Comparative study on molecular mechanism of diabetic myopathy in two different types of streptozotocin-induced diabetic models

Saliu, Tolulope Peter; Kumrungsee, Thanutchaporn; Miyata, Kenshu; Tominaga, H.; Yazawa, Nao; Hashimoto, Kenkichi; Kamesawa, Mion

doi:10.1016/j.lfs.2021.120183

Cited by 6 publications

(5 citation statements)

References 65 publications

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“…Therefore, STZ is widely used experimentally to induce animal models for type 1 DM [35]. A recent study demonstrated that STZ-induced type 1 DM is suitable for studying the molecular mechanism of diabetic myopathy in animal models [36]. Diabetic rats used in this study exhibit hyperglycemia, elevated levels of pro-inflammatory cytokine skeletal muscle mRNA expression (TNF-), MDA levels of proinflammatory cytokine (TNF-α), and atrophy-related genes (FBXO32 and MuRF1) MDA levels (a marker of oxidative stress), as well as muscle fiber atrophy as indicated by histological assessment.…”

Section: Discussionmentioning

confidence: 99%

“…Hyperglycemia, a key feature of diabetes, plays a pivotal role in developing several diabetes complications [39], including diabetic myopathy [36]. General mechanisms of hyperglycemia-mediated pathophysiological complications and organ dysfunction include enhancing oxidative stress, upsurging polyol pathway, activating protein kinase C (PKC), and enhancing hexosamine biosynthetic pathway (HBP), promoting the formation of advanced glycation end-products (AGEs), and finally altering gene expressions [39].…”

Section: Discussionmentioning

confidence: 99%

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Molecular and cellular effects of gold nanoparticles treatment in experimental diabetic myopathy

Al-Shwaheen

Aljabali

Alomari

et al. 2022

Heliyon

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Molecular and cellular effects of gold nanoparticles treatment in experimental diabetic myopathy

Al-Shwaheen

Aljabali

Alomari

et al. 2022

Heliyon

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“…Some controversy exists around the single high dose streptozotocin model used in the present study, compared with repeated low-dose streptozotocin models, with nonspecific toxicity being a potential confounding factor [23]. When compared, the lower streptozotocin model can also produce undesirable effects such as higher inflammatory markers in muscles [24]. We chose the high streptozotocin model, as it ablates all pancreatic beta cells, resulting in insulin dependent diabetes, to mimic human insulin dependent diabetes.…”

Section: Induction Of Diabetes and Hyperglycaemiamentioning

confidence: 99%

Increased Diabetes Complications in a Mouse Model of Oxidative Stress Due to ‘Mismatched’ Mitochondrial DNA

Januszewski,

Blake,

Zhang

et al. 2024

Antioxidants

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Associations between chronic diabetes complications and mitochondrial dysfunction represent a subject of major importance, given the diabetes pandemic and high personal and socioeconomic costs of diabetes and its complications. Modelling diabetes complications in inbred laboratory animals is challenging due to incomplete recapitulation of human features, but offer mechanistic insights and preclinical testing. As mitochondrial-based oxidative stress is implicated in human diabetic complications, herein we evaluate diabetes in a unique mouse model that harbors a mitochondrial DNA from a divergent mouse species (the ‘xenomitochondrial mouse’), which has mild mitochondrial dysfunction and increased oxidative stress. We use the streptozotocin-induced diabetes model with insulin supplementation, with 20-weeks diabetes. We compare C57BL/6 mice and the ‘xenomitochondrial’ mouse, with measures of heart and kidney function, histology, and skin oxidative stress markers. Compared to C57BL/6 mice, the xenomitochondrial mouse has increased diabetic heart and kidney damage, with cardiac dysfunction, and increased cardiac and renal fibrosis. Our results show that mitochondrial oxidative stress consequent to divergent mtDNA can worsen diabetes complications. This has implications for novel therapeutics to counter diabetes complications, and for genetic studies of risk, as mtDNA genotypes may contribute to clinical outcomes.

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“…Finally, as mentioned above, given the importance of simulating the pathophysiology and symptomatology of T2DM, there are several animal biomodels that involve genetically modified rodents, but one of the most used biomodels is the induction of obesity and chemical pancreatic damage [ 21 , 22 ]. These models used in the present study combine a high-fat diet with low-dose streptozotocin (HFD/STZ) which mimics the generation of insulin resistance, β-cell dysfunction, the metabolic characteristics, cytokine levels, and oxidative stress similar to those observed in patients with T2DM [ 23 , 24 ].…”

Section: Introductionmentioning

confidence: 99%

Antidiabetic Effect of Passiflora ligularis Leaves in High Fat-Diet/Streptozotocin-Induced Diabetic Mice

Rey,

Echeverry,

Valderrama

et al. 2024

Nutrients

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Type 2 diabetes mellitus (T2DM) is a major global public health concern, prompting the ongoing search for new treatment options. Medicinal plants have emerged as one such alternative. Our objective was to evaluate the antidiabetic effect of an extract from the leaves of Passiflora ligularis (P. ligularis). For this purpose, T2DM was first induced in mice using a high-fat diet and low doses of streptozotocin. Subsequently, an aqueous extract or an ethanolic extract of P. ligularis leaves was administered for 21 days. The following relevant results were found: fasting blood glucose levels were reduced by up to 41%, and by 29% after an oral glucose overload. The homeostasis model assessment of insulin resistance (HOMA-IR) was reduced by 59%. Histopathologically, better preservation of pancreatic tissue was observed. Regarding oxidative stress parameters, there was an increase of up to 48% in superoxide dismutase (SOD), an increase in catalase (CAT) activity by 35% to 80%, and a decrease in lipid peroxidation (MDA) by 35% to 80% in the liver, kidney, or pancreas. Lastly, regarding the lipid profile, triglycerides (TG) were reduced by up to 30%, total cholesterol (TC) by 35%, and low-density lipoproteins (LDL) by up to 32%, while treatments increased high-density lipoproteins (HDL) by up to 35%. With all the above, we can conclude that P. ligularis leaves showed antihyperglycemic, hypolipidemic, and antioxidant effects, making this species promising for the treatment of T2DM.

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Comparative study on molecular mechanism of diabetic myopathy in two different types of streptozotocin-induced diabetic models

Cited by 6 publications

References 65 publications

Molecular and cellular effects of gold nanoparticles treatment in experimental diabetic myopathy

Molecular and cellular effects of gold nanoparticles treatment in experimental diabetic myopathy

Increased Diabetes Complications in a Mouse Model of Oxidative Stress Due to ‘Mismatched’ Mitochondrial DNA

Antidiabetic Effect of Passiflora ligularis Leaves in High Fat-Diet/Streptozotocin-Induced Diabetic Mice

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