A Cardiac Amino-Terminal GRK2 Peptide Inhibits Maladaptive Adipocyte Hypertrophy and Insulin Resistance During Diet-Induced Obesity

Manaserh, Iyad H.; Błędzka, Kamila; Junker, Alex; Grondolsky, Jessica; Schumacher, Sarah M.

doi:10.1016/j.jacbts.2022.01.010

Cited by 8 publications

(7 citation statements)

References 61 publications

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“…Glucagon-like peptide-1 receptor analogues, cardiac amino-terminal GRK2 peptides, and protease A-digested crude-chalaza hydrolysates could suppress blood lipids and obesity in mice orally administered with HFD. [27][28][29] The liver is an important tissue for lipid metabolism in the body. Cholesterol-7𝛼-hydroxylase (CYP7A1) is contained in the liver tissue, which can convert cholesterol into bile acid and leave the body to reduce the cholesterol content in the body.…”

Section: Discussionmentioning

confidence: 99%

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Hypolipidemic and Anti‐Obesity Effect of Anserine on Mice Orally Administered with High‐Fat Diet via Regulating SREBP‐1, NLRP3, and UCP‐1

Luo,

Chen,

et al. 2024

Molecular Nutrition Food Res

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To investigate the efficacy of anserine on antiobesity, C57BL/6 mice are orally administered with a high‐fat diet (HFD) and different doses of anserine (60, 120, and 240 mg/kg/day) for 16 weeks. Body weight, lipid, and epididymal fat content in mice are measured, and their liver damage is observed. The results display that the body weight, epididymal fat content, and low‐density lipoprotein cholesterol (LDL‐C) content in anserine groups are decreased by 4.36–18.71%, 7.57–35.12%, and 24.32–44.40%, respectively. To further investigate the antiobesity mechanism of anserine, the expression of SREBP‐1, NLRP3, NF‐κB p65 (p65), and p‐NF‐κB p65 (p‐p65) proteins in the liver and peroxisome proliferator‐activated receptor gamma coactivator 1α (PGC1‐α) and UCP‐1 proteins in brown adipose tissue (BAT) is analyzed by Western blot. Results show that anserine can significantly decrease the expression of the NLRP3, p65, p‐p65, and the SREBP‐1 proteins and increase the expression of the PGC1‐α and UCP‐1 proteins. This study demonstrates that anserine lowered blood lipids and prevented obesity; its antiobesity mechanism may be related to the activation of brown fat by inflammation.

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Section: Discussionmentioning

confidence: 99%

“…Glucagon‐like peptide‐1 receptor analogues, cardiac amino‐terminal GRK2 peptides, and protease A‐digested crude‐chalaza hydrolysates could suppress blood lipids and obesity in mice orally administered with HFD. [ 27–29 ]…”

Section: Discussionmentioning

confidence: 99%

Hypolipidemic and Anti‐Obesity Effect of Anserine on Mice Orally Administered with High‐Fat Diet via Regulating SREBP‐1, NLRP3, and UCP‐1

Luo,

Chen,

et al. 2024

Molecular Nutrition Food Res

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“…The findings of Manaserh et al 2 also raise a number of additional interesting questions. For example, cardiomyocyte-specific βARKnt expression was shown to modestly increase fibrotic area in the heart with high-fat feeding, despite no difference in fibrosis in mice fed normal chow.…”

mentioning

confidence: 93%

mentioning

confidence: 99%

“…In this issue of JACC: Basic to Translational Science , Manaserh et al 2 further examined the role of βARK1 in the heart-fat axis, highlighting novel links between cardiac β-adrenergic signaling and systemic metabolism. 2 Mice expressing βARKnt specifically in the heart were provided a high fat diet (HFD) and were shown to gain weight similar to nontransgenic littermate controls. However, the authors observed striking differences in glucose handling: although fasting glucose levels, glucose tolerance, and insulin tolerance were worsened by HFD in control mice, the βARKnt mice were largely protected against diet-induced insulin resistance.…”

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confidence: 99%

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Cardiac GRK2 and the Communicative Axis Between Heart and Fat

Hill

2022

JACC: Basic to Translational Science

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Progress in the treatment of diabetic cardiomyopathy, a systematic review

Shou,

Li,

Fang

et al. 2024

Pharmacology Res & Perspec

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Diabetic cardiomyopathy (DCM) is a condition characterized by myocardial dysfunction that occurs in individuals with diabetes, in the absence of coronary artery disease, valve disease, and other conventional cardiovascular risk factors such as hypertension and dyslipidemia. It is considered a significant and consequential complication of diabetes in the field of cardiovascular medicine. The primary pathological manifestations include myocardial hypertrophy, myocardial fibrosis, and impaired ventricular function, which can lead to widespread myocardial necrosis. Ultimately, this can progress to the development of heart failure, arrhythmias, and cardiogenic shock, with severe cases even resulting in sudden cardiac death. Despite several decades of both fundamental and clinical research conducted globally, there are currently no specific targeted therapies available for DCM in clinical practice, and the incidence and mortality rates of heart failure remain persistently high. Thus, this article provides an overview of the current treatment modalities and novel techniques pertaining to DCM, aiming to offer valuable insights and support to researchers dedicated to investigating this complex condition.

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A Cardiac Amino-Terminal GRK2 Peptide Inhibits Maladaptive Adipocyte Hypertrophy and Insulin Resistance During Diet-Induced Obesity

Cited by 8 publications

References 61 publications

Hypolipidemic and Anti‐Obesity Effect of Anserine on Mice Orally Administered with High‐Fat Diet via Regulating SREBP‐1, NLRP3, and UCP‐1

Hypolipidemic and Anti‐Obesity Effect of Anserine on Mice Orally Administered with High‐Fat Diet via Regulating SREBP‐1, NLRP3, and UCP‐1

Cardiac GRK2 and the Communicative Axis Between Heart and Fat

Progress in the treatment of diabetic cardiomyopathy, a systematic review

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