ArticleMolecular biology reports2024
Madhuca longifolia-hydro-ethanolic-fraction reverses mitochondrial dysfunction and modulates selective GLUT expression in diabetic mice fed with high fat diet.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- Chromosome-level genome ofiScience · 2026Article
- Gut Microbiota Diversity and Function in Adults With Type 2 Diabetes, Alzheimer's Disease, and Both Conditions.International journal of microbiology · 2026Article
- Regorafenib modulates glucose metabolism, insulin/GLP-1 signaling, and tau pathology in an STZ-induced model of Alzheimer's disease.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Protective effects of Parabacteroides distasonis against high-fat diet-induced brain injury in mice.NPJ science of food · 2025Article
- Pathophysiology of Prediabetes Hyperinsulinemia and Insulin Resistance in the Cardiovascular System.Biomedicines · 2025Review
- Exploring the potential of pheophorbide A, a chlorophyll-derived compound in modulating GLUT for maintaining glucose homeostasis.Frontiers in endocrinology · 2024Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMetabolic disorder is characterized as chronic low-grade inflammation which elevates the systemic inflammatory markers. The proposed hypothesis behind this includes occurrence of hypoxia due to intake of high fat diet leading to oxidative stress and mitochondrial dysfunction.
aimIn the present work our aim was to elucidate the possible mechanism of action of hydroethanolic fraction of M. longifolia leaves against the metabolic disorder. METHOD AND
resultsIn the present investigation, effect of Madhuca longifolia hydroethanolic fraction (MLHEF) on HFD induced obesity and diabetes through mitochondrial action and selective GLUT expression has been studied. In present work, it was observed that HFD (50% of diet) on chronic administration aggravates the metabolic problems by causing reduced imbalanced oxidative stress, ATP production, and altered selective GLUT protein expression. Long term HFD administration reduced (p < 0.001) the SOD, CAT level significantly along with elevated liver function marker AST and ALT. MLHEF administration diminishes this oxidative stress. HFD administration also causes decreased ATP/ADP ratio owing to suppressed mitochondrial function and elevating LDH level. This oxidative imbalance further leads to dysregulated GLUT expression in hepatocytes, skeletal muscles and white adipose tissue. HFD leads to significant (p < 0.001) upregulation in GLUT 1 and 3 expression while significant (p < 0.001) downregulation in GLUT 2 and 4 expressions in WAT, liver and skeletal muscles. Administration of MLHEF significantly (p < 0.001) reduced the LDH level and also reduces the mitochondrial dysfunction.
conclusionImbalances in GLUT levels were significantly reversed in order to maintain GLUT expression in tissues on the administration of MLHEF.
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