ArticlePloS one2017
The desert gerbil Psammomys obesus as a model for metformin-sensitive nutritional type 2 diabetes to protect hepatocellular metabolic damage: Impact of mitochondrial redox state.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Progress in experimental models to investigate the in vivo and in vitro antidiabetic activity of drugs.Animal models and experimental medicine · 2024Review
- Role of glycolysis in diabetic atherosclerosis.World journal of diabetes · 2023Review
- Anti-Obesity and Anti-Dyslipidemic Effects ofFoods (Basel, Switzerland) · 2023Article
- Species Differences in Tryptophan Metabolism and Disposition.International journal of tryptophan research : IJTR · 2022Review
- Pup ultrasonic isolation calls of six gerbil species and the relationship between acoustic traits and body size.Royal Society open science · 2021Article
- The Metformin Mechanism on Gluconeogenesis and AMPK Activation: The Metabolite Perspective.International journal of molecular sciences · 2020Review
- Low metformin causes a more oxidized mitochondrial NADH/NAD redox state in hepatocytes and inhibits gluconeogenesis by a redox-independent mechanism.The Journal of biological chemistry · 2019Article
- Article
- Psammomys obesus: a Natural Diet-Controlled Model for Diabetes and Cardiovascular Diseases.Current atherosclerosis reports · 2018Review
Corrections and comments
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Authors and funding
6 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionWhile metformin (MET) is the most widely prescribed antidiabetic drug worldwide, its beneficial effects in Psammomys obesus (P. obesus), a rodent model that mimics most of the metabolic features of human diabetes, have not been explored thoroughly. Here, we sought to investigate whether MET might improve insulin sensitivity, glucose homeostasis, lipid profile as well as cellular redox and energy balance in P. obesus maintained on a high energy diet (HED). MATERIALS AND
methodsP. obesus gerbils were randomly assigned to receive either a natural diet (ND) consisting of halophytic plants (control group) or a HED (diabetic group) for a period of 24 weeks. MET (50 mg/kg per os) was administered in both animal groups after 12 weeks of feeding, i.e., the time required for the manifestation of insulin resistance in P. obesus fed a HED. Parallel in vitro experiments were conducted on isolated hepatocytes that were shortly incubated (30 min) with MET and energetic substrates (lactate + pyruvate or alanine, in the presence of octanoate).
resultsIn vivo, MET lowered glycemia, glycosylated haemoglobin, circulating insulin and fatty acid levels in diabetic P. obesus. It also largely reversed HED-induced hepatic lipid alterations. In vitro, MET increased glycolysis but decreased both gluconeogenesis and ketogenesis in the presence of glucogenic precursors and medium-chain fatty acid. Importantly, these changes were associated with an increase in cytosolic and mitochondrial redox states along with a decline in respiration capacity.
conclusionsMET prevents the progression of insulin resistance in diabetes-prone P. obesus, possibly through a tight control of gluconeogenesis and fatty acid β-oxidation depending upon mitochondrial function. While the latter is increasingly becoming a therapeutic issue in diabetes, the gut microbiota is another promising target that would need to be considered as well.
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