Anti-insulin resistant effect of ferulic acid on high fat diet-induced obese mice

Jarinyaporn Naowaboot; Pritsana Piyabhan; Pholawat Tingpej; Narongsuk Munkong; Wason Parklak; Patchareewan Pannangpetch

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Anti-insulin resistant effect of ferulic acid on high fat diet-induced obese mice

Author: Jarinyaporn NAOWABOOT ¹ ; Pritsana PIYABHAN ² ; Pholawat TINGPEJ ³ ; Narongsuk MUNKONG ⁴ ; Wason PARKLAK ⁵ ; Patchareewan PANNANGPETCH ⁶
Author Information

1. Division of Pharmacology, Department of Preclinical Science, Faculty of Medicine, Thammasat University, Rangsit Campus
2. Division of Physiology, Department of Preclinical Science, Faculty of Medicine, Thammasat University, Rangsit Campus
3. Division of Microbiology, Department of Preclinical Science, Faculty of Medicine, Thammasat University, Rangsit Campus
4. Division of Pathology, School of Medicine, University of Phayao
5. Graduate Academy, Faculty of Medicine, Thammasat University, Rangsit Campus
6. Department of Pharmacology, Faculty of Medicine, Khon Kaen University
Publication Type:Journal Article
Keywords: Ferulic acid; Insulin resistance; Obesity
From:Asian Pacific Journal of Tropical Biomedicine 2018;8(12):604-608
CountryChina
Language:Chinese
Abstract: Objective: To evaluate the insulin sensitivity action of ferulic acid (FA) in skeletal muscle and hypothalamus of high-fat diet (HFD)-induced obese mice. Methods: Obese mouse model was induced by HFD (45 kcal% lard fat) for 16 weeks. After 8 weeks of HFD feeding, these obese mice were orally treated with FA at doses of 25 and 50 mg/kg/day for 8 weeks. At the end of all treatments, the epididymal fat, pancreas, skeletal muscle and hypothalamus were removed for biochemical parameter and protein expression examinations. Results: FA treatment significantly decreased leptin level in fat tissue and insulin level in pancreas (P < 0.05). Interestingly, obese mice treated with FA increased the protein expressions of insulin receptor substrate-1, phosphatidylinositol 3-kinase, and phosphorylated-protein kinase B in both muscle and brain (P < 0.05). The phosphorylations of adenosine monophosphate-activated protein kinase and acetyl-CoA carboxylase in muscle, and leptin receptor protein in hypothalamus were also increased (P < 0.05). The pancreatic islets histology showed smaller size in obese mice treated with FA compared to untreated obese mice. Conclusions: These findings indicate the beneficial effect of FA in improving insulin resistance in HFD-induced obese mice. These effects are probably mediated via modulating the insulin receptor substrate/phosphatidylinositol 3-kinase/protein kinase B or adenosine monophosphate-activated protein kinase pathways.