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Myocardial hypertrophy and enhanced left ventricular contractility in Zucker diabetic fatty rats
Abstract
Heart failure is known to be a complication of insulin-dependent (IDDM) and noninsulin-dependent diabetes mellitus (NIDDM) even in the absence of coronary heart disease or hypertension. The mechanisms leading to diabetic cardiomyopathy are unknown. The aim of the study was to characterize structural and functional alterations in hyperinsulinemic Zucker diabetic fatty (ZDF) rats treated with or without insulin. Diabetic animals showed a twofold increase in cardiomyocyte volume with increased left ventricular ANP but not BNP mRNA levels in spite of a reduced plasma renin activity (PRA) 2 months after onset of diabetes compared to nondiabetic littermates. These changes were associated with an increase in left ventricular performance as assessed by echocardiography. Insulin treatment led to a significant increase in body weight (BW), total heart weight, myocardial protein content, and left ventricular mass (LVM). Perivascular fibrosis and laminin thickness were significantly augmented in diabetic rat myocardium irrespective of insulin treatment, whereas interstitial collagen I and fibronectin were similarly found in diabetic and control myocardium. Initial stages of diabetic cardiomyopathy in hyperinsulinemic rats are characterized by cardiomyocyte hypertrophy and enhanced cardiac contractility. It is suggested that hyperinsulinemia may be involved in cardiac hypertrophy.
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“In genetically obese Zucker fatty rats, LVH is present in young animals shortly after the development of diabetes. This is associated with increased LV function by echocardiography (104); however, they eventually develop significant LV dysfunction in vivo as evidenced by decreased fractional shortening. This can be reversed with TZD treatment (394).”
From Cardiac remodeling in obesity (2008) · cites this paper as [104]
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Abel, E. D., Litwin, S. E., & Sweeney, G. (2008) · Physiological Reviews · doi:10.1152/physrev.00017.2007 · Cited by 736
“echocardiography (104); however, they eventually de-”
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“Obese hyperinsulinemic Zucker rats also develop perivascular cardiac fibrosis, associated with cardiac hypertrophy (23) and diastolic dysfunction (24).”
BackgroundTuleta, I., & Frangogiannis, N. G. (2020) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2020.166044 · Cited by 229
“• Zucker rats develop myocardial fibrosis [310], hepatic fibrosis accompanied by NASH [311], and renal fibrosis that may precede hyperglycemia [312].”
BackgroundMurine Models of Heart Failure With Preserved Ejection Fraction
Valero‐Muñoz, M., Backman, W., & Sam, F. (2017) · JACC Basic to Translational Science · doi:10.1016/j.jacbts.2017.07.013 · Cited by 217
“Systolic function is similar (49) or slightly decreased (51) in SAMP8 compared with SAMR1, but LVEF appears preserved.”
BackgroundInfluentialAdiponectin Protects Against Angiotensin II–Induced Cardiac Fibrosis Through Activation of PPAR-α
Fujita, K., Maeda, N., Sonoda, M., Ohashi, K., Hibuse, T., Nishizawa, H., Nishida, M., Hiuge, A., Kurata, A., Kihara, S., et al. (2008) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.107.156687 · Cited by 185
Mechanisms for increased myocardial fatty acid utilization following short-term high-fat feeding
Wright, J. J., Kim, J., Buchanan, J., Boudina, S., Sena, S., Bakirtzi, K., Ilkun, O. L., Theobald, H. A., Cooksey, R. C., Kandror, K. V., et al. (2009) · Cardiovascular Research · doi:10.1093/cvr/cvp017 · Cited by 179
“Similarly, in Zucker fatty rat hearts, glucose utilization is depressed prior to evidence of cardiac dysfunction,(10) but at a time when there is left ventricular hypertrophy.(11) Proposed mechanisms include reduced expression of glucose transporters, myocardial insulin resistance, and increased sarcolemmal localizati…”
BackgroundAsghar, O., Alsunni, A. A., Khavandi, K., Khavandi, A., Withers, S., Greenstein, A. S., Heagerty, A. M., & Malik, R. A. (2009) · Clinical Science · doi:10.1042/cs20080500 · Cited by 162
Habbout, A., Li, N., Rochette, L., & Vergely, C. (2013) · Journal of Nutrition · doi:10.3945/jn.112.172825 · Cited by 138
The Nrf2 pathway in the progression of renal disease
Zoja, C., Benigni, A., & Remuzzi, G. (2013) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gft224 · Cited by 135
Molecular Mechanisms of Obesity-Linked Cardiac Dysfunction: An Up-Date on Current Knowledge
Gutiérrez‐Cuevas, J., Sandoval-Rodriguez, A. S., Meza-Ríos, A., Monroy-Ramírez, H. C., Galicia‐Moreno, M., Garcia-Bañuelos, J. J., Santos, A., & Armendáriz‐Borunda, J. (2021) · Cells · doi:10.3390/cells10030629 · Cited by 133
“ZDF rats Rats develop obesity and insulin resistance at a young age Maintained on RMH-B rat chow Male rats showed an increase in cardiomyocyte size, LV performance, also developed perivascular fibrosis and cardiac hypertrophy [137]”
BackgroundAnalogs of bardoxolone methyl worsen diabetic nephropathy in rats with additional adverse effects
Zoja, C., Corna, D., Nava, V., Locatelli, M., Abbate, M., Gaspari, F., Carrara, F., Sangalli, F., Remuzzi, G., & Benigni, A. (2012) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00376.2012 · Cited by 101
“They are characterized by altered metabolic profile, hyperlipidemia, progressive renal disease, and cardiac abnormalities (3, 8, 33).”
BackgroundRenal Expression of FGF23 in Progressive Renal Disease of Diabetes and the Effect of Ace Inhibitor
Zanchi, C., Locatelli, M., Benigni, A., Corna, D., Tomasoni, S., Rottoli, D., Gaspari, F., Remuzzi, G., & Zoja, C. (2013) · PLoS ONE · doi:10.1371/journal.pone.0070775 · Cited by 98
Radovits, T., Korkmaz, S., Loganathan, S., Barnucz, E., Bömicke, T., Arif, R., Karck, M., & Szabo, G. B. (2009) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00165.2009 · Cited by 95
“Although during the first months of diabetes duration (when hyperinsulinemia is dominating) ZDF diabetic rats have been reported to have significantly higher body weights compared with lean controls (8, 28, 32), the lower body weight of ZDF diabetic compared with ZDF lean rats at an older age is a common finding that…”
BackgroundInfluentialDiabetes in Zucker Diabetic Fatty Rat
Shiota, M., & Printz, R. L. (2012) · Methods in molecular biology · doi:10.1007/978-1-62703-068-7_8 · Cited by 94
Cardiovascular Complications of Sleep Apnea: Role of Oxidative Stress
Badran, M., Ayas, N., & Laher, I. (2014) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2014/985258 · Cited by 99
“These animals show many of the cardiopulmonary deficits described in obese humans, such as respiratory control dysfunction, chest wall limitation, upper airway narrowing, hypertension, myocardial hypertrophy, and poor exercise capacity [56–58].”
BackgroundŚlusarz, A., & Pulakat, L. (2015) · Journal of Cardiovascular Medicine · doi:10.2459/jcm.0000000000000246 · Cited by 89
Magnetic resonance imaging of progressive cardiomyopathic changes in the db/db mouse
Yue, P., Arai, T., Terashima, M., Sheikh, A. Y., Cao, F., Charo, D., Hoyt, G., Robbins, R. C., Ashley, E. A., Wu, J., et al. (2007) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00856.2006 · Cited by 81
“Although to our knowledge no studies have evaluated ANP expression in db/db mice, ANP upregulation has been detected in other models of Type 2 diabetes (27, 30).”
BackgroundCardiovascular dysfunction in Zucker obese and Zucker diabetic fatty rats: role of hydronephrosis
Marsh, S. A., Powell, P. C., Agarwal, A., Dell’Italia, L. J., & Chatham, J. C. (2007) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.01362.2006 · Cited by 74
“A number of laboratories, including our own, have used obese Zucker and ZDF rats to investigate the consequences of insulin resistance and Type 2 diabetes on cardiac function (9, 30, 31).”
BackgroundMethodInfluentialWu, X. Y., Sun, Z., Foskett, A. M., Trzeciakowski, J. P., Meininger, G. A., & Muthuchamy, M. (2010) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.01156.2009 · Cited by 73
Updating Experimental Models of Diabetic Cardiomyopathy
Fuentes‐Antrás, J., Picatoste, B., Gómez‐Hernández, A., Egido, J., Tuñón, J., & Lorenzo, Ó. (2015) · Journal of Diabetes Research · doi:10.1155/2015/656795 · Cited by 74
“∼ [2 7] ↑ [1 0, 28 ] ↑ [1 2, 30 ] ↑ [1 3] ↑ [3 2]”
Howarth, F. C., Qureshi, M. A., Hassan, Z. A., Kury, L. T. A., Isaev, D. S., Parekh, K., Yammahi, S., Öz, M., Adrian, T. E., & Adeghate, E. A. (2011) · Experimental Physiology · doi:10.1113/expphysiol.2010.055574 · Cited by 66
“At 19 weeks of age, increased ejection fraction and fractional shortening and cardiomyocyte volume have been reported in ZDF rats (Fredersdorf et al. 2004).”
BackgroundInteraction of diet and diabetes on cardiovascular function in rats
Marsh, S. A., Dell’Italia, L. J., & Chatham, J. C. (2008) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00421.2008 · Cited by 66
“It is often reported that diabetes is associated with cardiac hypertrophy (13, 16, 17); however, in contrast, we found that LV weight relative to tibia length was actually lower in all three diabetic groups compared with age-matched, nondiabetic controls (Table 2).”
ResultCardiovascular Consequences of Sleep Apnea
Golbidi, S., Badran, M., Ayas, N., & Laher, I. (2011) · Lung · doi:10.1007/s00408-011-9340-1 · Cited by 62
“These animals show many of the cardiopulmonary deficits described in obese humans, such as respiratory control dysfunction, chest wall limitation, upper airway narrowing, hypertension, myocardial hypertrophy, and poor exercise capacity [116–118].”
BackgroundLeft ventricle structural remodelling in the prediabetic Goto-Kakizaki rat
D’Souza, A., Howarth, F. C., Yanni, J., Dobrzynski, H., Boyett, M. R., Adeghate, E. A., Bidasee, K. R., & Singh, J. (2011) · Experimental Physiology · doi:10.1113/expphysiol.2011.058271 · Cited by 62
“Differential expression of BNP and ANP, i.e. no change in ANP message levels observed in this work, is comparable to previous studies of diabetic cardiomyopathy (Fredersdorf et al. 2004) as well as decompensated experimental HF (Langenickel et al. 2000).”
ResultZoja, C., Cattaneo, S. G. D. A., Fiordaliso, F., Lionetti, V., Zambelli, V., Salio, M., Corna, D., Pagani, C., Rottoli, D., Bisighini, C., et al. (2011) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00122.2011 · Cited by 61
“The inbred obese ZDF rats, that carry the Lepr mutation, develop non-insulin-dependent diabetes and progressive renal disease in association with cardiac abnormalities (4, 23), which renders ZDF rats a suitable model for studying renal and cardiovascular alterations in type 2 diabetes.”
BackgroundResultInsights into obstructive sleep apnea research
Badran, M., Ayas, N., & Laher, I. (2014) · Sleep Medicine · doi:10.1016/j.sleep.2014.01.009 · Cited by 63
“These animals show many of the cardiopulmonary deficits described in obese humans, such as respiratory control dysfunction, chest wall limitation, upper airway narrowing, hypertension, myocardial hypertrophy, and poor exercise capacity [144–146].”
BackgroundDaniels, A., Linz, D., van Bilsen, M., Rütten, H., Sadowski, T., Ruf, S. G., Juretschke, H., Neumann‐Haefelin, C., Munts, C., Vusse, G. J., et al. (2012) · European Journal of Heart Failure · doi:10.1093/eurjhf/hfr166 · Cited by 58
“One study even reported enhanced LV contractility in ZDF rats.(12) Collectively, these experimental data illustrate the lack of consensus about the nature and severity of the disturbances in cardiac performance in this animal model of type 2 DM.”
BackgroundXi, S., Zhou, G., Zhang, X., Zhang, W., Cai, L., & Zhao, C. (2009) · Experimental & Molecular Medicine · doi:10.3858/emm.2009.41.8.059 · Cited by 55
Effects of exercise training on cardiac apoptosis in obese rats
Lee, S., Shyu, W.-C., Cheng, I.-S., Kuo, C., Chan, Y., Lin, Y.-M., Tasi, C., Tsai, C., Ho, T.-J., & Huang, C.-Y. (2012) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2011.11.002 · Cited by 56
Fredersdorf, S., Thumann, C., Zimmermann, W., Vetter, R., Graf, T., Luchner, A., Riegger, G. A. J., Schunkert, H., Thomas Eschenhagen, A., & Weil, J. (2012) · Cardiovascular Diabetology · doi:10.1186/1475-2840-11-57 · Cited by 54
Self-citationJoshi, D., Gupta, R. K., Dubey, A., Shiwalkar, A., Pathak, P., Gupta, R. C., Chauthaiwale, V. M., & Dutt, C. (2009) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0b013e3181ac3a34 · Cited by 52
“Augmented perivascular fibrosis and laminin thickness have been observed in the myocardium by others too.(23,24) In the persistent severely diabetic Ob-ZSF1 rats we observed widespread necrosis similar to that reported in diabetic patients.”
ResultHabbout, A., Delemasure, S., Goirand, F., Guilland, J., Chabod, F., Sediki, M., Rochette, L., & Vergely, C. (2012) · Biochimie · doi:10.1016/j.biochi.2011.09.023 · Cited by 52
“Indeed, studies have highlighted the role of leptin and insulin in the elongation of cardiac myocytes [45], ventricular hypertrophy [46, 47], and heart failure [48].”
BackgroundVavrinec, P., Henning, R. H., Landheer, S. W., Wang, Y., Deelman, L., van Dokkum, R. P., & Buikema, H. (2014) · Current Vascular Pharmacology · doi:10.2174/15701611113116660151 · Cited by 51
“Other studies with ZDF rats have reported both no differences in blood pressures as well as increased blood pressure compared to lean controls, seemingly depending on the age of the animals at the moment of study and the method employed [40-42].”
BackgroundMore Activated Cardiac Mitochondrial‐dependent Apoptotic Pathway in Obese Zucker Rats
Lu, M., Tzang, B., Kuo, W., Wu, F., Chen, Y.-S., Tsai, C., Huang, C., & Lee, S. (2007) · Obesity · doi:10.1038/oby.2007.315 · Cited by 47
“Introduction The obese Zucker rat, a genetic model of severe obesity, presents many of the same cardiopulmonary deficits as noted in obese humans, including respiratory control dysfunction (1–4), chest wall limitations (5), upper airway narrowing (6), hypertension (7), myocardial hypertrophy (8), and poor exercise cap…”
BackgroundPovlsen, J. A., Løfgren, B., Dalgas, C., Birkler, R. I. D., Johannsen, M., Støttrup, N. B., & Bøtker, H. E. (2013) · PLoS ONE · doi:10.1371/journal.pone.0064093 · Cited by 45
“In addition to hyperlipidemia and hypercholesterolemia, ZDF rats develop several obesity- and hyperglycemia-related complications including arterial hypertension, cardiomyopathy, cardiac hypertrophy and nephropathy [29,30].”
BackgroundBaynes, J., & Murray, D. B. (2009) · Oxidative Medicine and Cellular Longevity · doi:10.4161/oxim.2.5.9831 · Cited by 47
“On the other hand, work by Fredersdorf et al.23 investigating insulin’s affect on myocardial morphology and function in non insulin dependent diabetes concluded that at 19 weeks of age the ZDF rat exhibited LV hypertrophy and enhanced contractility as assessed by echocardiography.”
MethodResultInfluentialRiojas-Hernández, A., Bernal‐Ramírez, J., Rodríguez-Mier, D., Morales, E., Domínguez-Barragán, E. M., Borja-Villa, C., Rivera-Álvarez, I., García‐Rivas, G., Altamirano, J., & García, N. (2015) · Life Sciences · doi:10.1016/j.lfs.2015.09.018 · Cited by 45
“ac damage have been described as a consequence of enhanced intracellular lipid accumulation, due to increased transport of long-chain fatty acids [30], accompanied by an increase in NADPH oxidase activity, and the parallel increase in pro-apoptotic proteins [20,22].”
BackgroundCardiac Fas Receptor‐dependent Apoptotic Pathway in Obese Zucker Rats
Lee, S., Tzang, B., Kuo, W., Lin, Y., Yang, A., Chen, S. H., Tsai, F., Wu, F., Lu, M., & Huang, C. (2007) · Obesity · doi:10.1038/oby.2007.286 · Cited by 42
“Introduction The obese Zucker rat, a genetic model of severe obesity, presents with many of the same cardiopulmonary deficits as noted in obese humans, including respiratory control dysfunction (1–3), chest wall limitations (4), upper airway narrowing (5), hypertension (6), myocardial hypertrophy (7), and poor exercis…”
BackgroundSchäfer, S., Huber, J., Wihler, C., Rütten, H., Busch, A. E., & Linz, W. (2005) · European Journal of Heart Failure · doi:10.1016/j.ejheart.2005.04.011 · Cited by 43
“Earlier reports describing reduced myocardial systolic function in Zucker diabetic fatty [13] and Goto-Kakizaki rats [14] could not be reproduced by another group [15].”
BackgroundHuang, T. H.-W., He, L., Qin, Q., Yang, Q., Peng, G., Harada, M., Qi, Y., YAMAHARA, J., Roufogalis, B. D., & Li, Y. J. (2007) · Diabetes Obesity and Metabolism · doi:10.1111/j.1463-1326.2007.00750.x · Cited by 39
Engineered Heart Tissue Model of Diabetic Myocardium
Song, H., Zandstra, P. W., & Radisic, M. (2011) · Tissue Engineering Part A · doi:10.1089/ten.tea.2010.0617 · Cited by 39
“These rats result from the breeding between SHHF rats and ZDF rats.”
InfluentialOkere, I. C., Chandler, M. P., McElfresh, T. A., Rennison, J. H., Kung, T. A., Hoit, B. D., Ernsberger, P. R., Young, M. E., & Stanley, W. C. (2006) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/j.1440-1681.2007.04545.x · Cited by 36
Hodrea, J., Saeed, A., Molnár, Á., Fintha, A., Bárczi, A., Wagner, L. J., Szabo, A. J., Fekete, A., & Balogh, D. B. (2022) · PLoS ONE · doi:10.1371/journal.pone.0263285 · Cited by 35
Howarth, F. C., Qureshi, M. A., Hassan, Z. A., Isaev, D. S., Parekh, K., John, A., Öz, M., Raza, H., Adeghate, E. A., & Adrian, T. E. (2011) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-011-1112-y · Cited by 34
“Increased ejection fraction and fractional shortening and increased myocyte volume have been reported in 19-week ZDF rats [28].”
BackgroundRadovits, T., Korkmaz, S., Mátyás, C., Oláh, A., Németh, B. T., Páli, S., Hirschberg, K., Zubarevich, A., Gwanmesia, P., Li, S., et al. (2015) · Journal of Diabetes Research · doi:10.1155/2015/728741 · Cited by 31
“reported no myocardial collagen deposition in ZDF diabetic animals at 14 weeks of age [27]; other studies demonstrated only perivascular but not interstitial myocardial fibrosis [24] at the age of 19 weeks, while a robust fibrotic remodelling of the left ventricle has been described in 45-week-old ZDF rats [28].”
BackgroundResultGarcia, J. A. D., dos Santos, L., de Moura, A. L., Ricardo, K. F. S., Wanschel, A. C. B. A., Shishido, S. M., Spadari-Bratfisch, R. C., de Souza, H. P., & Krieger, M. H. (2008) · Journal of Cardiovascular Pharmacology · doi:10.1097/fjc.0b013e31815c39d4 · Cited by 30
Baldi, J. C., Wilson, G. A., Wilson, L. C., WILKINS, G. T., & Lamberts, R. R. (2016) · Sports Medicine · doi:10.1007/s40279-016-0542-9 · Cited by 32
Vasopeptidase inhibition has beneficial cardiac effects in spontaneously diabetic Goto–Kakizaki rats
Grönholm, T., Cheng, Z. J., Palojoki, E., Eriksson, A., Bäcklund, T., Vuolteenaho, O. J., Finckenberg, P., Laine, M., Mervaala, E. M. A., & Tikkanen, I. T. (2005) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2005.07.015 · Cited by 29
“Also in another diabetic rat model, the Zucker diabetic fatty rat, the expression of ANP mRNA was increased, probably due to hyperglycemia-induced volume expansion (Fredersdorf et al., 2004).”
BackgroundPulmonary arterial dysfunction in insulin resistant obese Zucker rats
Moral‐Sanz, J., Menéndez, C., Moreno, L., Moreno, E., Cogolludo, A. L., & Pérez‐Vizcaíno, F. (2011) · Respiratory Research · doi:10.1186/1465-9921-12-51 · Cited by 29
“For this purpose we have used a well established genetic model of obesity and insulin resistance, the obese Zucker rat, characterized by a missense mutation in the leptin receptor [28] and associated with several cardiovascular complications [22,29].”
MethodFernandes, T. M., Casaes, L., Soci, Ú. P. R., Silveira, A. C., Gomes, J. L. P., Barretti, D. L. M., Roque, F. R., & de Oliveira, E. M. (2018) · Obesity Facts · doi:10.1159/000454835 · Cited by 30
Sex, sex steroids, and diabetic cardiomyopathy: making the case for experimental focus
Reichelt, M. E., Mellor, K. M., Bell, J. R., Chandramouli, C., Headrick, J. P., & Delbridge, L. M. D. (2013) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00141.2013 · Cited by 24
Obesity and sudden cardiac death: Prevalence, pathogenesis, prevention and intervention
Yao, Y., Jia, X., & Li, B. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2022.1044923 · Cited by 25
“Obese hyperinsulinemic Zucker rats also showed perivascular cardiac fibrosis, associated with increased left ventricular mass and cardiac hypertrophy (Fredersdorf et al., 2004).”
BackgroundInducible nitric oxide synthase depresses cardiac contractile function in Zucker diabetic fatty rats
Song, D., Kuo, K., Yao, R., Hutchings, S., & Pang, C. C. Y. (2007) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2007.09.043 · Cited by 21
“, 2000) or increased (Fredersdorf et al., 2004) baseline”
BackgroundContractile Smooth Muscle and Active Stress Generation in Porcine Common Carotids
Zhou, B., Prim, D. A., Romito, E. A., McNamara, L. P., Spinale, F. G., Shazly, T. M., & Eberth, J. F. (2017) · Journal of Biomechanical Engineering · doi:10.1115/1.4037949 · Cited by 20
The coexistence of nocturnal sustained hypoxia and obesity additively increases cardiac apoptosis
Lee, S., Kuo, W., Bau, D., Ko, F.-Y., Wu, F., Kuo, C., Tsai, F., Wang, P. S., Lu, M.-C., & Huang, C. (2008) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00152.2007 · Cited by 20
Cosson, E., Valensi, P. E., Laude, D., Mesangeau, D., & Dabiré, H. (2009) · Diabetes & Metabolism · doi:10.1016/j.diabet.2009.02.007 · Cited by 19
Yalçın, F., Shiota, M., Greenberg, N. L., Thomas, J. D., & Shiota, T. (2008) · Echocardiography · doi:10.1111/j.1540-8175.2007.00603.x · Cited by 19
Cardiac Hypertrophy-Related Pathways in Obesity
Chen, W.-K. (2014) · The Chinese Journal of Physiology · doi:10.4077/cjp.2014.bab146 · Cited by 18
“The obese Zucker rat, a genetic model of morbid obesity, presents many of the same cardiopulmonary deficits noted in obese humans including respiratory control dysfunction (24, 25, 27), chest wall limitations (12), upper airway narrowing (34), hypertension (2), myocardial hypertrophy (13), cardiac apoptosis (29, 30) a…”
BackgroundSeldin, M. M., Kim, E. D., Romay, M. C., Li, S., Rau, C. D., Wang, J., Krishnan, K. C., Wang, Y., Deb, A., & Lusis, A. J. (2017) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00068.2016 · Cited by 18
van Lunteren, E., & Moyer, M. (2007) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00191.2007 · Cited by 18
“Atrial natriuretic peptide levels are increased in the plasma as well as heart atrium and ventricle of streptozotocin-diabetic rats (25), and gene expression is increased in the heart left ventricle of Zucker diabetic fatty rats (17).”
BackgroundIn vivo creatine kinase reaction kinetics at rest and stress in type II diabetic rat heart
Bashir, A., Coggan, A. R., & Gropler, R. J. (2015) · Physiological Reports · doi:10.14814/phy2.12248 · Cited by 17
“Previous studies have reported enhanced, similar, and reduction in heart function in ZDF rats (Fredersdorf et al. 2004; van den Brom et al. 2010; Daniels et al. 2012).”
ResultFibronectin increases the force production of mouse papillary muscles via α5β1 integrin
Wu, X. Y., Chakraborty, S., Heaps, C. L., Davis, M. J., Meininger, G. A., & Muthuchamy, M. (2010) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2010.10.003 · Cited by 17
“An imbalance in the production and the degradation of ECM proteinsmay lead to structural alterations such as basement membrane thickening and ECM protein deposition in tissues during the development of cardiovascular diseases [22,26,42,47–59].”
BackgroundResch, M., Schmid, P., Amann, K., Fredersdorf, S., Weil, J., Schach, C., Birner, C. M., Griese, D. P., Kreuzer, P. M., Brunner, S., et al. (2011) · Cardiovascular Diabetology · doi:10.1186/1475-2840-10-94 · Cited by 16
“We previously reported a state of hyporeninemic hyperaldosteronism in a model of type II diabetes mellitus, the Zucker Diabetic Fatty ZDF-rat [17].”
BackgroundResultSelf-citationColton, H. M., Stokes, A. H., Yoon, L. W., Quaile, M. P., Novak, P. J., Falls, J. G., Kimbrough, C. L., Cariello, N. F., Jordan, H. L., & Berridge, B. R. (2011) · Toxicological Sciences · doi:10.1093/toxsci/kfr003 · Cited by 16
“ANP and BNP are synthesized and stored as full-length prohormones and, on secretion, are cleaved to yield equimolar amounts of N-terminal proNP (NT-proNP) and the active NP hormone.”
BackgroundInfluentialSong, D., Yao, R., & Pang, C. C. Y. (2008) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2008.06.036 · Cited by 16
“TheZDFrats, at 18weeksof age, havebeenshown tohave unchanged systolic blood pressure and decreased heart rate (Fredersdorf et al., 2004).”
BackgroundmTORC1 inhibitors rapamycin and metformin affect cardiovascular markers differentially in ZDF rats
Nistala, R., Raja, A., & Pulakat, L. (2017) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/cjpp-2016-0567 · Cited by 16
Hubesch, G., Hanthazi, A., Acheampong, A., Chomette, L., Lasolle, H., Hupkens, E., Jespers, P., Vegh, G., Wembonyama, C. W. M., Verhoeven, C., et al. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2021.809885 · Cited by 15
“Additionally, obesity was mostly experimentally induced with specific genetic manipulations targeting the leptin signaling (58, 59, 62, 63).”
BackgroundResch, M., Bergler, T., Fredersdorf, S., Griese, D. P., Weil, J., Kreuzer, P. M., Brunner, S., Riegger, G. A. J., Luchner, A., & Endemann, D. (2010) · Hypertension Research · doi:10.1038/hr.2010.132 · Cited by 15
Self-citationOtani, K., Funada, H., Teranishi, R., Okada, M., & Yamawaki, H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23084228 · Cited by 14
“Another report demonstrated in ZDF rats that fractional shortening and EF were rather increased with the existence of cardiomyocyte hypertrophy at 19 weeks old, indicating that the cardiac dysfunction was not obvious [28].”
BackgroundHaley, J. M., Thackeray, J. T., Thorn, S., & DaSilva, J. N. (2015) · PLoS ONE · doi:10.1371/journal.pone.0127581 · Cited by 13
“Similar contradictions exist in assessing systolic function in ZDF rats, with reports showing reduced %EF by 14 weeks [20,27], while others indicate normal systolic function in 44 week old ZDF [41] or even increased function in 19 week ZDF animals [42].”
BackgroundVasopeptidase inhibition attenuates proteinuria and podocyte injury in Zucker diabetic fatty rats
Fredersdorf, S., Weil, J., Ulucan, C., Birner, C. M., Büttner, R., Schubert, T. E. O., Böger, C. A., Debl, K., Muders, F., Riegger, G. A. J., et al. (2007) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-007-0147-9 · Cited by 11
“In addition, our group has observed additional cardiac adaptations with enhanced cardiac contractility, myocardial hypertrophy and perivascular fibrosis during early stages of diabetes mellitus (Fredersdorf et al. 2002, 2004).”
MethodSelf-citationShushakova, N., Park, J. K., Menne, J., & Fliser, D. (2009) · European Journal of Clinical Investigation · doi:10.1111/j.1365-2362.2009.02165.x · Cited by 9
Cook, R. F., Bussey, C. T., Mellor, K. M., Cragg, P. A., & Lamberts, R. R. (2017) · Experimental Physiology · doi:10.1113/ep086293 · Cited by 9
“β-Adrenergic receptor subtype regulation of resting HR in diabetes In this study, we derived a calculated conscious HR from the direct recording of ABP and showed that resting HR is reduced by 17% in diabetic rats compared with non-diabetic rats, as also described by others (Fredersdorf et al. 2004; Thaung et al. 2015…”
ResultRussell, J. C., & Proctor, S. D. (2007) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0707226 · Cited by 9
“…and inflammatory British Journal of Pharmacology (2007) 151 216–225 processes (Fasshause et al., 2004) with lower plasma concentrations reported in both obese humans and some rodent models of obesity/insulin resistance (Altomonte et al., 2003; Alemzadeh and Tushaus, 2004; Fredersdorf et al., 2004).”
BackgroundDebin, R., Lauzier, B., Sicard, P., Delemasure, S., Amoureux, S., Duvillard, L., Vergely, C., Cottin, Y., & Rochette, L. (2009) · Fundamental and Clinical Pharmacology · doi:10.1111/j.1472-8206.2008.00659.x · Cited by 8
Furumoto, T., Fujii, S., Onozuka, H., Zaman, A. K. M. T., Goto, D., Sugawara, T., Mikami, T., Watanabe, S., Abe, K., Terauchi, Y., et al. (2005) · Coronary Artery Disease · doi:10.1097/00019501-200503000-00007 · Cited by 6
Kamada, K., Saku, K., Tohyama, T., Kawada, T., Mannoji, H., Abe, K., Nishikawa, T., Sunagawa, G., Kishi, T., Sunagawa, K., et al. (2018) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00515.2018 · Cited by 6
Shmygol, A., Bru‐Mercier, G., Sultan, A. S., & Howarth, F. C. (2024) · Clinical Science · doi:10.1042/cs20242144 · Cited by 5
Chen, J., Wang, H., Chang, W., Jao, C.-C., Wu, B., Shyu, W., & Lee, S. (2010) · Hypertension Research · doi:10.1038/hr.2010.109 · Cited by 5
The effect of non-insulin dependent diabetes mellitus on uncontrolled hemorrhage in a rodent model
Sinert, R. H., Finkelstein, D., Pius, M., Baron, B. J., Adar, E., Rizzo, P., & Shahidi, H. (2005) · Resuscitation · doi:10.1016/j.resuscitation.2004.12.026 · Cited by 5
Sun, G., Zhang, G., Jackson, C. V., & Wang, Y. (2018) · Cardiology Research and Cardiovascular Medicine · doi:10.29011/2575-7083.000033 · Cited by 4
Howarth, F. C., Qureshi, M. A., Hassan, Z. A., Kury, L. A., Isaev, D. S., Parekh, K. A., Yammahi, S. R. R. K. D., John, A., Öz, M., Raza, H., et al. (2012) · Hamdan Medical Journal · doi:10.7707/hmj.v5i2.140 · Cited by 4
Zimering, M. B. (2021) · doi:10.31038/edmj.2021523 · Cited by 3
“Chronic hypertension is a significant risk factor for the later occurrence of adverse cerebrovascular, cardiovascular and renal outcomes in humans [20-22].”
BackgroundChronic Diabetic Complications: Endothelial Cells at the Frontline
Khan, Z. A., & Chakrabarti, S. (2010) · BENTHAM SCIENCE PUBLISHERS eBooks · doi:10.2174/978160805160111001010121 · Cited by 3
Wingard, M. C., Dalal, S., Shook, P. L., Ramirez, P. R., Raza, M. U., Johnson, P. M., Connelly, B. A., Thewke, D. P., Singh, M., & Singh, K. (2022) · Physiological Reports · doi:10.14814/phy2.15434 · Cited by 2
Biomarkers of Myocardial Fibrosis in Diabetes, Echocardiography, and Magnetic Resonance Imaging
Madsen, P. L. (2022) · Biomarkers in disease · doi:10.1007/978-3-030-81303-1_45-1 · Cited by 2
Clinical Applications in Extra-Cardiac Diseases
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“In contrast, at the age of 19 weeks, Fredersdorf et al. (2004) have reported increased left ventricular myocyte volume from the immunohistological tissue morphology analysis.”
Kumar, C. U., Reddy, S. S., & Reddy, G. B. (2022) · Proceedings of the National Academy of Sciences India Section B Biological Sciences · doi:10.1007/s40011-021-01305-3 · Cited by 1
“Hyperinsulinemic obese Zucker rats also show cardiac hypertrophy along with fibrosis [28].”
BackgroundMorphological quantification of myocardial pathology in the Zucker diabetic fatty rat
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“Quantitative immunohistochemistry of areas positive for fibronectin and collagen I showed no increase in interstitial collagen I or fibronectin [15].”
BackgroundArranjo estrutural das fibras de colágeno do coração de cães normais e diabéticos
Benedicto, H. G. (2005) · doi:10.11606/t.10.2005.tde-06062007-160152 · Cited by 1
Diabetic cardiomyopathy: phenotypes, mechanisms, and therapeutic targets
Johnson, E. J. (2015) · Research Exchange (Washington State University) · Cited by 1
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Song, D. (2008) · cIRcle (University of British Columbia) · doi:10.14288/1.0066398
“In vivo echocardiographic measurements have shown depressed (Zhou et al., 2000) or increased (Fredersdorf et al., 2004) baseline cardiac contractile function of 19-20 week old Zucker diabetic fatty (ZDF) rats, an animal model of type 2 diabetes.”
Role of cardiac FoxO1 in conditions of insulin resistance, nutrient excess, and diabetes
Puthanveetil, P. (2012) · cIRcle (University of British Columbia) · doi:10.14288/1.0072615
Metadata
- Authors
- Fredersdorf, S., Thumann, C., Ulucan, C., Griese, D. P., Luchner, A., Riegger, G. A. J., Kromer, E. P., & Weil, J.
- Affiliations
- University Hospital Regensburg (DE)
- Corresponding author
- Weil, Joachim
- Venue
- Cardiovascular Pathology
- Publisher
- Elsevier BV
- Published
- 2004-01
- Volume
- 13
- Issue
- 1
- Pages
- 11-19
- ISSN
- 1054-8807 (ISSN-L)
- OpenAlex
- W2165355897
- Cited by
- 115
- References
- 46
- Citations by year
- 2026: 5 · 2024: 2 · 2022: 9 · 2021: 3 · 2020: 1 · 2019: 1 · 2018: 3 · 2017: 8 · 2016: 2 · 2015: 8 · 2014: 5 · 2013: 5 · 2012: 7
- FWCI
- 3.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cardiovascular Pathology (publishedVersion)
- PubMed (publishedVersion)
- University of Regensburg Publication Server (University of Regensburg) (acceptedVersion)
- Funders
- Universität Regensburg
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Keywords
- diabetic cardiomyopathy, cardiac hypertrophy, left ventricular contractility, hyperinsulinemia, insulin therapy, Zucker diabetic fatty rats, heart failure, atrial natriuretic peptide, brain natriuretic peptide, plasma renin activity, myocardial fibrosis, laminin, type I collagen, fibronectin, left ventricular mass, cardiomyocyte volume
- MeSH terms
- Animals, Diabetes Mellitus, Experimental, Echocardiography, Fibronectins, Fibrosis, Cardiomegaly, Heart Ventricles, Hyperinsulinism, Image Processing, Computer-Assisted, Immunohistochemistry, Insulin, Laminin, Male, Myocardial Contraction, Myocardium, Atrial Natriuretic Factor, Rats, Zucker, RNA, Messenger, Blotting, Northern, Ventricular Function, Collagen Type I, Rats
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