Insulin resistance induces hyperleptinemia, cardiac contractile dysfunction but not cardiac leptin resistance in ventricular myocytes

Hintz, Kadon K.; Aberle, Nicholas S.; Ren, Jun

doi:10.1038/sj.ijo.0802389

Cited by 62 publications

(55 citation statements)

References 25 publications

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“…Data from our present study revealed that ventricular myocytes from sucrose-fed mice exhibited depressed PS amplitude, reduced ±dL/dt and prolonged TR 90 associated with normal TPS and HWD. Most of these data are consistent with our previous findings using a similar hyperinsulinaemic insulin-resistance model in rats [6,26]. The fact that Fig.…”

Section: Discussionsupporting

confidence: 92%

“…Consistent with the previous findings [5,6,19], sucrose induced hyperinsulinaemia, which was not affected by the catalase transgene (Table 1). Following acute i.p.…”

Section: Experimental Animalssupporting

confidence: 93%

“…b Total Akt expression; c pAkt expression; and d pAkt/Akt ratio. Means±SEM, n=8 and 4 for non-insulin-and insulin-stimulated groups, respectively, *p<0.05 vs FVB-starch group, #p<0.05 vs corresponding non-insulin-stimulated group our early observation showed either normal TR 90 and ±dL/dt or shortened TPS after sucrose-diet feeding may be attributed to relatively short feeding duration (7-10 weeks) [6] and the difference in experimental species (rats vs mice). These mechanical defects are strikingly similar to those reported in ventricular myocytes from full-blown diabetes [9,18,26].…”

Section: Discussionmentioning

confidence: 68%

“…Individuals with insulin resistance exhibit a high incidence of cardiovascular diseases such as ventricular dysfunction [1][2][3]. Compromised heart function associated with insulin resistance is characterised by impaired cardiac efficiency, reduced ventricular function and coronary heart disease [2][3][4][5][6][7]. Many of these dysfunctions are reminiscent of those found in diabetic individuals with compromised heart function.…”

Section: Introductionmentioning

confidence: 99%

“…However, the role of oxidative stress in cardiac dysfunction under insulin resistance is essentially unknown. We used a sucrose-diet-induced insulinresistance model with hyperinsulinaemia and hypertriglyceridaemia [5,6,19]. It is believed that changes in fatty acid composition and membrane fluidity may contribute to the elevated cholesterol content and cholesterol:phospholipid ratio [19].…”

Section: Introductionmentioning

confidence: 99%

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Cardiac overexpression of catalase rescues cardiac contractile dysfunction induced by insulin resistance: role of oxidative stress, protein carbonyl formation and insulin sensitivity

et al. 2006

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Aims/hypothesis: Insulin resistance leads to oxidative stress and cardiac dysfunction. This study examined the impact of catalase on insulin-resistanceinduced cardiac dysfunction, oxidative damage and insulin sensitivity. Methods: Insulin resistance was initiated in FVB and catalase-transgenic mice by 12 weeks of sucrose feeding. Contractile and intracellular Ca 2+ properties were evaluated in cardiomyocytes including peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR 90 ), half-width duration (HWD), maximal velocity of shortening/relengthening (±dL/dt), fura-fluorescence intensity change (ΔFFI) and intracellular Ca 2+ clearance rate (τ). Reactive oxygen species (ROS) and protein damage were evaluated with dichlorodihydrofluorescein and protein carbonyl formation. Results: Sucrose-fed mice displayed hyperinsulinaemia, impaired glucose tolerance and normal body weight. Myocytes from FVB sucrose-fed mice exhibited depressed PS and ±dL/dt, prolonged TR 90 and τ, and reduced ΔFFI associated with normal TPS and HWD compared with those from starch-fed control mice. ROS and protein carbonyl formation were elevated in FVB sucrose-fed mice. Insulin sensitivity was reduced, evidenced by impaired insulin-stimulated 2-deoxy-D-[ 3 H] glucose uptake. Western blot analysis indicated that sucrose feeding: (1) inhibited insulin-stimulated phosphorylation of insulin receptor and Akt; (2) enhanced proteintyrosine phosphatase 1B (PTP1B) expression; and (3) suppressed endothelial nitric oxide synthase (eNOS) and Na + -Ca 2+ exchanger expression without affecting peroxisome proliferator-activated receptor γ (PPARγ), sarco(endo)plasmic reticulum Ca 2+ -ATPase isozyme 2a and phospholamban. Catalase ablated insulin-resistanceinduced mechanical dysfunction, ROS production and protein damage, and reduced eNOS, but not insulin insensitivity. Catalase itself decreased resting FFI and enhanced expression of PTP1B and PPARγ. Conclusions/ interpretation: These data indicate that catalase rescues insulin-resistance-induced cardiac dysfunction related to ROS production and protein oxidation but probably does not improve insulin sensitivity.

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Section: Discussionsupporting

confidence: 92%

“…Consistent with the previous findings [5,6,19], sucrose induced hyperinsulinaemia, which was not affected by the catalase transgene (Table 1). Following acute i.p.…”

Section: Experimental Animalssupporting

confidence: 93%

Section: Discussionmentioning

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cardiac overexpression of catalase rescues cardiac contractile dysfunction induced by insulin resistance: role of oxidative stress, protein carbonyl formation and insulin sensitivity

et al. 2006

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Adipokine Production by Adipose Tissue: A Novel Target for Treating Metabolic Syndrome and its Sequelae

et al. 2011

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Signal Transduction in the Cardiovascular System in Health and Disease

Srivastava¹,

Anand‐Srivastava²

2008

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except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. Cover illustration:Printed on acid-free paper 9 8 7 6 5 4 3 2 1 springer.com PrefaceIn recent years, there has been a surge of interest in studies related to the role of a variety of signaling pathways in the control of cardiovascular physiology. Evidence has also accumulated to suggest that an aberration in the signal transduction pathways contributes to the pathophysiology of cardiovascular disease. Several components of the signaling pathways have been identified as potential targets for the development of new therapies of cardiovascular disease. Therefore, this volume has been compiled to highlight the contributions of different signaling systems in modulating normal cardiovascular functions and how a perturbation in these signaling events leads to abnormal cell functions and cardiovascular disorders. This volume has been divided into five sections dealing with five key signaling pathways regulating different aspects of cardiovascular physiology. The first section describes the role of G-protein-coupled receptor (GPCR) signaling in cardiovascular functions. In this section, Anand-Srivastava has elegantly summarized studies showing that the expression levels of various G-proteins as well as responsiveness of adenylyl cyclase systems to various stimuli such as β-adrenergic receptor (βAR) agonist and vasoactive peptides are defective in various models of hypertension, congestive heart failure (CHF), cardiac hypertrophy, and other diseases. Dent et al. have highlighted studies showing how the alterations in different components of the βAR signaling system contribute to CHF and suggest that βAR blockade could be used as a strategy to treat CHF. Continuing on the same theme, Vacek et al. have reviewed the pathophysiological mechanisms involved in CHF and sudden cardiac death, with an emphasis on the role of homocysteine-induced cross talk between NMDA receptor and GPCRs, while Moolman et al. have elaborated on the contributions of adenosine, cAMP/PKA system as well as p 38mapk in eliciting a cardioprotective response during early preconditioning. This section also has two elegant articles on the role of angiotensin II in cardiovascular pathophysiology: Engberding and Grindling and Schaffer and Mozaffari have provided indepth accounts of various signaling pathways induced by angiotensin II and how the dysregulation of this pathway contributes to heightened growth, proliferation, hypertrophy, and cell survival death responses associated with various cardiovascular abnormalities. v vi PrefaceThe second section foc...

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Insulin resistance induces hyperleptinemia, cardiac contractile dysfunction but not cardiac leptin resistance in ventricular myocytes

Cited by 62 publications

References 25 publications

Cardiac overexpression of catalase rescues cardiac contractile dysfunction induced by insulin resistance: role of oxidative stress, protein carbonyl formation and insulin sensitivity

Cardiac overexpression of catalase rescues cardiac contractile dysfunction induced by insulin resistance: role of oxidative stress, protein carbonyl formation and insulin sensitivity

Adipokine Production by Adipose Tissue: A Novel Target for Treating Metabolic Syndrome and its Sequelae

Signal Transduction in the Cardiovascular System in Health and Disease

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