Association of mitochondrial dysfunction and lipid metabolism with type 2 diabetes mellitus: A review of literature

Haghani, Karimeh; Asadi, Pouyan; Taheripak, Gholamreza; Noori-Zadeh, Ali; Darabi, Shahram; Bakhtiyari, Salar

doi:10.1007/s11515-018-1521-3

Cited by 3 publications

(2 citation statements)

References 109 publications

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“…Insulin resistance is a major pathogenic factor of T2DM. Insulin maintains glucose homeostasis as an effective regulator of glucose metabolism (14). Insulin resistance means the reduced sensitivity of tissues to insulin-mediated biologic activity (15), which will result in increased adverse events such as obesity, hypertension, and dyslipidemia in patients with T2DM (16).…”

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confidence: 99%

MiR-21 antagomir improves insulin resistance and lipid metabolism disorder in streptozotocin-induced type 2 diabetes mellitus rats

Wang¹,

Yang²,

Yang³

et al. 2020

Ann Palliat Med

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Background: Type 2 diabetes mellitus (T2DM) is a major cause of death with an increasing incidence at an epidemic rate. The existing treatments for T2DM lack long-term effective blood glucose control. In this study, the effects of miR-21 antagomir on T2DM and the related mechanism were investigated using streptozotocin (STZ)-induced T2DM rats.Methods: 30 T2DM rats were randomly divided into 3 groups (n=10): T2DM group, T2DM rats with miR-21 antagomir group, T2DM rats with NC antagomir group. The expression of miR-21 in rats was detected by qRT-PCR. blood glucose, triacylglycerol (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-Cho), insulin, adiponectin, ITT and GTT were detected. The expression of TIMP3 in si-TIMP3 rats and the expression of TIMP3 in T2DM rats with miR-21 antagomir and si-TIMP3 was detected by Western blotting.Results: We found that miR-21 antagomir reduced blood glucose concentration in T2DM rats. MiR-21 antagomir improved lipid metabolic disorder by decreasing the levels of triacylglycerol (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-Cho) and increasing the level of high-density lipoprotein cholesterol (HDL-Cho). Also, miR-21 antagomir reduced the value of homeostasis model assessment of insulin resistance (HOMA-IR), hemoglobin A1c (HbAc1), plasma insulin, and up-regulated the plasma adiponectin. These results, combined with insulin tolerance tests (ITT) and glucose tolerance tests (GTT) results, showed that miR-21 improved insulin resistance in STZ-induced T2DM rats. Then the target relationship between miR-21 and tissue inhibitor of metalloproteinases 3 (TIMP3) was proved by luciferase reporter assay. More impressively, miR-21 significantly increased the expression level of TIMP3 in STZ-induced T2DM rats. Conclusion:Our study taken together has shown that miR-21 antagomir improved insulin resistance and lipid metabolism disorder in STZ-induced T2DM rats by up-regulating the expression level of TIMP3. This study suggested that miR-21 antagomir could be used as an effective therapeutic strategy and the underlying mechanism was revealed.

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Section: Introductionmentioning

confidence: 99%

MiR-21 antagomir improves insulin resistance and lipid metabolism disorder in streptozotocin-induced type 2 diabetes mellitus rats

Wang¹,

Yang²,

Yang³

et al. 2020

Ann Palliat Med

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“…Moreover, it is known that the mitochondria are the main regulators of cellular metabolism and apoptosis [ 4 ]. In addition, damaged or malfunctioning mitochondria are increasingly recognized as the main cause of improper functioning of not only inflammation but also lipid metabolism [ 5 , 6 ].…”

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confidence: 99%

Molecular Aspects of Inflammation and Lipid Metabolism in Health and Disease: The Role of the Mitochondria

Sukhorukov,

Orekhov

2024

IJMS

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ApoEVs Transfer Mitochondrial Component to Modulate Macrophages in Periodontal Regeneration

Liu,

Lyu,

et al. 2024

Oral Diseases

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ObjectiveMacrophages are key players in the host immune response to periodontal pathogens and tissue repair. The aim of this study was to explore the potential of apoptotic cell‐derived extracellular vesicles (ApoEVs) in modulating the mitochondrial function of macrophages as a mean to enhance periodontal tissue regeneration.Subjects and MethodsApoEVs were extracted from periodontal ligament stem cells (PDLSCs) and characterized to observe their effects on macrophage function. In vivo experiments, ApoEVs were mixed with hyaluronic acid and injected into the periodontal pockets of rats with periodontitis to observe their impact on periodontal tissue regeneration and the immune microenvironment. Functional assays were conducted to confirm whether ApoEVs contained mitochondrial components and which specific components were transferred to regulate macrophage function.ResultsThe experimental findings showed that treatment of ApoEVs efficiently restored the homeostasis of macrophage and improved tissue regeneration in a periodontitis rat model. Mechanism investigation demonstrated that the efferocytosis of ApoEVs resulted in the transfer of mitochondrial components from PDLSCs to macrophage. The increased mitochondrial components within macrophages improved mitochondrial function and polarization of macrophages towards the anti‐inflammatory M2 phenotype, resulting in the improvement of inflammatory environment in periodontal tissues.ConclusionApoEVs can transfer mtDNA to enhance mitochondrial function in macrophages, fostering their transition to an anti‐inflammatory phenotype. Ultimately, this process improves the immune microenvironment in periodontitis and promotes periodontal tissue regeneration.

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Association of mitochondrial dysfunction and lipid metabolism with type 2 diabetes mellitus: A review of literature

Cited by 3 publications

References 109 publications

MiR-21 antagomir improves insulin resistance and lipid metabolism disorder in streptozotocin-induced type 2 diabetes mellitus rats

MiR-21 antagomir improves insulin resistance and lipid metabolism disorder in streptozotocin-induced type 2 diabetes mellitus rats

Molecular Aspects of Inflammation and Lipid Metabolism in Health and Disease: The Role of the Mitochondria

ApoEVs Transfer Mitochondrial Component to Modulate Macrophages in Periodontal Regeneration

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