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Nilsson, Stefan K.
Alternative names
Publications (10 of 26) Show all publications
Jönsson, S., Becirovic-Agic, M., Isackson, H., Tveitarås, M. K., Skogstrand, T., Narfström, F., . . . Hultström, M. (2019). Angiotensin II and salt-induced decompensation in Balb/CJ mice is aggravated by fluid retention related to low oxidative stress. American Journal of Physiology - Renal Physiology, 316(5), F914-F933
Open this publication in new window or tab >>Angiotensin II and salt-induced decompensation in Balb/CJ mice is aggravated by fluid retention related to low oxidative stress
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2019 (English)In: American Journal of Physiology - Renal Physiology, ISSN 1931-857X, E-ISSN 1522-1466, Vol. 316, no 5, p. F914-F933Article in journal (Refereed) Published
Abstract [en]

Balb/CJ mice are more sensitive to treatment with angiotensin II (ANG II) and high-salt diet compared with C57BL/6J mice. Together with higher mortality, they develop edema, signs of heart failure, and acute kidney injury. The aim of the present study was to identify differences in renal gene regulation that may affect kidney function and fluid balance, which could contribute to decompensation in Balb/CJ mice after ANG II + salt treatment. Male Balb/CJ and C57BL/6J mice were divided into the following five different treatment groups: control, ANG II, salt, ANG II + salt. and ANG II + salt + N-acetylcysteine. Gene expression microarrays were used to explore differential gene expression after treatment and between the strains. Published data from the Mouse Genome Database were used to identify the associated genomic differences. The glomerular filtration rate (GFR) was measured using inulin clearance, and fluid balance was measured using metabolic cages. Gene ontology enrichment analysis of gene expression microarrays identified glutathione transferase (antioxidant system) as highly enriched among differentially expressed genes. Balb/CJ mice had similar GFR compared with C57BL/6J mice but excreted less Na+ and water, although net fluid and electrolyte balance did not differ, suggesting that Balb/CJ mice may be inherently more prone to decompensation. Interestingly, C57BL/6J mice had higher urinary oxidative stress despite their relative protection from decompensation. In addition, treatment with the antioxidant N-acetylcysteine decreased oxidative stress in C57BL/6J mice, reduced urine excretion, and increased mortality. Balb/CJ mice are more sensitive than C57BL/6J to ANG II + salt, in part mediated by lower oxidative stress, which favors fluid and Na+ retention.

Place, publisher, year, edition, pages
American Physiological Society, 2019
Keywords
fluid balance, kidney function, mice, microarray, oxidative stress
National Category
Physiology
Identifiers
urn:nbn:se:umu:diva-159399 (URN)10.1152/ajprenal.00483.2018 (DOI)000467160100016 ()30785350 (PubMedID)
Available from: 2019-06-10 Created: 2019-06-10 Last updated: 2019-06-10Bibliographically approved
Nyrén, R., Makoveichuk, E., Malla, S., Kersten, S., Nilsson, S. K., Ericsson, M. & Olivecrona, G. (2019). Lipoprotein lipase in mouse kidney: effects of nutritional status and high-fat diet. American Journal of Physiology - Renal Physiology, 316(3), F558-F571
Open this publication in new window or tab >>Lipoprotein lipase in mouse kidney: effects of nutritional status and high-fat diet
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2019 (English)In: American Journal of Physiology - Renal Physiology, ISSN 1931-857X, E-ISSN 1522-1466, Vol. 316, no 3, p. F558-F571Article in journal (Refereed) Published
Abstract [en]

Activity of lipoprotein lipase (LPL) is high in mouse kidney, but the reason is poorly understood. The aim was to characterize localization, regulation, and function of LPL in kidney of C57BL/6J mice. We found LPL mainly in proximal tubules, localized inside the tubular epithelial cells, under all conditions studied. In fed mice, some LPL, colocalized with the endothelial markers CD31 and GPIHBP1 and could be removed by perfusion with heparin. indicating a vascular location. The role of angiopoietin-like protein 4 (ANGPTL4) for nutritional modulation of LPL activity was studied in wild-type and Angptl4(-/-) mice. In Angptl4(-/-) mice, kidney LPL activity remained high in fasted animals, indicating that ANGPTL4 is involved in suppression of LPL activity on fasting, like in adipose tissue. The amount of ANGPTL4 protein in kidney was low, and the protein appeared smaller in size, compared with ANGPTL4 in heart and adipose tissue. To study the influence of obesity, mice were challenged with high-fat diet for 22 wk, and LPL was studied after an overnight fast compared with fasted mice given food for 3 h. High-fat diet caused blunting of the normal adaptation of LPL activity to feeding/fasting in adipose tissue, but in kidneys this adaptation was lost only in male mice. LPL activity increases to high levels in mouse kidney after feeding, but as no difference in uptake of chylomicron triglycerides in kidneys is found between fasted and fed states, our data confinn that LPL appears to have a minor role for lipid uptake in this organ.

Place, publisher, year, edition, pages
American Physiological Society, 2019
Keywords
angiopoietin-like protein 4, high-fat diet, lipoprotein lipase, mouse, triglyceride uptake
National Category
Physiology
Identifiers
urn:nbn:se:umu:diva-158108 (URN)10.1152/ajprenal.00474.2018 (DOI)000462008700015 ()30698048 (PubMedID)
Funder
Swedish Research Council, 2015-02942Swedish Heart Lung Foundation, 2016-245-32M
Available from: 2019-04-12 Created: 2019-04-12 Last updated: 2019-04-12Bibliographically approved
Teixeira Damasceno, N. R., Landfors, F., De Lira Teixeira, L., Fonseca, H., Gidlund, M., Wennberg, P., . . . Nilsson, S. K. (2019). Low Plasma Titer Of Autoantibodies Against Degraded Apob100 Is Independently Associated With Myocardial Infarction. Paper presented at 87th Congress of the European-Atherosclerosis-Society (EAS), MAY 26-29, 2019, Maastricht, Netherlands. Atherosclerosis, 287, E221-E221
Open this publication in new window or tab >>Low Plasma Titer Of Autoantibodies Against Degraded Apob100 Is Independently Associated With Myocardial Infarction
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2019 (English)In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 287, p. E221-E221Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
Elsevier, 2019
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-163695 (URN)10.1016/j.atherosclerosis.2019.06.676 (DOI)000482110800674 ()
Conference
87th Congress of the European-Atherosclerosis-Society (EAS), MAY 26-29, 2019, Maastricht, Netherlands
Available from: 2019-10-16 Created: 2019-10-16 Last updated: 2019-10-16Bibliographically approved
Recirovic-Agic, M., Jönsson, S., Tveitarås, M. K., Skogstrand, T., Karlsen, T. V., Lidén, Å., . . . Hultstrom, M. (2019). Time course of decompensation after angiotensin II and high-salt diet in Balb/CJ mice suggests pulmonary hypertension-induced cardiorenal syndrome. American Journal of Physiology. Regulatory Integrative and Comparative Physiology, 316(5), R563-R570
Open this publication in new window or tab >>Time course of decompensation after angiotensin II and high-salt diet in Balb/CJ mice suggests pulmonary hypertension-induced cardiorenal syndrome
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2019 (English)In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 316, no 5, p. R563-R570Article in journal (Refereed) Published
Abstract [en]

The genetic background of a mouse strain determines its susceptibility to disease. C57BL/6J and Balb/CJ are two widely used inbred mouse strains that we found react dramatically differently to angiotensin II and high-salt diet (ANG II + Salt). Balb/CJ show increased mortality associated with anuria and edema formation while C57BL/6J develop arterial hypertension but do not decompensate and die. Clinical symptoms of heart failure in Balb/CJ mice gave the hypothesis that ANG II + Salt impairs cardiac function and induces cardiac remodeling in male Balb/CJ but not in male C57BL/6J mice. To test this hypothesis, we measured cardiac function using echocardiography before treatment and every day for 7 days during treatment with ANG II + Salt. Interestingly, pulsed wave Doppler of pulmonary artery flow indicated increased pulmonary vascular resistance and right ventricle systolic pressure in Balb/CJ mice, already 24 h after ANG II + Salt treatment was started. In addition, Balb/CJ mice showed abnormal diastolic filling indicated by reduced early and late filling and increased isovolumic relaxation time. Furthermore, Balb/CJ exhibited lower cardiac output compared with C57BL/6J even though they retained more sodium and water, as assessed using metabolic cages. Left posterior wall thickness increased during ANG II + Salt treatment but did not differ between the strains. In conclusion, ANG II + Salt treatment causes early restriction of pulmonary flow and reduced left ventricular filling and cardiac output in Balb/CJ, which results in fluid retention and peripheral edema. This makes Balb/CJ a potential model to study the adaptive capacity of the heart for identifying new disease mechanisms and drug targets.

Place, publisher, year, edition, pages
the American Physiological Society, 2019
Keywords
animal model, congestive heart failure, pulmonary hypertension, right-sided heart failure
National Category
Physiology Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-159872 (URN)10.1152/ajpregu.00373.2018 (DOI)000468436400001 ()30840486 (PubMedID)
Funder
Åke Wiberg FoundationSwedish Heart Lung Foundation
Available from: 2019-06-10 Created: 2019-06-10 Last updated: 2019-06-10Bibliographically approved
Näslund, U., Ng, N., Lundgren, A., Fhärm, E., Grönlund, C., Johansson, H., . . . Norberg, M. (2019). Visualization of asymptomatic atherosclerotic disease for optimum cardiovascular prevention (VIPVIZA): a pragmatic, open-label, randomised controlled trial. The Lancet, 393(10167), 133-142
Open this publication in new window or tab >>Visualization of asymptomatic atherosclerotic disease for optimum cardiovascular prevention (VIPVIZA): a pragmatic, open-label, randomised controlled trial
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2019 (English)In: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 393, no 10167, p. 133-142Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Primary prevention of cardiovascular disease often fails because of poor adherence among practitioners and individuals to prevention guidelines. We aimed to investigate whether ultrasound-based pictorial information about subclinical carotid atherosclerosis, targeting both primary care physicians and individuals, improves prevention.

METHODS: Visualization of asymptomatic atherosclerotic disease for optimum cardiovascular prevention (VIPVIZA) is a pragmatic, open-label, randomised controlled trial that was integrated within the Västerbotten Intervention Programme, an ongoing population-based cardiovascular disease prevention programme in northern Sweden. Individuals aged 40, 50, or 60 years with one or more conventional risk factors were eligible to participate. Participants underwent clinical examination, blood sampling, and ultrasound assessment of carotid intima media wall thickness and plaque formation. Participants were randomly assigned 1:1 with a computer-generated randomisation list to an intervention group (pictorial representation of carotid ultrasound plus a nurse phone call to confirm understanding) or a control group (not informed). The primary outcomes, Framingham risk score (FRS) and European systematic coronary risk evaluation (SCORE), were assessed after 1 year among participants who were followed up. This study is registered with ClinicalTrials.gov, number NCT01849575.

FINDINGS: 3532 individuals were enrolled between April 29, 2013, and June 7, 2016, of which 1783 were randomly assigned to the control group and 1749 were assigned to the intervention group. 3175 participants completed the 1-year follow-up. At the 1-year follow-up, FRS and SCORE differed significantly between groups (FRS 1·07 [95% CI 0·11 to 2·03, p=0·0017] and SCORE 0·16 [0·02 to 0·30, p=0·0010]). FRS decreased from baseline to the 1-year follow-up in the intervention group and increased in the control group (-0·58 [95% CI -0·86 to -0·30] vs 0·35 [0·08 to 0·63]). SCORE increased in both groups (0·13 [95% CI 0·09 to 0·18] vs 0·27 [0·23 to 0·30]).

INTERPRETATION: This study provides evidence of the contributory role of pictorial presentation of silent atherosclerosis for prevention of cardiovascular disease. It supports further development of methods to reduce the major problem of low adherence to medication and lifestyle modification.

Place, publisher, year, edition, pages
Elsevier, 2019
National Category
Public Health, Global Health, Social Medicine and Epidemiology Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-154318 (URN)10.1016/S0140-6736(18)32818-6 (DOI)000455437100026 ()30522919 (PubMedID)
Funder
Västerbotten County Council, Dnr ALFVLL-298001Swedish Research Council, Dnr 521-2013-2708Swedish Research Council, 2016-01891Swedish Heart Lung Foundation, Dnr 20150369Swedish Heart Lung Foundation, 20170481
Available from: 2018-12-17 Created: 2018-12-17 Last updated: 2019-02-22Bibliographically approved
Bartelt, A., John, C., Schaltenberg, N., Berbee, J. F. P., Worthmann, A., Cherradi, M. L., . . . Heeren, J. (2017). Thermogenic adipocytes promote HDL turnover and reverse cholesterol transport. Nature Communications, 8, Article ID 15010.
Open this publication in new window or tab >>Thermogenic adipocytes promote HDL turnover and reverse cholesterol transport
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2017 (English)In: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 8, article id 15010Article in journal (Refereed) Published
Abstract [en]

Brown and beige adipocytes combust nutrients for thermogenesis and through their metabolic activity decrease pro-atherogenic remnant lipoproteins in hyperlipidemic mice. However, whether the activation of thermogenic adipocytes affects the metabolism and anti-atherogenic properties of high-density lipoproteins (HDL) is unknown. Here, we report a reduction in atherosclerosis in response to pharmacological stimulation of thermogenesis linked to increased HDL levels in APOE(star)3-Leiden. CETP mice. Both cold-induced and pharmacological thermogenic activation enhances HDL remodelling, which is associated with specific lipidomic changes in mouse and human HDL. Furthermore, thermogenic stimulation promotes HDL-cholesterol clearance and increases macrophage-to-faeces reverse cholesterol transport in mice. Mechanistically, we show that intravascular lipolysis by adipocyte lipoprotein lipase and hepatic uptake of HDL by scavenger receptor B-I are the driving forces of HDL-cholesterol disposal in liver. Our findings corroborate the notion that high metabolic activity of thermogenic adipocytes confers atheroprotective properties via increased systemic cholesterol flux through the HDL compartment.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2017
National Category
Medicinal Chemistry
Identifiers
urn:nbn:se:umu:diva-134812 (URN)10.1038/ncomms15010 (DOI)000399524700001 ()28422089 (PubMedID)
Available from: 2017-05-30 Created: 2017-05-30 Last updated: 2018-06-09Bibliographically approved
Nilsson, J., Ericsson, M., Joibari, M. M., Anderson, F., Carlsson, L., Nilsson, S. K., . . . Burén, J. (2016). A low-carbohydrate high-fat diet decreases lean mass and impairs cardiac function in pair-fed female C57BL/6J mice. Nutrition & Metabolism, 13, Article ID 79.
Open this publication in new window or tab >>A low-carbohydrate high-fat diet decreases lean mass and impairs cardiac function in pair-fed female C57BL/6J mice
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2016 (English)In: Nutrition & Metabolism, ISSN 1743-7075, E-ISSN 1743-7075, Vol. 13, article id 79Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Excess body fat is a major health issue and a risk factor for the development of numerous chronic diseases. Low-carbohydrate diets like the Atkins Diet are popular for rapid weight loss, but the long-term consequences remain the subject of debate. The Scandinavian low-carbohydrate high-fat (LCHF) diet, which has been popular in Scandinavian countries for about a decade, has very low carbohydrate content (~5 E %) but is rich in fat and includes a high proportion of saturated fatty acids. Here we investigated the metabolic and physiological consequences of a diet with a macronutrient composition similar to the Scandinavian LCHF diet and its effects on the organs, tissues, and metabolism of weight stable mice.

METHODS: Female C57BL/6J mice were iso-energetically pair-fed for 4 weeks with standard chow or a LCHF diet. We measured body composition using echo MRI and the aerobic capacity before and after 2 and 4 weeks on diet. Cardiac function was assessed by echocardiography before and after 4 weeks on diet. The metabolic rate was measured by indirect calorimetry the fourth week of the diet. Mice were sacrificed after 4 weeks and the organ weight, triglyceride levels, and blood chemistry were analyzed, and the expression of key ketogenic, metabolic, hormonal, and inflammation genes were measured in the heart, liver, and adipose tissue depots of the mice using real-time PCR.

RESULTS: The increase in body weight of mice fed a LCHF diet was similar to that in controls. However, while control mice maintained their body composition throughout the study, LCHF mice gained fat mass at the expense of lean mass after 2 weeks. The LCHF diet increased cardiac triglyceride content, impaired cardiac function, and reduced aerobic capacity. It also induced pronounced alterations in gene expression and substrate metabolism, indicating a unique metabolic state.

CONCLUSIONS: Pair-fed mice eating LCHF increased their percentage of body fat at the expense of lean mass already after 2 weeks, and after 4 weeks the function of the heart deteriorated. These findings highlight the urgent need to investigate the effects of a LCHF diet on health parameters in humans.

Place, publisher, year, edition, pages
BioMed Central, 2016
Keywords
Low-carbohydrate diet, Heart, Mouse
National Category
Clinical Medicine Physiology Nutrition and Dietetics Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-128938 (URN)10.1186/s12986-016-0132-8 (DOI)000388140200001 ()27891164 (PubMedID)
Available from: 2016-12-20 Created: 2016-12-20 Last updated: 2018-06-09Bibliographically approved
Hellström, M., Ericsson, M., Johansson, B., Faraz, M., Anderson, F., Henriksson, R., . . . Hedman, H. (2016). Cardiac hypertrophy and decreased high-density lipoprotein cholesterol in Lrig3-deficient mice. American Journal of Physiology. Regulatory Integrative and Comparative Physiology, 310(11), R1045-R1052
Open this publication in new window or tab >>Cardiac hypertrophy and decreased high-density lipoprotein cholesterol in Lrig3-deficient mice
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2016 (English)In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology, ISSN 0363-6119, E-ISSN 1522-1490, Vol. 310, no 11, p. R1045-R1052Article in journal (Refereed) Published
Abstract [en]

Genetic factors confer risk for cardiovascular disease. Recently, large genome-wide population studies have shown associations between genomic loci close to LRIG3 and heart failure and plasma high-density lipoprotein (HDL) cholesterol level. Here, we ablated Lrig3 in mice and investigated the importance of Lrig3 for heart function and plasma lipid levels. Quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to analyze Lrig3 expression in the hearts of wild-type and Lrig3-deficient mice. In addition, molecular, physiological, and functional parameters such as organ weights, heart rate, blood pressure, heart structure and function, gene expression in the heart, and plasma insulin, glucose, and lipid levels were evaluated. The Lrig3-deficient mice were smaller than the wild-type mice but otherwise appeared grossly normal. Lrig3 was expressed at detectable but relatively low levels in adult mouse hearts. At 9 mo of age, ad libitum-fed Lrig3-deficient mice had lower insulin levels than wildtype mice. At 12 mo of age, Lrig3-deficient mice exhibited increased blood pressure, and the Lrig3-deficient female mice displayed signs of cardiac hypertrophy as assessed by echocardiography, heart-to-body weight ratio, and expression of the cardiac hypertrophy marker gene Nppa. Additionally, Lrig3-deficient mice had reduced plasma HDL cholesterol and free glycerol. These findings in mice complement the human epidemiological results and suggest that Lrig3 may influence heart function and plasma lipid levels in mice and humans.

National Category
Physiology
Identifiers
urn:nbn:se:umu:diva-122617 (URN)10.1152/ajpregu.00309.2015 (DOI)000377021700004 ()27009049 (PubMedID)
Available from: 2016-06-20 Created: 2016-06-20 Last updated: 2018-06-07Bibliographically approved
Avall, K., Ali, Y., Leibiger, I. B., Leibiger, B., Moede, T., Paschen, M., . . . Juntti-Berggren, L. (2015). Apolipoprotein CIII links islet insulin resistance to beta-cell failure in diabetes. Proceedings of the National Academy of Sciences of the United States of America, 112(20), E2611-E2619
Open this publication in new window or tab >>Apolipoprotein CIII links islet insulin resistance to beta-cell failure in diabetes
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2015 (English)In: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 112, no 20, p. E2611-E2619Article in journal (Refereed) Published
Abstract [en]

Insulin resistance and beta-cell failure are the major defects in type 2 diabetes mellitus. However, the molecular mechanisms linking these two defects remain unknown. Elevated levels of apolipoprotein CIII (apoCIII) are associated not only with insulin resistance but also with cardiovascular disorders and inflammation. We now demonstrate that local apoCIII production is connected to pancreatic islet insulin resistance and beta-cell failure. An increase in islet apoCIII causes promotion of a local inflammatory milieu, increased mitochondrial metabolism, deranged regulation of beta-cell cytoplasmic free Ca2+ concentration ([Ca2+](i)) and apoptosis. Decreasing apoCIII in vivo results in improved glucose tolerance, and pancreatic apoCIII knockout islets transplanted into diabetic mice, with high systemic levels of the apolipoprotein, demonstrate a normal [Ca2+](i) response pattern and no hallmarks of inflammation. Hence, under conditions of islet insulin resistance, locally produced apoCIII is an important diabetogenic factor involved in impairment of beta-cell function and may thus constitute a novel target for the treatment of type 2 diabetes mellitus.

Keywords
diabetes, apoCIII, insulin resistance, pancreatic islets
National Category
Cell and Molecular Biology Endocrinology and Diabetes
Identifiers
urn:nbn:se:umu:diva-106130 (URN)10.1073/pnas.1423849112 (DOI)000354729500011 ()25941406 (PubMedID)
Available from: 2015-07-14 Created: 2015-07-09 Last updated: 2018-06-07Bibliographically approved
Caraballo, R., Larsson, M., Nilsson, S. K., Ericsson, M., Qian, W., Tran, N. P., . . . Elofsson, M. (2015). Structure-activity relationships for lipoprotein lipase agonists that lower plasma triglycerides in vivo. European Journal of Medicinal Chemistry, 103, 191-209
Open this publication in new window or tab >>Structure-activity relationships for lipoprotein lipase agonists that lower plasma triglycerides in vivo
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2015 (English)In: European Journal of Medicinal Chemistry, ISSN 0223-5234, E-ISSN 1768-3254, Vol. 103, p. 191-209Article in journal (Refereed) Published
Abstract [en]

The risk of cardiovascular events increases in individuals with elevated plasma triglyceride (TG) levels, therefore advocating the need for efficient TG-lowering drugs. In the blood circulation, TG levels are regulated by lipoprotein lipase (LPL), an unstable enzyme that is only active as a non-covalently associated homodimer. We recently reported on a N-phenylphthalimide derivative (1) that stabilizes LPL in vitro, and moderately lowers triglycerides in vivo (Biochem. Biophys. Res. Common. 2014, 450, 1063). Herein, we establish structure activity relationships of 51 N-phenylphthalimide analogs of the screening hit 1. In vitro evaluation highlighted that modifications on the phthalimide moiety were not tolerated and that lipophilic substituents on the central phenyl ring were functionally essential. The substitution pattern on the central phenyl ring also proved important to stabilize LPL However, in vitro testing demonstrated rapid degradation of the phthalimide fragment in plasma which was addressed by replacing the phthalimide scaffold with other heterocyclic fragments. The in vitro potency was retained or improved and substance 80 proved stable in plasma and efficiently lowered plasma TGs in vivo. 2015 The Authors. Published by Elsevier Masson SAS.

Place, publisher, year, edition, pages
Elsevier, 2015
Keywords
Lipoprotein lipase, LPL, Triglyceride, Structure-activity relationship, Agonist
National Category
Chemical Sciences
Identifiers
urn:nbn:se:umu:diva-111481 (URN)10.1016/j.ejmech.2015.08.058 (DOI)000363344700015 ()26355531 (PubMedID)
Available from: 2015-12-08 Created: 2015-11-13 Last updated: 2018-06-07Bibliographically approved
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