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3. One-leg inactivity induces a reduction in mitochondrial oxidative capacity, intramyocellular lipid accumulation and reduced insulin signalling upon lipid infusion: a human study with unilateral limb suspension

Author

Bilet, Lena, Phielix, Esther, van de Weijer, Tineke, Gemmink, Anne, Bosma, Madeleen, Moonen-Kornips, Esther, Jorgensen, Johanna A., Schaart, Gert, Zhang, Dongyan, Meijer, Kenneth, Hopman, Maria, Hesselink, Matthijs K. C., Ouwens, D. Margriet, Shulman, Gerald I., Schrauwen-Hinderling, Vera B., and Schrauwen, Patrick

Published
2020
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8. Assessment of circulating Wnt1 inducible signalling pathway protein 1 (WISP-1)/CCN4 as a novel biomarker of obesity

Author

Tacke, Christopher, Aleksandrova, Krasimira, Rehfeldt, Miriam, Murahovschi, Veronica, Markova, Mariya, Kemper, Margrit, Hornemann, Silke, Kaiser, Ulrike, Honig, Caroline, Gerbracht, Christiana, Kabisch, Stefan, Hörbelt, Tina, Ouwens, D. Margriet, Weickert, Martin O., Boeing, Heiner, Pfeiffer, Andreas F. H., Pivovarova, Olga, and Rudovich, Natalia

Published
2018
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10. Secretome profiling of primary human skeletal muscle cells

Author

Hartwig, Sonja, Raschke, Silja, Knebel, Birgit, Scheler, Mika, Irmler, Martin, Passlack, Waltraud, Muller, Stefan, Hanisch, Franz-Georg, Franz, Thomas, Li, Xinping, Dicken, Hans-Dieter, Eckardt, Kristin, Beckers, Johannes, de Angelis, Martin Hrabe, Weigert, Cora, Häring, Hans-Ulrich, Al-Hasani, Hadi, Ouwens, D. Margriet, Eckel, Jürgen, Kotzka, Jorg, and Lehr, Stefan

Published
2014
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12. CDH13 abundance interferes with adipocyte differentiation and is a novel biomarker for adipose tissue health

Author

Göddeke, Simon, Knebel, Birgit, Fahlbusch, Pia, Hörbelt, Tina, Poschmann, Gereon, Velde, Frederique, Benninghoff, Tim, Al-Hasani, Hadi, Jacob, Sylvia, Nieuwenhove, Yves, Lapauw, Bruno, Lehr, Stefan, Ouwens, D., and Kotzka, Jorg

Abstract

CDH13, an atypical member of the cadherin superfamily, has been identified in adipocyte secretomes of lean mouse models. CDH13 abundance differs in mouse models according to their susceptibility to develop metabolic disorders, but the role of CDH13 in adipose tissue is unknown. Secreted CDH13 protein levels and mRNA levels in visceral adipose tissue were determined in lean and obese mouse models. In vitro studies were performed in 3T3-L1 adipocytes to determine the role of CDH13 in adipocyte differentiation. The pathophysiological impact of visceral adipose tissue CDH13mRNA and circulating CDH13 levels were determined in humans (normal-weight men n= 37, obese men n= 109 including n= 51 type 2 diabetes patients) and in obese patients (n= 14) pre- and post-metabolic surgery. This study shows that in visceral adipose tissue CDH13 protein secretion and mRNA levels were decreased in obese mouse models. Mechanistically, CDH13 affects lipid metabolism during adipogenesis but not in mature adipocytes. CDH13 knockdown during adipogenesis reduced fatty acid uptake and lipid content in developing adipocytes. Furthermore, CDH13 depletion during adipogenesis lowered the induction of PPARγand C/EBPαexpression. These observations are of pathophysiological impact since visceral adipose tissue CDH13mRNA and circulating CDH13 levels were decreased in obese men compared to normal-weight controls. Weight loss induced by bariatric surgery restored circulating CDH13 to levels found in normal-weight controls. CDH13 levels in adipose tissue and the circulation are affected by obesity in mouse models and humans and are restored by weight loss in humans. CDH13 interferes with the differentiation potential of adipocytes and therefore is a marker for plasticity of fat tissue that might reflect the health status of adipose tissue.

Published
2024
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13. Interactive contribution of hyperinsulinemia, hyperglycemia, and mammalian target of rapamycin signaling to valvular interstitial cell differentiation and matrix remodeling

Author

Selig, Jessica I., primary, Krug, H. Viviana, additional, Küppers, Caroline, additional, Ouwens, D. Margriet, additional, Kraft, Felix A., additional, Adler, Elena, additional, Bauer, Sebastian J., additional, Lichtenberg, Artur, additional, Akhyari, Payam, additional, and Barth, Mareike, additional

Published
2022
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18. Postprandial renal hemodynamic effects of DPP-4 inhibitor linagliptin versus sulfonylurea glimepiride in adults with type 2 diabetes (RENALIS):a pre-defined sub-study of a randomized, double-blind trial

Author

Muskiet, Marcel H A, Tonneijck, Lennart, Smits, Mark M, Kramer, Mark H H, Ouwens, D Margriet, Hartmann, Bolette, Holst, Jens J, Danser, A H Jan, Joles, Jaap A, van Raalte, Daniël H, Muskiet, Marcel H A, Tonneijck, Lennart, Smits, Mark M, Kramer, Mark H H, Ouwens, D Margriet, Hartmann, Bolette, Holst, Jens J, Danser, A H Jan, Joles, Jaap A, and van Raalte, Daniël H

Abstract

AIMS: To determine the effect of dipeptidyl-peptidase (DPP)-4-inhibitor linagliptin on postprandial glomerular hyperfiltration compared to the sulfonylurea glimepiride in adults with type 2 diabetes (T2DM).MATERIALS AND METHODS: In this pre-defined sub-study within a randomized, double-blind, parallel-group, intervention-trial, overweight people with T2DM without renal-impairment were treated with once-daily linagliptin 5 mg (N = 10) or glimepiride 1 mg (N = 13) as add-on to metformin for 8 weeks. After a standardized liquid protein-rich meal, GFR and effective renal plasma flow were determined by inulin and para-aminohippuric acid clearance, respectively, based on timed urine-sampling. Intrarenal hemodynamics were estimated using Gomez'-equations. Glucoregulatory/vasoactive hormones, urinary-pH and fractional excretions (FE) of sodium, potassium and urea were measured.RESULTS: Linagliptin compared to glimepiride increased postprandial filtration fraction (FF; mean-difference 2.1%; P = 0.016) and estimated glomerular hydraulic pressure (mean-difference 3.0 mmHg; P = 0.050), and tended to increase GFR (P = 0.08) and estimated efferent renal arteriolar resistance (RE ; P = 0.08) from baseline to Week-8. No differences in FE were noted. Glimepiride reduced HbA1c more than linagliptin (mean-difference - 0.40%; P = 0.004), without between-group differences in time-averaged postprandial glucose-levels. In the linagliptin-group, change in FF correlated with change in mean arterial pressure (R = 0.807; P = 0.009) and time-averaged-mean glucagon (R = 0.782; P = 0.008), but not with changes in glucose, insulin, intact GLP-1, renin or FENa . Change in glucagon was associated with change in RE (R = 0.830; P = 0.003).CONCLUSIONS: In contrast to our hypothesis, linagliptin compared to glimepiride does not reduce postprandial hyperfiltration, yet seems to increase FF after meal-ingestion by increasing blood pressure or RE . This article is protected by copy

Published
2022

19. Postprandial renal haemodynamic effects of the dipeptidyl peptidase-4 inhibitor linagliptin versus the sulphonylurea glimepiride in adults with type 2 diabetes (RENALIS):A predefined substudy of a randomized, double-blind trial

Author

Muskiet, Marcel H.A., Tonneijck, Lennart, Smits, Mark M., Kramer, Mark H.H., Ouwens, D. Margriet, Hartmann, Bolette, Holst, Jens J., Danser, A. H.Jan, Joles, Jaap A., van Raalte, Daniël H., Muskiet, Marcel H.A., Tonneijck, Lennart, Smits, Mark M., Kramer, Mark H.H., Ouwens, D. Margriet, Hartmann, Bolette, Holst, Jens J., Danser, A. H.Jan, Joles, Jaap A., and van Raalte, Daniël H.

Abstract

Aim: To determine the effect of the dipeptidyl peptidase-4 inhibitor linagliptin on postprandial glomerular hyperfiltration compared with the sulphonylurea glimepiride in adults with type 2 diabetes (T2D). Materials and Methods: In this predefined substudy within a randomized, double-blind, parallel-group, intervention trial, overweight people with T2D without renal impairment were treated with once-daily linagliptin 5 mg (N = 10) or glimepiride 1 mg (N = 13) as an add-on to metformin for 8 weeks. After a standardized liquid protein-rich meal, the glomerular filtration rate (GFR) and effective renal plasma flow were determined by inulin and para-aminohippuric acid clearance, respectively, based on timed urine sampling. Intrarenal haemodynamics were estimated using the Gomez equations. Glucoregulatory/vasoactive hormones, urinary pH and fractional excretions (FE) of sodium, potassium and urea were measured. Results: Compared with glimepiride, linagliptin increased the postprandial filtration fraction (FF; mean difference 2.1%-point; P =.016) and estimated glomerular hydraulic pressure (mean difference 3.0 mmHg; P =.050), and tended to increase GFR (P =.08) and estimated efferent renal arteriolar resistance (RE; P =.08) from baseline to week 8. No differences in FE were noted. Glimepiride reduced HbA1c more than linagliptin (mean difference −0.40%; P =.004), without between-group differences in time-averaged postprandial glucose levels. In the linagliptin group, change in FF correlated with change in mean arterial pressure (R = 0.807; P =.009) and time-averaged mean glucagon (R = 0.782; P =.008), but not with changes in glucose, insulin, intact glucagon-like peptide-1, renin or FENa. Change in glucagon was associated with change in RE (R = 0.830; P =.003). Conclusions: In contrast to our hypothesis, compared with glimepiride, linagliptin does not reduce postprandial hyperfiltration, yet appears to increase FF after meal ingestion by

Published
2022

20. Postprandial renal haemodynamic effects of the dipeptidyl peptidase-4 inhibitor linagliptin versus the sulphonylurea glimepiride in adults with type 2 diabetes (RENALIS): a pre-defined sub-study of a randomized, double-blind trial

Author

MS Nefrologie, Regenerative Medicine and Stem Cells, Muskiet, Marcel H A, Tonneijck, Lennart, Smits, Mark M, Kramer, Mark H H, Ouwens, D Margriet, Hartmann, Bolette, Holst, Jens J, Danser, A H Jan, Joles, Jaap A, van Raalte, Daniël H, MS Nefrologie, Regenerative Medicine and Stem Cells, Muskiet, Marcel H A, Tonneijck, Lennart, Smits, Mark M, Kramer, Mark H H, Ouwens, D Margriet, Hartmann, Bolette, Holst, Jens J, Danser, A H Jan, Joles, Jaap A, and van Raalte, Daniël H

Published
2022

30. Postprandial renal haemodynamic effects of the dipeptidyl peptidase‐4 inhibitor linagliptin versus the sulphonylurea glimepiride in adults with type 2 diabetes (RENALIS): A predefined substudy of a randomized, double‐blind trial

Author

Muskiet, Marcel H. A., primary, Tonneijck, Lennart, additional, Smits, Mark M., additional, Kramer, Mark H. H., additional, Ouwens, D. Margriet, additional, Hartmann, Bolette, additional, Holst, Jens J., additional, Danser, A. H. Jan, additional, Joles, Jaap A., additional, and van Raalte, Daniël H., additional

Published
2021
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34. Differential regulation of cardiac glucose and fatty acid uptake by endosomal pH and actin filaments

Author

Steinbusch, Laura K.M., Wijnen, Wino, Schwenk, Robert W., Coumans, Will A., Hoebers, Nicole T.H., Ouwens, D. Margriet, Diamant, Michaela, Bonen, Arend, Glatz, Jan F.C., and Luiken, Joost J.F.P.

Subjects
Actin -- Physiological aspects, Fatty acids -- Physiological aspects, Glucose metabolism -- Physiological aspects, Substrates (Biochemistry) -- Physiological aspects, Biological sciences
Abstract

Insulin and contraction stimulate both cardiac glucose and long-chain fatty acid (LCFA) uptake via translocation of the substrate transporters GLUT4 and CD36, respectively, from intracellular compartments to the sarcolemma. Little is known about the role of vesicular trafficking elements in insulin- and contraction-stimulated glucose and LCFA uptake in the heart, especially whether certain trafficking elements are specifically involved in GLUT4 versus CD36 translocation. Therefore, we studied the role of coat proteins, actin- and microtubule-filaments and endosomal pH on glucose and LCFA uptake into primary cardiomyocytes under basal conditions and during stimulation with insulin or oligomycin (contraction-like AMP-activated protein kinase activator). Inhibition of coat protein targeting to Golgi/endosomes decreased insulin/oligomycin-stimulated glucose (-42%/-51%) and LCFA (-39%/-68%) uptake. Actin disruption decreased insulin/oligomycin-stimulated glucose uptake (-41%/-75%), while not affecting LCFA uptake. Microtubule disruption did not affect substrate uptake under any condition. Endosomal alkalinization increased basal sarcolemmal CD36 (2-fold), but not GLUT4, content, and concomitantly decreased basal intracellular membrane GLUT4 and CD36 content (-60% and -62%, respectively), indicating successful CD36 translocation and incomplete GLUT4 translocation. Additionally, endosomal alkalinization elevated basal LCFA uptake (1.4-fold) in a nonadditive manner to insulin/oligomycin, and decreased insulin/oligomycin-stimulated glucose uptake (-32%/-68%). In conclusion, 1) CD36 translocation, just like GLUT4 translocation, is a vesicle-mediated process depending on coat proteins, and 2) GLUT4 and CD36 trafficking are differentially dependent on endosomal pH and actin filaments. The latter conclusion suggests novel strategies to alter cardiac substrate preference as part of metabolic modulation therapy. cardiac substrate uptake; CD36 translocation; vesicular trafficking; coat proteins doi: 10.1152/ajpcell.00334.2009.

Published
2010

39. The small chain fatty acid butyrate antagonizes the TCR-stimulation-induced metabolic shift in murine epidermal gamma delta T cells

Author

Häselbarth, Lukas, Ouwens, D. Margriet, Teichweyde, Nadine, Hochrath, Katrin, Merches, Katja, and Esser, Charlotte

Subjects
Original Article, propionate, dendritic epidermal T cells, acetate, butyrate, metabolism, short chain fatty acids
Abstract

The metabolic requirements change during cell proliferation and differentiation. Upon antigen-stimulation, effector T cells switch from adenosine-triphospate (ATP)-production by oxidative phosphorylation in the mitochondria to glycolysis. In the gut it was shown that short chain fatty acids (SCFA), fermentation products of the microbiota in colon, ameliorate inflammatory reactions by supporting the differentiation of regulatory T cells. SCFA are a major energy source, but they are also anabolic metabolites, histone-deacetylase-inhibitors and activators of G protein receptors. Recently, it was reported that a topical application of the SCFA butyrate promotes regulatory T cells in the skin. Here we ask if the SCFA butyrate, propionate and acetate affect the energy metabolism and inflammatory potential of dendritic epidermal T cells (DETC), the innate resident skin γδ T cell population. Using the Seahorse™ technology, we measured glycolysis and oxidative phosphorylation (OXPHOS) in a murine DETC cell line, 7-17, upon TCR-stimulation by CD3/CD28 crosslinking, with or without SCFA addition. TCR engagement resulted in a change of the ratio glycolysis/OXPHOS. A similar metabolic shift has been described for activated CD4 T cells. Addition of 5 mM SCFA, in particular butyrate, antagonized the effect. Stimulated DETC secrete cytokines, e.g. the pro-inflammatory cytokine interferon-gamma (IFNγ), and thereby regulate skin homeostasis. Addition of butyrate and propionate to the cultures at non-toxic concentrations decreased secretion of IFNγ by DETC and increased the expression of the immunoregulatory surface receptor CD69. We hypothesize that SCFA can dampen the inflammatory activity of DETC., EXCLI Journal;Vol. 19 2020

Published
2020

45. Hepatic Wnt1 Inducible Signaling Pathway Protein 1 (WISP-1/CCN4) Associates with Markers of Liver Fibrosis in Severe Obesity

Author

Pivovarova-Ramich, Olga, primary, Loske, Jennifer, additional, Hornemann, Silke, additional, Markova, Mariya, additional, Seebeck, Nicole, additional, Rosenthal, Anke, additional, Klauschen, Frederick, additional, Castro, José, additional, Buschow, René, additional, Grune, Tilman, additional, Lange, Volker, additional, Rudovich, Natalia, additional, and Ouwens, D., additional

Published
2021
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46. Acute hepatic steatosis in mice by blocking [beta]-oxidation does not reduce insulin sensitivity of very-low-density lipoprotein production

Author

Grefhorst, Aldo, Hoekstra, Jildou, Derks, Terry G. J., Ouwens, D. Margriet, Bailer, Julius F.W., Havinga, Rick, Havekes, Louis M., Romijn, Johannes A., and Kuipers, Folkert

Subjects
Liver -- Research, Mice -- Research, Triglycerides -- Research, Biological sciences
Abstract

Accumulation of triglycerides (TG) in the liver is generally associated with hepatic insulin resistance. We questioned whether acute hepatic steatosis induced by pharmacological blockade of [beta]-oxidation affects hepatic insulin sensitivity, i.e., insulin-mediated suppression of VLDL production and insulin-induced activation of phosphatidylinositol 3-kinase (PI3-kinase) and PKB. Tetradecylglycidic acid (TDGA), an inhibitor of carnitine palmitoyl transferase-1 (CPT1), was used for this purpose. Male C57BL/6J mice received 30 mg/kg TDGA or its solvent intraperitoneally and were subsequently fasted for 12 h. CPT 1 inhibition resulted in severe microvesicular hepatic steatosis (19.9 [+ or -] 8.3 vs. 112.4 [+ or -] 25.2 nmol TG/mg liver, control vs. treated, P < 0.05) with elevated plasma nonesterified fatty acid (0.68 [+ or -] 0.25 vs. 1.21 [+ or -] 0.41 mM, P < 0.05) and plasma TG (0.39 [+ or -] 0.16 vs. 0.60 [+ or -] 0.10 mM, P < 0.05) concentrations. VLDL-TG production rate was not affected on CPT1 inhibition (74.9 [+ or -] 15.2 vs. 79.1 [+ or -] 12.8 [micro]mol TG x [kg.sup.-1] x [min.sup.-1] control vs. treated)although treated mice secreted larger VLDL particles (59.3 [+ or -] 3.6 vs. 66.6 [+ or -] 4.5 nm diameter, P < 0.05). Infusion of insulin under euglycemic conditions suppressed VLDL production rate in control and treated mice by 43 and 54%, respectively, with formation of smaller VLDL particles (51.2 [+ or -] 2.5 and 53.2 [+ or -] 2.8 nm diameter). Insulin-induced insulin receptor substrate (IRS)1- and IRS2-associated PI3-kinase activity and PKB-phosphorylation were not affected on TDGA treatment. In conclusion, acute hepatic steatosis caused by pharmacological inhibition of [beta]-oxidation is not associated with reduced hepatic insulin sensitivity, indicating that hepatocellular fat content per se is not causally related to insulin resistance. tetradecylglycidic acid; triglycerides; carnitine palmitoyl transferase-1

Published
2005

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