ArticleDiabetology & metabolic syndrome2015
Regulation of hepatic TRB3/Akt interaction induced by physical exercise and its effect on the hepatic glucose production in an insulin resistance state.
Article in Diabetology & metabolic syndrome, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 31 citations in OpenAlex.
- Investigating the impact of physical activity on BMI, motor skills, and sleep patterns in elementary school children.Frontiers in public health · 2025Trial
- Transcriptomic responses and molecular mechanisms of glucagon-regulated glucose metabolism in Japanese flounder (Frontiers in physiology · 2026Article
- NAD metabolic therapy in metabolic dysfunction-associated steatotic liver disease: Possible roles of gut microbiota.iScience · 2024Review
- Spirulina liquid extract prevents metabolic disturbances and improves liver sphingolipids profile in hamster fed a high-fat diet.European journal of nutrition · 2021Article
- Endoplasmic reticulum stress as the basis of obesity and metabolic diseases: focus on adipose tissue, liver, and pancreas.European journal of nutrition · 2021Review
- Zinc Supplementation and Strength Exercise in Rats with Type 2 Diabetes: Akt and PTP1B Phosphorylation in Nonalcoholic Fatty Liver.Biological trace element research · 2021Article
- Mitochondria in Sex Hormone-Induced Disorder of Energy Metabolism in Males and Females.Frontiers in endocrinology · 2021Review
- ER-Mitochondria Contacts and Insulin Resistance Modulation through Exercise Intervention.International journal of molecular sciences · 2020Review
- Spexin alleviates insulin resistance and inhibits hepatic gluconeogenesis via the FoxO1/PGC-1α pathway in high-fat-diet-induced rats and insulin resistant cells.International journal of biological sciences · 2019Article
- Repression of Transcriptional Activity of Forkhead Box O1 by Histone Deacetylase Inhibitors Ameliorates Hyperglycemia in Type 2 Diabetic Rats.International journal of molecular sciences · 2018Article
- Matrine Inhibits Neuroblastoma Cell Proliferation and Migration by Enhancing Tribbles 3 Expression.Oncology research · 2018Article
- Silencing of TRB3 Ameliorates Diabetic Tubule Interstitial Nephropathy via PI3K/AKT Signaling in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To maintain euglycemia in healthy organisms, hepatic glucose production is increased during fasting and decreased during the postprandial period. This whole process is supported by insulin levels. These responses are associated with the insulin signaling pathway and the reduction in the activity of key gluconeogenic enzymes, resulting in a decrease of hepatic glucose production. On the other hand, defects in the liver insulin signaling pathway might promote inadequate suppression of gluconeogenesis, leading to hyperglycemia during fasting and after meals. The hepatocyte nuclear factor 4, the transcription cofactor PGC1-α, and the transcription factor Foxo1 have fundamental roles in regulating gluconeogenesis. The loss of insulin action is associated with the production of pro-inflammatory biomolecules in obesity conditions. Among the molecular mechanisms involved, we emphasize in this review the participation of TRB3 protein (a mammalian homolog of Drosophila tribbles), which is able to inhibit Akt activity and, thereby, maintain Foxo1 activity in the nucleus of hepatocytes, inducing hyperglycemia. In contrast, physical exercise has been shown as an important tool to reduce insulin resistance in the liver by reducing the inflammatory process, including the inhibition of TRB3 and, therefore, suppressing gluconeogenesis. The understanding of these new mechanisms by which physical exercise regulates glucose homeostasis has critical importance for the understanding and prevention of diabetes.
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