Profile of cardiac lipid metabolism in STZ-induced diabetic mice

Li, Wenjie; Yao, Min; Wang, Ruonan; Shi, Yun; Hou, Lianguo; Hou, Ziyuan; Lian, Kaoqi; Zhang, Nan; Wang, Yaqi; Li, Weiwei; Wang, Wei; Jiang, Lingling

doi:10.1186/s12944-018-0872-8

Cited by 35 publications

(27 citation statements)

References 45 publications

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“…Insulin deficiency decreases glucose delivery in cardiomyocytes and use of fatty acids as an alternative energy source. This elevation increases subsequent triglyceride synthesis in the heart leading to cellular lipotoxicity and the beginning of cardiac dysfunction [20]. In accordance with these reports, in the present study, hyperlipidemia characterized by increased levels of cholesterol, triglycerides, LDL and VLDL were observed in untreated diabetic animals.…”

Section: Discussionsupporting

confidence: 92%

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Sodium current inhibitor ranolazine ameliorates experimentally induced diabetic cardiomyopathy

Gandhi¹,

Singh²,

Patel³

et al. 2020

JRP

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Ranolazine is an anti-ischemic drug with glucose lowering effect. Our study scrutinized the effect of ranolazine on Streptozotocin (STZ) induced diabetic cardiomyopathy, emphasizing role of Sarcoplasmic Endoplasmic Reticulum Calcium ATPase (SERCA) pump. STZ induced diabetic rats showed significant hyperglycaemia with weight loss, hyperlipidaemia, increased cardiovascular risk indices as well as atherogenic index of plasma, Left Ventricular (LV) dysfunction, abnormal electrocardiography (ECG) and elevated cardiac biomarkers (CK-MB, LDH and AST). Twelve weeks ranolazine treatment ameliorated diabetes associated biochemical alterations and LV function along with ECG. The diabetic heart showed increased lipid peroxidation and compromised antioxidant defence mechanism which was reversed by ranolazine treatment. Reduced SERCA expressions were recognised in STZ treated diabetic rats. Ranolazine amplified SERCA expressions thus by regulating intracellular calcium homeostasis and keeping diabetic cardiomyopathy at bay. Ranolazine also prevented histological alterations in the heart and pancreas. Our results may open novel avenues for designing treatment strategies using ranolazine against diabetic cardiomyopathy.

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Section: Discussionsupporting

confidence: 92%

“…In diabetic state, due to decrease in glucose uptake by cardiac cells, the fatty acid is used as a fuel [20]. The oxidation of this causes increase in lipid levels which are also observed in the current study.…”

Section: Effect On Lipid Profile In Stz Induced Dcmsupporting

confidence: 80%

Sodium current inhibitor ranolazine ameliorates experimentally induced diabetic cardiomyopathy

Gandhi¹,

Singh²,

Patel³

et al. 2020

JRP

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“…Phosphocholine is attributed to toxic lipid species, and was found to be higher in diabetic mice. 34 It is normal that phosphocholine serum levels are higher in these patients. Formate is associated with vitamin B12 metabolism.…”

Section: Discussionmentioning

confidence: 95%

“…In these untreated patients, higher serum methionine levels may indicate a worsened physiological state of MetS. Phosphocholine is attributed to toxic lipid species, and was found to be higher in diabetic mice 34 . It is normal that phosphocholine serum levels are higher in these patients.…”

Section: Discussionmentioning

confidence: 98%

Serum Metabolomic Profiles Associated With Untreated Metabolic Syndrome Patients in the Chinese Population

Wang

Zhuang

et al. 2020

Clinical Translational Sci

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Metabolomics is a promising technology for elucidating the mechanisms of metabolic syndrome (MetS). However, measurements in patients with MetS under different conditions vary. Metabolomics experiments in different populations and pathophysiological conditions are, therefore, indispensable. We performed a serum metabolomics investigation in untreated patients with MetS in the Chinese population. Untreated patients with MetS were recruited to this study. Metabolites were measured using a traditional 1H nuclear magnetic resonance (NMR) experiment followed by principal component analysis (PCA) and orthogonal partial least squares discriminant analysis (OPLS‐DA). Key metabolic pathways were identified by searching the Kyoto Encyclopedia of Genes and Genomes Pathway Database. A total of 28 patients with MetS and 30 healthy subjects were enrolled. All patients were untreated because they were unaware of or neglected to treat their MetS. By 1H NMR, we identified 49 known substances. Following PCA and OPLS‐DA, 36 metabolites were confirmed to be closely associated with MetS compared with the control group; 33 metabolites were increased, whereas 3 metabolites were reduced. Importantly, 14 metabolites that changed in the serum of these untreated patients with MetS were previously unreported. Pathway analysis revealed the top 15 metabolic pathways associated with untreated MetS, which included 3 amino acid metabolic pathways. Our data suggest that untreated patients exhibit a worse pathophysiologic manifestation, which may result in more rapid progression of MetS. Thus, we propose that health education be reinforced to improve the public’s knowledge, attitude, and practice regarding MetS. The rates of “untreated” patients due to unawareness and neglect must be reduced immediately.

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“…Indeed, it is known that 3-ketoacyl-CoA thiolase abolishes BNIP3-mediated apoptosis and mitochondrial damage [83]. It was shown that 3-ketoacyl-CoA thiolase increased in the heart of STZ-induced diabetic mice [84]. The -3.4-fold decrease in the disulfide-isomerase protein level may also contribute to the suppression of apoptosis (Table 5) [85].…”

Section: Resultsmentioning

confidence: 99%

Prediabetes Induced by Fructose-Enriched Diet Influences Cardiac Lipidome and Proteome and Leads to Deterioration of Cardiac Function prior to the Development of Excessive Oxidative Stress and Cell Damage

Szűcs

Sója

Péter

et al. 2019

Oxidative Medicine and Cellular Longevity

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Prediabetes is a condition affecting more than 35% of the population. In some forms, excessive carbohydrate intake (primarily refined sugar) plays a prominent role. Prediabetes is a symptomless, mostly unrecognized disease which increases cardiovascular risk. In our work, we examined the effect of a fructose-enriched diet on cardiac function and lipidome as well as proteome of cardiac muscle. Male Wistar rats were divided into two groups. The control group received a normal diet while the fructose-fed group received 60% fructose-supplemented chow for 24 weeks. Fasting blood glucose measurement and oral glucose tolerance test (OGTT) showed slightly but significantly elevated values due to fructose feeding indicating development of a prediabetic condition. Both echocardiography and isolated working heart perfusion performed at the end of the feeding protocol demonstrated diastolic cardiac dysfunction in the fructose-fed group. Mass spectrometry-based, high-performance lipidomic and proteomic analyses were executed from cardiac tissue. The lipidomic analysis revealed complex rearrangement of the whole lipidome with special emphasis on defects in cardiolipin remodeling. The proteomic analysis showed significant changes in 75 cardiac proteins due to fructose feeding including mitochondria-, apoptosis-, and oxidative stress-related proteins. Nevertheless, just very weak or no signs of apoptosis induction and oxidative stress were detected in the hearts of fructose-fed rats. Our results suggest that fructose feeding induces marked alterations in the cardiac lipidome, especially in cardiolipin remodeling, which leads to mitochondrial dysfunction and impaired cardiac function. However, at the same time, several adaptive responses are induced at the proteome level in order to maintain a homeostatic balance. These findings demonstrate that even very early stages of prediabetes can impair cardiac function and can result in significant changes in the lipidome and proteome of the heart prior to the development of excessive oxidative stress and cell damage.

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Profile of cardiac lipid metabolism in STZ-induced diabetic mice

Cited by 35 publications

References 45 publications

Sodium current inhibitor ranolazine ameliorates experimentally induced diabetic cardiomyopathy

Sodium current inhibitor ranolazine ameliorates experimentally induced diabetic cardiomyopathy

Serum Metabolomic Profiles Associated With Untreated Metabolic Syndrome Patients in the Chinese Population

Prediabetes Induced by Fructose-Enriched Diet Influences Cardiac Lipidome and Proteome and Leads to Deterioration of Cardiac Function prior to the Development of Excessive Oxidative Stress and Cell Damage

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