Curcumin attenuates cardiomyocyte hypertrophy induced by high glucose and insulin via the PPARγ/Akt/NO signaling pathway

Chen, Rongchun; Peng, Xing; Du, Weimin; Wu, Yang; Huang, Bo; Xue, Lingui; Wu, Qin; Qiu, Hongmei; Jiang, Qingsong

doi:10.1016/j.diabres.2015.02.012

Cited by 31 publications

(21 citation statements)

References 26 publications

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“…Our data clearly demonstrate that both hyperglycemia (25 mM) and hyperinsulinemia (>100 nM) are necessary for generating insulin resistance in LMCs during 48 h treatment (Fig. 2, ), which is consistent with the insulin resistance responses across different cell lines (59, 60). Although a direct causal relationship between oxidative stress and insulin resistance has not been clearly established, there is a significant evidence of a link between these 2 mechanisms in several metabolic diseases (66–68).…”

Section: Discussionsupporting

confidence: 87%

“…Insulin resistance mechanisms have been studied in several muscle types but remain undefined in the lymphatic muscle (58)(59)(60)(61). In ventricular cardiomyocytes, hyperglycemia alone have been shown to induce insulin resistance by significantly decreasing glucose uptake and promoting myocyte dysfunction, even in low-insulin conditions (62,63).…”

Section: Discussionmentioning

confidence: 99%

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Hyperglycemia‐ and hyperinsulinemia‐induced insulin resistance causes alterations in cellular bioenergetics and activation of inflammatory signaling in lymphatic muscle

Lee

Fluckey²,

Chakraborty

et al. 2017

FASEB j.

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Insulin resistance is a well-known risk factor for obesity, metabolic syndrome (MetSyn) and associated cardiovascular diseases, but its mechanisms are undefined in the lymphatics. Mesenteric lymphatic vessels from MetSyn or LPS-injected rats exhibited impaired intrinsic contractile activity and associated inflammatory changes. Hence, we hypothesized that insulin resistance in lymphatic muscle cells (LMCs) affects cell bioenergetics and signaling pathways that consequently alter contractility. LMCs were treated with different concentrations of insulin or glucose or both at various time points to determine insulin resistance. Onset of insulin resistance significantly impaired glucose uptake, mitochondrial function, oxygen consumption rates, glycolysis, lactic acid, and ATP production in LMCs. Hyperglycemia and hyperinsulinemia also impaired the PI3K/Akt while enhancing the ERK/p38MAPK/JNK pathways in LMCs. Increased NF-κB nuclear translocation and macrophage chemoattractant protein-1 and VCAM-1 levels in insulin-resistant LMCs indicated activation of inflammatory mechanisms. In addition, increased phosphorylation of myosin light chain-20, a key regulator of lymphatic muscle contraction, was observed in insulin-resistant LMCs. Therefore, our data elucidate the mechanisms of insulin resistance in LMCs and provide the first evidence that hyperglycemia and hyperinsulinemia promote insulin resistance and impair lymphatic contractile status by reducing glucose uptake, altering cellular metabolic pathways, and activating inflammatory signaling cascades.-Lee, Y., Fluckey, J. D., Chakraborty, S., Muthuchamy, M. Hyperglycemia- and hyperinsulinemia-induced insulin resistance causes alterations in cellular bioenergetics and activation of inflammatory signaling in lymphatic muscle.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Hyperglycemia‐ and hyperinsulinemia‐induced insulin resistance causes alterations in cellular bioenergetics and activation of inflammatory signaling in lymphatic muscle

Lee

Fluckey²,

Chakraborty

et al. 2017

FASEB j.

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“…In contrast to insulin, hyperglycemia did not alter glucose uptake at any of the time points (Figure B). Previous studies showed both hyperglycemia and hyperinsulinemia were necessary to develop insulin resistance in various cell types, including LMCs . In the presence of insulin and HG, LECs showed an increase in glucose uptake within 5 minutes (+2.46‐fold vs control, P < 0.001).…”

Section: Resultsmentioning

confidence: 85%

Insulin resistance disrupts cell integrity, mitochondrial function, and inflammatory signaling in lymphatic endothelium

et al. 2018

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“…Moreover, it was suggested that exosomal 15d-PGJ2 was already activated by PPAR-γ before entering recipient cells, because PPAR-γ was also enriched in exosomes from human plasma (Looze et al, 2009). Because PPARγ activation was demonstrated to attenuate cardiomyocyte hypertrophy induced by high glucose and insulin (Chen et al, 2015; Peng et al, 2015), exosomal 15d-PGJ2 is a promising strategy for preventing cardiomyopathy in patients with diabetes.…”

Section: Other Types Of Exosomal Cargoesmentioning

confidence: 99%

Exosomes: A Rising Star in Failing Hearts

Chen

Yang

2017

Front. Physiol.

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Although exosomes were previously recognized as a mechanism for discharging useless cellular components, growing evidence has elucidated their roles in conveying information between cells. They contribute to cell–cell communication by carrying nucleic acids, proteins and lipids that can, in turn, regulate behavior of the target cells. Recent research suggested that exosomes extensively participate in progression of diverse cardiovascular diseases (CVDs), such as myocardial infarction, cardiomyopathy, pulmonary arterial hypertension and others. Here, we summarize effects of exosome-derived molecules (mainly microRNAs and proteins) on cardiac function, to examine their potential applications as biomarkers or therapeutics in CVDs.

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Curcumin attenuates cardiomyocyte hypertrophy induced by high glucose and insulin via the PPARγ/Akt/NO signaling pathway

Cited by 31 publications

References 26 publications

Hyperglycemia‐ and hyperinsulinemia‐induced insulin resistance causes alterations in cellular bioenergetics and activation of inflammatory signaling in lymphatic muscle

Hyperglycemia‐ and hyperinsulinemia‐induced insulin resistance causes alterations in cellular bioenergetics and activation of inflammatory signaling in lymphatic muscle

Insulin resistance disrupts cell integrity, mitochondrial function, and inflammatory signaling in lymphatic endothelium

Exosomes: A Rising Star in Failing Hearts

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