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

2003 ◽  
Vol 27 (10) ◽  
pp. 1196-1203 ◽  
Author(s):  
K K Hintz ◽  
N S Aberle ◽  
J Ren
Keyword(s):  
Insulin Resistance ◽  
Ventricular Myocytes ◽  
Leptin Resistance ◽  
Contractile Dysfunction ◽  
Cardiac Contractile ◽  
Cardiac Contractile Dysfunction

scholarly journals Transgenic overexpression of insulin-like growth factor I prevents streptozotocin-induced cardiac contractile dysfunction and beta-adrenergic response in ventricular myocytes

2004 ◽  
Vol 180 (1) ◽  
pp. 175-182 ◽  
Author(s):  
FL Norby ◽  
J Kajstura ◽  
P Anversa ◽  
J Ren ◽  
Keyword(s):  
Contractile Response ◽  
Ventricular Myocytes ◽  
Contractile Dysfunction ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Factor I ◽  
Cardiac Contractile ◽  
Adrenergic Response ◽  
Igf I ◽  
Cardiac Contractile Dysfunction

Diabetic cardiomyopathy is characterized by cardiac dysfunction and altered level/function of insulin-like growth factor I (IGF-I). Both endogenous and exogenous IGF-I have been shown to effectively alleviate diabetes-induced cardiac dysfunction and oxidative stress. This study was designed to examine the effect of cardiac overexpression of IGF-I on streptozotocin (STZ)-induced cardiac contractile dysfunction in mouse myocytes. Both IGF-I heterozygous transgenic mice and their wild-type FVB littermates were made diabetic with a single injection of STZ (200 mg/kg, i.p.) and maintained for 2 weeks. The following mechanical indices were evaluated in ventricular myocytes: peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR90) and maximal velocity of shortening/relengthening (+/- dL/dt). Intracellular Ca2+ was evaluated as resting and peak intracellular Ca2+ levels, Ca2+-induced Ca2+ release and intracellular Ca2+ decay rate (tau). STZ led to hyperglycemia in FVB and IGF-I mice. STZ treatment prolonged TPS and TR90, reduced Ca2+-induced Ca2+ release, increased resting intracellular Ca2+ levels and slowed tau associated with normal PS and +/- dL/dt. All of which, except the elevated resting intracellular Ca2+, were prevented by the IGF-I transgene. In addition, myocytes from STZ-treated FVB mice displayed an attenuated contractile response to the beta-adrenergic agonist isoproterenol, which was restored by the IGF-I transgene. Contractile response to the alpha-adrenergic agonist phenylephrine and angiotensin II was not affected by either STZ treatment or IGF-I. These results validate the beneficial role of IGF-I in diabetic cardiomyopathy, possibly due to an improved beta-adrenergic response.

scholarly journals Zbtb20 deficiency causes cardiac contractile dysfunction in mice

2020 ◽  
Vol 34 (10) ◽  
pp. 13862-13876
Author(s):  
An‐Jing Ren ◽  
Chao Chen ◽  
Sha Zhang ◽  
Mengna Liu ◽  
Chunchun Wei ◽  
...  
Keyword(s):  
Contractile Dysfunction ◽  
Cardiac Contractile ◽  
Cardiac Contractile Dysfunction
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