ArticleMolecular metabolism2017
Intestinal SIRT3 overexpression in mice improves whole body glucose homeostasis independent of body weight.
Article in Molecular metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Bioenergetic adaptations of small intestinal epithelial cells reduce cell differentiation enhancing intestinal permeability in obese mice.Molecular metabolism · 2025Article
- Exploring histone deacetylases in type 2 diabetes mellitus: pathophysiological insights and therapeutic avenues.Clinical epigenetics · 2024Review
- Interactions between Intestinal Homeostasis and NADNutrients · 2023Review
- Berberine remodels adipose tissue to attenuate metabolic disorders by activating sirtuin 3.Acta pharmacologica Sinica · 2022Article
- Small Intestinal Tuft Cell Activity Associates With Energy Metabolism in Diet-Induced Obesity.Frontiers in immunology · 2021Article
- Article
- Deletion of intestinal Hdac3 remodels the lipidome of enterocytes and protects mice from diet-induced obesity.Nature communications · 2019Article
- Roux-en-Y gastric bypass surgery reprograms enterocyte triglyceride metabolism and postprandial secretion in rats.Molecular metabolism · 2019Article
- Striatal dopamine 2 receptor upregulation during development predisposes to diet-induced obesity by reducing energy output in mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Enhancing enterocyte fatty acid oxidation in mice affects glycemic control depending on dietary fat.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIntestinal metabolism might play a greater role in regulating whole body metabolism than previously believed. We aimed to enhance enterocyte metabolism in mice and investigate if it plays a role in diet-induced obesity (DIO) and its comorbidities.
methodsUsing the cre-loxP system, we overexpressed the mitochondrial NAD
resultsThere were no genotype differences in any of the parameters tested when the mice were fed CD. Also, iSIRT3 mice were equally susceptible to the development of DIO as S3fl mice when fed HFD. They were, however, better able than S3fl mice to regulate their blood glucose levels in response to exogenous insulin and glucose, indicating that they were protected from developing insulin resistance. This improved glucose homeostasis was accompanied by an increase in enterocyte metabolic activity and an upregulation of ketogenic gene expression in the small intestine.
conclusionEnhancing enterocyte oxidative metabolism can improve whole body glucose homeostasis.
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Registered trials
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