ArticlePloS one2018
Sarcopoterium spinosum extract improved insulin sensitivity in mice models of glucose intolerance and diabetes.
Article in PloS one, 2018. 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, 18 citations in OpenAlex.
- Activation of the Insulin Receptor byACS omega · 2025Article
- The Anti-Inflammatory Potential of an Ethanolic Extract fromInternational journal of molecular sciences · 2024Article
- Integration of the Connectivity Map and Pathway Analysis to Predict Plant Extract's Medicinal Properties-The Study Case ofPlants (Basel, Switzerland) · 2022Article
- Article
- Middle East Medicinal Plants in the Treatment of Diabetes: A Review.Molecules (Basel, Switzerland) · 2021Review
- Plant Extracts for Type 2 Diabetes: From Traditional Medicine to Modern Drug Discovery.Antioxidants (Basel, Switzerland) · 2021Review
- Approaches to Decrease Hyperglycemia by Targeting Impaired Hepatic Glucose Homeostasis Using Medicinal Plants.Frontiers in pharmacology · 2021Review
- Article
- Activation of Insulin Signaling in Adipocytes and Myotubes byNutrients · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe glucose lowering properties of Sarcopoterium spinosum, a traditional medicinal plant, were previously validated by us using KK-Ay mice as a genetic model for type 2 diabetes (T2D).
objectiveTo clarify the effects of Sarcopoterium spinosum extract (SSE) on diet-induced glucose intolerance and to investigate SSE effects on carbohydrate and lipid metabolism in target tissues of both high-fat-diet (HFD)-fed and KK-Ay mice.
resultsMice were given SSE (70 mg/day) for 6 weeks. SSE improved glucose tolerance and insulin sensitivity in HFD-fed mice as was demonstrated previously in KK-Ay mice. Higher insulin sensitivity was validated by lower serum insulin and activation of the insulin signaling cascade in skeletal muscle and liver of SSE-treated mice in both models. H&E staining of the livers demonstrated lower severity of steatosis in SSE-treated mice. Several model-specific effects of SSE were observed-mRNA expression of proinflammatory genes and CD36 was reduced in SSE-treated KK-Ay mice. Hepatic mRNA expression of PEPCK was also reduced in SSE-treated KK-Ay mice, while other genes involved in carbohydrates and lipid metabolism were not affected. HFD-fed mice treated by SSE had elevated hepatic glycogen stores. Gluconeogenic gene expression was not affected, while GCK expression was increased. HFD-induced hepatic steatosis was not affected by SSE. However, while genes involved in lipid metabolism were downregulated by HFD, this was not found in HFD-fed mice given SSE, demonstrating an expression profile which is similar to that of standard diet-fed mice.
conclusionOur study supports the insulin sensitizing activity of SSE and suggests that this extract might improve other manifestations of the metabolic syndrome.
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