneously assess individual and population behavior from experimental data. Lipoproteins and plasma lipids are key mediators for cardiovascular disease in metabolic disorders suchdoi:10.1371/journal.pone.0138538 pmid:26422201 pmcid:PMC4589417 fatcat:ltidr5xe6fey3feh7ojr5f27mq
more »... as diabetes mellitus type 2. By the use of mathematical models and tracer experiments fluxes and production rates of lipoproteins may be estimated. Results We developed a mixed effects model to study lipoprotein kinetics in a data set of 15 healthy individuals and 15 patients with type 2 diabetes. We compare the traditional and the mixed effects approach in terms of group estimates at various sample and data set sizes. Conclusion We conclude that the mixed effects approach provided better estimates using the full data set as well as with both sparse and truncated data sets. Sample size estimates showed that to compare lipoprotein secretion the mixed effects approach needed almost half the sample size as the traditional method.
Interestingly, these lipid disturbances are not isolated abnormalities but metabolically linked to each other (Taskinen, 2005) , and they appear years before type 2 diabetes is diagnosed (Taskinen, 2003 ... ., 2014; Taskinen and Boren, 2015) . The formation of VLDL 1 is highly associated with fatty liver (Adiels et al., 2008; Boren et al., 2013) . ...doi:10.3389/fphys.2015.00342 pmid:26635628 pmcid:PMC4653309 fatcat:qajtzqwp7jdw3hts3pavxw72nu
Acknowledgments We thank Lea Hedman, for technical expertise; Heljä-Marja Surcel, for serological samples; and Aki Koskinen, for statistical analysis. Financial support. ...doi:10.1086/593190 pmid:18991512 fatcat:ylhrgz3l3bdqbgak6n5g6gm5ma
Taskinen MR, Boren J. New insights into the pathophysiology of dyslipidemia in type 2 diabetes. Atherosclerosis. 2015;239(2): 483-95. 12. Adiels M, Olofsson SO, Taskinen MR, Boren J. ...doi:10.1007/s11883-019-0791-9 pmid:31111320 pmcid:PMC6527792 fatcat:2z3fyqib4ff7pifk5at53dhpl4
Turbidity (absorbance at 470 nm) measurements revealed human serum low density lipoprotein (LDL) to cause, within a few minutes and at physiological pH and [NaCl], the aggregation of liquid crystalline large unilamellar liposomes (LUVs) of dimyristoylphosphatidylglycerol (DMPG). No evidence for concomitant lipid or aqueous contents mixing was obtained with fluorescent assays for these processes, in keeping with the lack of fusion of LUVs. Involvement of apoB is implicated by the finding thatdoi:10.1016/s0005-2736(98)00102-3 pmid:9733956 fatcat:4bh7eqnmifdarhfgyih2jbpj5a
more »... ptic digestion of LDL abrogates its ability to cause aggregation. Aggregation is not caused by VLDL, HDL 2 , or HDL 3 . Interestingly, also oxidised LDL failed to aggregate DMPG vesicles. Aggregation of DMPG LUVs by LDL did depend on the ionic strength of the medium as well as on the phase state of the lipid. More specifically, below the main transition temperature T m maximal aggregation was seen in the presence of 25^100 mM NaCl, whereas slightly higher (up to 150 mM) [NaCl] were required when T s T m . Aggregation due to LDL was also observed for dimyristoylphosphatidylserine as well as for dipalmitoylphosphatidylglycerol LUVs, whereas liposomes composed of either unsaturated acidic phospholipids or different phosphatidylcholines were not aggregated. Involvement of electrostatic attraction between the acidic phosphate of DMPG and cationic residues in apoB is suggested by the finding that increasing the content of dimyristoylphosphatidylcholine (DMPC) in DMPG liposomes reduced their aggregation and at X DMPC = 0.50 no response was evident. Notably, increasing the mole fraction of 1-palmitoyl-2-oleyl-PG (POPG) in DMPG LUVs progressively reduced their aggregation by LDL and at X POPG = 0.50 there was complete inhibition. The latter effect of POPG is likely to be due to augmented hydration of the unsaturated lipid constituting a barrier for the contact between apoB and the vesicle surface. In keeping with this view, the presence of the strongly hygroscopic polymer, poly(ethylene glycol) at 1% (by weight) enhanced the aggregation and could partly reverse the inhibition by POPG. ß
Taskinen MR, Boren J. Why is apolipoprotein CIII emerging as a novel therapeutic target to reduce the burden of cardiovascular disease? ...doi:10.3389/fendo.2020.00474 pmid:32849270 pmcid:PMC7399058 fatcat:h3ghsb5drrhrrgyemqlawoe2ey
Compliance with Ethical Standards Conflict of Interest Marja-Riitta Taskinen declares personal fees from Amgen, AstraZeneca, and Chiesi Pharma, grant support and personal fees from Sanofi Aventis and Novo ...doi:10.1007/s11883-016-0614-1 pmid:27613744 pmcid:PMC5018018 fatcat:3lqfshrzbbh53l3b2iwffuupzu
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