ArticleFrontiers in nutrition2022
Linking Mitochondrial Function to Insulin Resistance: Focusing on Comparing the Old and the Young.
Article in Frontiers in nutrition, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- The Benefits of Non-Pharmaceutic Interventions on Intrinsic Capacity in Insulin-Resistant Adult and Geriatric Populations-A Narrative Review.Journal of clinical medicine · 2026Review
- Inducible skeletal muscle-specific p53 deletion alleviates high-fat diet-induced insulin resistance by modulating mitochondria-associated membrane in obese mice.Redox biology · 2025Article
- Triglyceride-glucose index in predicting the risk of new-onset diabetes in the general population aged 45 years and older: a national prospective cohort study.BMC endocrine disorders · 2025Article
- Crosstalk between Adipose Tissue and Hepatic Mitochondria in the Development of the Inflammation and Liver Injury during Ageing in High-Fat Diet Fed Rats.International journal of molecular sciences · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term intake of high-energy diet can lead to decreased insulin sensitivity and even insulin resistance, eventually leading to diabetes. Diabetes often occurs in middle-aged and elderly people. However, there is growing evidence that the incidence rate of young body is increasing over the years. This means that insulin resistance can be caused by excessive energy intake in both young and old people. In this study, high-fat diet (HFD) and normal diet were fed to rats of elderly experimental group (EE), elderly control group (EC), young experimental group (YE), and young control group (YC), respectively, for 8 weeks, by which insulin resistance model was obtained. Insulin sensitivity was measured, histopathology changes in liver and skeletal muscle tissues were observed, and mitochondrial fusion and division and cell senescence were detected in four groups of rats. The results showed that both young and elderly rats developed significant insulin resistance, fat deposition, decline of mitochondrial function and mitochondrial biosynthesis in liver and skeletal muscle, and cell aging after HFD feeding. In addition, the degree of mitochondrial dysfunction and aging in young rats was similar to that of aged rats fed a normal diet after HFD. This experiment provides a reference for an in-depth study of the regulatory mechanisms of cellular energy metabolism in this state.
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