Comparisons of cardioprotective efficacy between fibroblast growth factor 21 and dipeptidyl peptidase‐4 inhibitor in prediabetic rats

Tanajak, Pongpan; Sa‐nguanmoo, Piangkwan; Apaijai, Nattayaporn; Wang, Xiaojie; Liang, Guang; Li, Xiaokun; Jiang, Chao; Chattipakorn, Siriporn C.; Chattipakorn, Nipon

doi:10.1111/1755-5922.12263

Cited by 8 publications

(12 citation statements)

References 49 publications

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“…Long-term HFD intake in several strains of rat and mouse can cause hyperlipidaemia, peripheral insulin resistance, moderate hyperglycaemia and IGT, together with increase in the expression of inflammation and oxidative stress markers. 124,125 In rodents on HFD feeding, insulin resistance is followed by insufficient β-cell compensation, resulting in hyperinsulinaemia and altered glucose metabolism. 126 The effects of HFD depend not only on the source and percentage of calories but also on the animal species and strains used.…”

Section: Prediabetesmentioning

confidence: 99%

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

et al. 2020

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Diet is a critical element determining human health and diseases, and unbalanced food habits are major risk factors for the development of obesity and related metabolic disorders. Despite technological and pharmacological advances, as well as intensification of awareness campaigns, the prevalence of metabolic disorders worldwide is still increasing. Thus, novel therapeutic approaches with increased efficacy are urgently required, which often depends on cellular and molecular investigations using robust animal models. In the absence of perfect rodent models, those induced by excessive consumption of fat and sugars better replicate the key aspects that are the root causes of human metabolic diseases. However, the results obtained using these models cannot be directly compared, particularly because of the use of different dietary protocols, and animal species and strains, among other confounding factors. This review article revisits diet-induced models of obesity and related metabolic disorders, namely, metabolic syndrome, prediabetes, diabetes and nonalcoholic fatty liver disease. A critical analysis focused on the main pathophysiological features of rodent models, as opposed to the criteria defined for humans, is provided as a practical guide with a translational perspective for the establishment of animal models of obesity-related metabolic diseases.

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Section: Prediabetesmentioning

confidence: 99%

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

et al. 2020

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“…Regarding cell death, cardiac apoptosis has been reported in HFD-fed rats (Hsieh et al 2016, Tanajak et al 2017, Chen et al 2019, while the report on cardiac necroptosis following HFD consumption is limited (Giricz et al 2017). Necroptosis is initiated by inflammation (Dhuriya & Sharma 2018), as we showed that cardiac TNF-α protein levels were upregulated in our prediabetic rats.…”

Section: Discussionmentioning

confidence: 46%

Necrostatin-1 reduces cardiac and mitochondrial dysfunction in prediabetic rats

Apaijai

Jinawong

Singhanat

et al. 2021

Journal of Endocrinology

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High fat diet (HFD) consumption induces prediabetes and left ventricular dysfunction through many pathways including the cell death pathway, necroptosis. Although benefits of necroptosis inhibitor (necrostatin-1 or Nec-1) in the brain of prediabetic rats have been shown, the effects of Nec-1 on cardiac autonomic function, blood pressure, and cardiac function, and the mechanisms involved have not been investigated. Male Wistar rats were fed with either a normal diet (n=8) or HFD (n=24) for 12 weeks to induce prediabetes. Prediabetic rats were randomly assigned into 3 interventional groups (n=8/group): 1) vehicle, 2) Nec-1 (1.65 mg/kg, sc injection), and 3) metformin (300 mg/kg, oral gavage feeding). Treatments lasted for 8 weeks. Normal saline was given to the vehicle group and a non-interventional group. Metabolic parameters, cardiac function and biochemical parameters were assessed. Prediabetic rats exhibited peripheral metabolic impairment as indicated by increased body weight, hyperinsulinemia with euglycemia, and dyslipidemia. Prediabetic rats also exhibited cardiac autonomic imbalance, high blood pressure, cardiac dysfunction, cardiac mitochondrial dysfunction, mitochondrial dynamic imbalance, and increased necroptosis and apoptosis. Treatment with Nec-1 did not affect peripheral metabolic parameters, however it effectively reduced cardiac autonomic imbalance, blood pressure, and cardiac dysfunction via reduced cardiac inflammation, necroptosis, mitochondrial dysfunction, and increased mitochondrial fusion. Treatment with metformin reduced peripheral metabolic impairment and cardiac dysfunction via decreased cardiac mitochondrial dysfunction, mitochondrial dynamic imbalance, and apoptosis. In summary, Nec-1 directly suppressed necroptosis, cardiac mitochondrial dysfunction, and increased mitochondrial fusion independent to peripheral metabolic function, leading to an improvement in cardiac function in prediabetic rats.

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“…Moreover, vildagliptin halted NLRP3 inflammasome activation and decreased IL-1β and IL-18 levels in free fatty acid-induced HUVECs [82].The anti-inflammatory properties of DPP-4i have been shown in different T1DM and T2DM animal models as well. Sitagliptin decreased serum levels of hs-CRP, IL-1β, MCP-1, and TNF-α in ZDF rats, while vildagliptin and linagliptin had a similar effect in high-fat diet-induced diabetic Wistar rats and western diet-induced diabetic C56Bl/6J mice [83][84][85]. In an STZ-induced T1DM diabetic Wistar rat model, sitagliptin also attenuated diabetic cardiomyopathy via the modulation of IL-6 levels and the JAK/STAT signaling pathway [86].…”

Section: Dpp-4imentioning

confidence: 92%

An Overview of the Cardioprotective Effects of Novel Antidiabetic Classes: Focus on Inflammation, Oxidative Stress, and Fibrosis

Balogh

Wagner

Fekete

2023

IJMS

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Metabolic diseases, particularly diabetes mellitus (DM), are significant global public health concerns. Despite the widespread use of standard-of-care therapies, cardiovascular disease (CVD) remains the leading cause of death among diabetic patients. Early and evidence-based interventions to reduce CVD are urgently needed. Large clinical trials have recently shown that sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RA) ameliorate adverse cardiorenal outcomes in patients with type 2 DM. These quite unexpected positive results represent a paradigm shift in type 2 DM management, from the sole importance of glycemic control to the simultaneous improvement of cardiovascular outcomes. Moreover, SGLT2i is also found to be cardio- and nephroprotective in non-diabetic patients. Several mechanisms, which may be potentially independent or at least separate from the reduction in blood glucose levels, have already been identified behind the beneficial effect of these drugs. However, there is still much to be understood regarding the exact pathomechanisms. This review provides an overview of the current literature and sheds light on the modes of action of novel antidiabetic drugs, focusing on inflammation, oxidative stress, and fibrosis.

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Comparisons of cardioprotective efficacy between fibroblast growth factor 21 and dipeptidyl peptidase‐4 inhibitor in prediabetic rats

Abstract: FGF21 exerts better metabolic regulation and inflammation reduction than vildagliptin. However, FGF21 and vildagliptin shared a similar efficacy for cardioprotection by improving HRV and LV function.

Cited by 8 publications

References 49 publications

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

Necrostatin-1 reduces cardiac and mitochondrial dysfunction in prediabetic rats

An Overview of the Cardioprotective Effects of Novel Antidiabetic Classes: Focus on Inflammation, Oxidative Stress, and Fibrosis

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