High-intensity interval training (HIIT) alleviated NAFLD feature via <i>miR-122</i> induction in liver of high-fat high-fructose diet induced diabetic rats

Kalaki-Jouybari, Fatemeh; Shanaki, Mehrnoosh; Delfan, Maryam; Gorgani-Firouzjae, Sattar; Khakdan, Soheyla

doi:10.1080/13813455.2018.1510968

Cited by 31 publications

(26 citation statements)

References 61 publications

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“…Similarly, Kalaki‐Jouybari et al 180 also reported a diabetic rat model in Wistar rats after supplementation with HFHSD (30% fat and 20% fructose) for 5 months. These authors confirmed the presence of T2DM features, such as hyperglycaemia (FBG > 200 mg/dl), insulin resistance (elevated HOMA‐IR), dyslipidaemia and hepatic steatosis 180 . However, both studies confirmed the diabetic phenotype in animals displaying FBG > 126 mg/dl, without discriminating between the time period of fasting.…”

Section: Diet‐induced Rodent Modelsmentioning

confidence: 87%

“…Upon dietary supplementation of fructose (25% in drinking water) within an HFD regimen of 4 months, Wistar rats displayed T2DM features comprising systemic hyperglycaemia (FBG > 126 mg/dl), insulin resistance (HOMA‐IR > 2.4), glucose intolerance, dyslipidaemia, oxidative stress associated with endothelial dysfunction and hepatic steatosis 159 . Similarly, Kalaki‐Jouybari et al 180 also reported a diabetic rat model in Wistar rats after supplementation with HFHSD (30% fat and 20% fructose) for 5 months. These authors confirmed the presence of T2DM features, such as hyperglycaemia (FBG > 200 mg/dl), insulin resistance (elevated HOMA‐IR), dyslipidaemia and hepatic steatosis 180 .…”

Section: Diet‐induced Rodent Modelsmentioning

confidence: 96%

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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: Diet‐induced Rodent Modelsmentioning

confidence: 87%

Section: Diet‐induced Rodent Modelsmentioning

confidence: 96%

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

et al. 2020

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“…32 Further, HIIT training reduced NAFLDrelated features by targeting miR122 induction in the liver of high-fat, high-fructose diet-induced diabetic rats. 15 Also, Khakdan et al demonstrated that HIIT intervention effectively improved heart function in an miR195 dependent manner and alleviated high-fat, high-fructose diet-induced cardiomyopathy in diabetic rats. 13 The main finding of this study was that the HFD considerably increased M1 markers and exercise interventions reversed them.…”

Section: Discussionmentioning

confidence: 99%

“…The results demonstrated that exercise intervention, especially HIIT, efficiently alleviated antidiabetic and hypolipidemic markers. 13,15 Recent evidence indicates that HIIT can improve insulin sensitivity and metabolic syndrome; however, the molecular mechanism of HIIT effects has not yet been well-defined. 16 Adipose-tissue inflammation is essential among several molecular mechanisms of the beneficial effects of training.…”

Section: Introductionmentioning

confidence: 99%

<p>High-Intensity Interval Training Reversed High-Fat Diet–Induced M1-Macrophage Polarization in Rat Adipose Tissue via Inhibition of NOTCH Signaling</p>

Shanaki¹,

Khosravi²,

Khoshdooni-Farahani³

et al. 2020

JIR

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Introduction: There is accumulating evidence on the beneficial effect of exercise intervention in the management of metabolic disorders; however, the molecular mechanism is still unclear. Here, the current study aimed to compare the effect of high-intensity interval training (HIIT) and continuous endurance training (CET) on serum and adipose-tissue markers of M1/M2 macrophage polarization. Methods: A total of 45 healthy male Wistar rats were divided into groups of normal chow (n=10) and high-fat diet (HFD) (n=35). Then, rats receiving the HFD were randomly divided into four groups. Training programs were performed for 5 days/week over 10 weeks. The CET protocol included 30 minutes running at 50%-60% of VO 2max . The HIIT protocol consisted of five repeated intervals of 2-minute sprints on the treadmill at 80%-90% VO 2max workload with 1 minute's 30%-35% VO 2max interval for each rat. Then, biochemical parameters were assessed. Macrophage-polarization markers were assessed at mRNA and protein levels by real-time PCR and Western blotting, respectively. Results: Both exercise-training programs, especially HIIT, reversed increased serum biochemical parameters (glucose, triglycerides, cholesterol, Homeostatic Model Assessment of Insulin Resistance, and hsCRP), M1-polarization markers (circulating IL6, TNFα, and adipose-tissue mRNA expression of IL6, TNFα and iNOS), M2 markers (CD206, CD163, and IL10 expression), as well as pIκKB, pNFκB, and NICD expression in HFD-induced diabetes. Conclusion: Our findings suggest that despite devoting less time, the HIIT workout is a more effective intervention for diabetes management. Moreover, HIIT reverses HFD-induced macrophage polarization by targeting the NFκB and NOTCH signaling pathways.

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“…The findings of animal studies [24,25,26,27,28] are highly suggestive of the physiological mechanism of the favorable impact of HIIT on NAFLD. Previous studies have shown that improved hepatic steatosis using HIIT is associated with increased hepatic mitochondrial function (citrate synthase activity and fatty acid oxidation), increased hepatic peroxisome proliferator-activated receptor (PPAR)-α content [24], increased hepatic PPAR-γ and glutathione peroxidase 4 gene expression [25], improved hepatic and adipose tissue insulin sensitivity independent of AMP-activated protein kinase phosphorylation of acetyl-CoA carboxylase [26], increased hepatic miR-122 expression [27], activated hepatic AMP-mediated protein kinase (AMPK) with upregulated adiponectin receptor 2 signaling pathway and downregulated NF-κB signaling pathway [28], and reduced hepatic M1 macrophage polarization markers [24], which suppress de novo hepatic lipogenesis [24,28]. AMPK-mediated improvement in mitochondrial function seems to play a key role in the treatment of NAFLD.…”

Section: Possible Physiological Mechanismsmentioning

confidence: 99%

Perspectives on Interval Exercise Interventions for Non-Alcoholic Fatty Liver Disease

Hamasaki¹

2019

Medicines

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Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and is associated with an increased risk of type 2 diabetes, cardiovascular disease, cirrhosis, and liver cancer. Exercise therapy is the most effective treatment for patients with NAFLD. High-intensity interval training (HIIT) is attracting attention as a time-efficient and an effective exercise modality for treating patients with NAFLD. Previous studies have shown that HIIT can reduce fat mass, visceral adipose tissue, and intrahepatic lipid levels and improve hepatic stiffness. HIIT may be an optimal exercise therapy to improve NAFLD in patients with a lack of time.

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High-intensity interval training (HIIT) alleviated NAFLD feature via miR-122 induction in liver of high-fat high-fructose diet induced diabetic rats

Cited by 31 publications

References 61 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

<p>High-Intensity Interval Training Reversed High-Fat Diet–Induced M1-Macrophage Polarization in Rat Adipose Tissue via Inhibition of NOTCH Signaling</p>

Perspectives on Interval Exercise Interventions for Non-Alcoholic Fatty Liver Disease

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