Siriporn Chattipakorn

Chiang Mai University, Amphoe Muang Chiang Mai, Chiang Mai, Thailand

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Publications (104)411.62 Total impact

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    ABSTRACT: Testosterone replacement improves metabolic parameters and cognitive function in hypogonadism. However, the effects of testosterone therapy on cognition in obese condition with testosterone deprivation have not been investigated. We hypothesized that testosterone replacement improves cognitive function in testosterone-deprived obese rats by restoring brain insulin sensitivity, brain mitochondrial function, and hippocampal synaptic plasticity. Thirty male Wistar rats had either a bilateral orchiectomy (ORX: O, n = 24) or a sham operation (S, n = 6). ORX rats were further divided into two groups fed with either a normal diet (NDO) or a high-fat diet (HFO) for 12 weeks. Then, ORX rats in each dietary group were divided into two subgroups (n = 6/subgroup) and were given either castor oil or testosterone (2 mg/kg/day, s.c.) for 4 weeks. At the end of this protocol, cognitive function, metabolic parameters, brain insulin sensitivity, hippocampal synaptic plasticity, and brain mitochondrial function were determined. We found that testosterone replacement increased peripheral insulin sensitivity, decreased circulation and brain oxidative stress levels, and attenuated brain mitochondrial ROS production in HFO rats. However, testosterone failed to restore hippocampal synaptic plasticity and cognitive function in HFO rats. In contrast, in NDO rats, testosterone decreased circulation and brain oxidative stress levels, attenuated brain mitochondrial ROS production, and restored hippocampal synaptic plasticity as well as cognitive function. These findings suggest that testosterone replacement improved peripheral insulin sensitivity and decreased oxidative stress levels, but failed to restore hippocampal synaptic plasticity and cognitive function in testosterone-deprived obese rats. However, it provided beneficial effects in reversing cognitive impairment in testosterone-deprived non-obese rats.
    Age 10/2015; 37(5):9827. DOI:10.1007/s11357-015-9827-4 · 3.45 Impact Factor
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    ABSTRACT: Iron-overload cardiomyopathy is a major cause of death in thalassemia patients due to the lack of an early detection strategy. Although cardiac magnetic resonance (CMR) T2* is used for early detection of cardiac iron accumulation, its availability is limited. Heart rate variability (HRV) has been used to evaluate cardiac autonomic function and found to be depressed in thalassemia. However, its direct correlation with cardiac iron accumulation has never been investigated. We investigated whether HRV can be used as an alternative indicator for early identification of cardiac iron deposition in thalassemia patients. Ninety-nine non-transfusion dependent thalassemia patients (23.00 (17.00, 32.75) years, 35 male) were enrolled. The correlation between HRV recorded using 24-hour Holter monitoring and non-transferrin bound iron (NTBI), hemoglobin (Hb), serum ferritin, LV ejection fraction (LVEF), and CMR-T2* were determined. The median NTBI value was 3.15 (1.11, 6.59) μM. Both time and frequency domains of HRV showed a significant correlation with the NTBI level, supporting HRV as a marker of iron overload. Moreover, the LF/HF ratio showed a significant correlation with CMR-T2* with the receiver operating characteristic (ROC) curve of 0.684±0.063, suggesting that it could represent the cardiac iron deposit in thalassemia patients. HRV was also significantly correlated with serum ferritin and Hb. This novel finding regarding the correlation between HRV and CMR-T2* indicates that HRV could be a potential marker in identifying early cardiac iron deposition prior to the development of LV dysfunction, and may be used as an alternative to CMR-T2* for screening cardiac iron status in thalassemia patients.
    PLoS ONE 06/2015; 10(6):e0130837. DOI:10.1371/journal.pone.0130837 · 3.23 Impact Factor
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    ABSTRACT: Brain mitochondrial dysfunction has been demonstrated in diabetic animals with neurodegeneration. Protocatechuic acid (PCA), a major metabolite of anthocyanin, has been shown to exert glycemic control and oxidative stress reduction in the heart. However, its effects on oxidative stress and mitochondrial function in the brain under diabetic condition have never been investigated. We found that PCA exerted glycemic control, attenuates brain mitochondrial dysfunction, and contributes to the prevention of brain oxidative stress in diabetic rats.
    Applied Physiology Nutrition and Metabolism 06/2015; DOI:10.1139/apnm-2015-0158 · 2.23 Impact Factor
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    ABSTRACT: It is unclear whether the DDP-IV inhibitor can counteract brain insulin resistance, brain mitochondrial dysfunction, impairment of hippocampal synaptic plasticity, and cognitive decline in testosterone-deprived obese rats. We hypothesized that DPP-4 inhibitor vildagliptin improves cognitive function in testosterone-deprived obese rats by restoring brain insulin sensitivity, brain mitochondrial function and hippocampal synaptic plasticity. Thirty male Wistar rats received either a sham-operated (S, n=6) or bilateral orchiectomy (ORX:O, n=24). ORX rats were divided into 2 groups and fed with either a normal diet (NDO) or a high-fat diet (HFO) for 12 weeks. Then, ORX rats in each dietary group were divided into 2 subgroups (n=6/subgroup) to receive either a vehicle or vildagliptin (3 mg/kg/day, p.o.) for 4 weeks. After treatment, cognitive function, metabolic parameters, brain insulin sensitivity, hippocampal synaptic plasticity and brain mitochondrial function were determined in each rat. We found that HFO rats exhibited peripheral and brain insulin resistance, brain mitochondrial dysfunction, impaired hippocampal synaptic plasticity and cognitive decline. NDO rats did not develop peripheral and brain insulin resistance; however, impaired hippocampal synaptic plasticity and cognitive decline occurred. Vildagliptin significantly improved peripheral insulin sensitivity, restored brain insulin sensitivity and decreased brain mitochondrial ROS production in HFO rats. However, vildagliptin did not restore hippocampal synaptic plasticity and cognitive function in both NDO and HFO rats. These findings suggest that vildagliptin could not counteract the impairment of hippocampal synaptic plasticity and cognitive decline in testosterone-deprived subjects, despite of its effects on improved peripheral and brain insulin sensitivity as well as brain mitochondrial function.
    Journal of Endocrinology 05/2015; DOI:10.1530/JOE-15-0099 · 3.59 Impact Factor
  • Wanpitak Pongkan · Siriporn C Chattipakorn · Nipon Chattipakorn
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    ABSTRACT: Testosterone is an anabolic steroid hormone, which is the major circulating androgen hormone in males. Testosterone levels decreasing below the normal physiological levels lead to a status known as androgen deficiency. Androgen deficiency has been shown to be a major risk factor in the development of several disorders, including obesity, metabolic syndrome, and ischemic heart disease. In the past decades, although several studies from animal models as well as clinical studies demonstrated that testosterone exerted cardioprotection, particularly during ischemia-reperfusion (I/R) injury, other preclinical and clinical studies have shown an inverse relationship between testosterone levels and cardioprotective effects. As a result, the effects of testosterone replacement on the heart remain controversial. In this review, reports regarding the roles of testosterone replacement in the heart following I/R injury are comprehensively summarized and discussed. At present, it may be concluded that chronic testosterone replacement at a physiological dose demonstrated cardioprotective effects, whereas acute testosterone replacement can cause adverse effects in the I/R heart. © The Author(s) 2015.
    Journal of Cardiovascular Pharmacology and Therapeutics 05/2015; DOI:10.1177/1074248415587977 · 3.07 Impact Factor
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    ABSTRACT: Chronic consumption of a high-fat diet (HF) causes peripheral insulin resistance, brain insulin resistance, brain mitochondrial dysfunction and cognitive impairment. Estrogen deprivation has also been found to impair cognition. However, the combined effect of both conditions on the brain is unclear. We hypothesized that estrogen deprivation causes brain insulin resistance, brain mitochondrial dysfunction, hippocampal synaptic dysfunction and cognitive impairment, and that consumption of a HF accelerates these impairments in an estrogen-deprived condition. Seventy-two female rats were divided into sham (S) and ovariectomized (O) groups. Rats in each group were further divided into two subgroups to be fed with either a normal diet (ND) or HF for 4, 8 and 12 weeks. At the end of each period, the Morris water maze test was carried out, after which the blood and brain were collected for metabolic and brain function analysis. Obesity, peripheral insulin resistance, increased brain oxidative stress and hippocampal synaptic dysfunction were observed at the eighth week in the NDO, HFS and HFO rats. However, these impairments were worse in the HFO rats. Interestingly, brain insulin resistance, brain mitochondrial dysfunction and cognitive impairment developed earlier (week eight) in the HFO rats, whereas these conditions were observed later at week 12 in the NDO and HFS rats. Either estrogen deprivation or HF appears to cause peripheral insulin resistance, increased brain oxidative stress, hippocampal synaptic dysfunction, brain mitochondrial dysfunction and brain insulin resistance, which together can lead to cognitive impairment. A HF accelerates and aggravates these deleterious effects under estrogen-deprived conditions. Copyright © 2015. Published by Elsevier Inc.
    Hormones and Behavior 05/2015; 72. DOI:10.1016/j.yhbeh.2015.04.023 · 4.51 Impact Factor
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    Sarawut Kumphune · Sirirat Surinkaew · Siriporn C Chattipakorn · Nipon Chattipakorn
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    ABSTRACT: Cardiac cell death and fatal arrhythmias during myocardial ischemia/reperfusion (I/R) can be reduced by p38 MAPK inhibition. However, the effects of p38 MAPK inhibition on cardiac mitochondria have not been investigated. We tested the hypothesis that p38 MAPK inhibition at different times during I/R protects cardiac mitochondrial functions. Adult Wistar rats were subjected to 30 min of left anterior descending coronary artery (LAD) occlusion, followed by 120 min of reperfusion. A 2 mg/kg bolus infusion of p38 MAPK inhibitor, SB203580, was given before or during ischemia, or at reperfusion. Mitochondrial function and ultrastructure were assessed and Western blots were performed. Administration of SB203580 at any time point of I/R significantly attenuated the mitochondrial ultrastructure change, mitochondrial swelling, by increasing the absorbance at 540 nm (I/R control 0.42 ± 0.03; pretreatment 0.58 ± 0.04; during ischemia 0.49 ± 0.02; at reperfusion 0.51 ± 0.02, p < 0.05), similar to reactive oxygen species (ROS) generation (I/R control 1300 ± 48; pretreatment 1150 ± 30; during ischemia 1000 ± 50; at reperfusion 1050 ± 55, p < 0.05). Only SB203580 given before or during ischemia attenuated mitochondrial membrane depolarization (I/R control 0.78 ± 0.04; pretreatment 1.02 ± 0.03; during ischemia 1.05 ± 0.12, p < 0.05). In addition, pre-treatment of SB203580 significantly reduced the phosphorylation of p53, CREB, Bax, cytochrome c, and cleaved caspase 3. The results from this study showed for the first time that p38 MAPK inhibition protects mitochondria from I/R injury.
    Pharmaceutical Biology 04/2015; DOI:10.3109/13880209.2015.1014569 · 1.34 Impact Factor
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    ABSTRACT: Women have a lower incidence of cardiovascular diseases (CVD) than men at a similar age but have an increased incidence of CVD and metabolic syndrome after menopause, indicating the possible protective effects of estrogen on cardiometabolic function. Although obesity is known to increase CVD risks, its impact on the heart on estrogen deprivation is still inconclusive. We investigated the effects of obese-insulin resistance on cardiometabolic function in estrogen-deprived ovariectomized rats. Adult female ovariectomized (O) or sham (S)-operated rats randomly received either normal diet (ND, 19.77 % fat) or high-fat diet (HF, 57.60 % fat) (n = 6/group) for 12 weeks. The heart rate variability (HRV), left ventricular (LV) performance, cardiac autonomic balance, cardiac mitochondrial function, metabolic parameters, oxidative stress, and apoptotic markers were determined at 4, 8, and 12 weeks. Insulin resistance developed at week 8 in NDO, HFS, and HFO rats as indicated by increased plasma insulin and HOMA index. However, only HFO rats had elevated plasma cholesterol level at week 8, whereas HFS rats had showed elevation at week 12. In addition, only HFO rats had depressed HRV, impaired LV performance indicated by decreased fractional shortening (%FS) and cardiac mitochondrial dysfunction indicated by increased mitochondrial ROS level, mitochondrial depolarization and swelling, as early as week 8, whereas other groups exhibited them at week 12. Either estrogen deprivation or obesity alone may impair metabolic parameters, cardiac autonomic balance, and LV and mitochondrial function. However, an obese insulin-resistant condition further accelerated and aggravated the development of these cardiometabolic impairments in estrogen-deprived rats.
    Age 04/2015; 37(2):9766. DOI:10.1007/s11357-015-9766-0 · 3.45 Impact Factor
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    Wanpitak Pongkan · Siriporn C Chattipakorn · Nipon Chattipakorn
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    ABSTRACT: Although testosterone deficiency is associated with increased risks of heart disease, the benefits of testosterone therapy are controversial. Moreover, current understanding on the cardiac effect of testosterone during cardiac ischemia-reperfusion (I/R) periods is unclear. We tested the hypothesis that testosterone replacement attenuates the impairment of left ventricular (LV) function and heart rate variability (HRV), and reduces the infarct size and arrhythmias caused by I/R injury in orchiectomized (ORX) rats. ORX or sham-operated male Wistar rats (n = 24) were randomly divided and received either testosterone (2 mg/kg, subcutaneously administered) or the vehicle for 8 weeks. The ejection fraction (EF) and HRV were determined at baseline and the 4th and 8th week. I/R was performed by left anterior descending coronary artery ligation for 30 minutes, followed by a 120-minute reperfusion. LV pressure, arrhythmia scores, infarct size and cardiac mitochondrial function were determined. Prior to I/R, EF and HRV were impaired in the ORX group, but were restored in the testosterone-treated group. During I/R, arrhythmia scores and the infarct size were greater, and cardiac mitochondrial function was impaired, whereas the time to 1st VT/VF onset and the LV end-systolic pressure were decreased in the ORX group when compared to the sham group. Testosterone replacement attenuated the impairment of these parameters in ORX rats during I/R injury, but did not show any benefit or adverse effect in non-ORX rats. Testosterone replacement restores cardiac function and autonomic regulation, and exerts cardioprotective effects during the I/R period via mitochondrial protection in ORX rats.
    PLoS ONE 03/2015; 10(3):e0122503. DOI:10.1371/journal.pone.0122503 · 3.23 Impact Factor
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    ABSTRACT: Adverse cardiac remodeling after myocardial infarction (MI) leads to progressive heart failure. Dipeptidyl peptidase-4 (DPP-4) inhibitor is a new antidiabetic drug that exerts cardioprotection. However, its role on cardiac function and remodeling in chronic MI is unclear. We hypothesized that DPP-4 inhibitor (vildagliptin) reduces adverse cardiac remodeling and improves cardiac function in chronic MI rats. These effects were also compared with enalapril and metformin. Male Wistar rats (n = 36) with chronic MI induced by left anterior descending coronary arterial ligation were divided into 6 groups to receive vehicle, vildagliptin (3 mg/kg/d), metformin (30 mg/kg/d), enalapril (10 mg/kg/d), combined metformin and enalapril, or combined vildagliptin and enalapril for 8 weeks. At the end of the study, plasma malondialdehyde, heart rate variability (HRV), left ventricular (LV) function, pathological and biochemical studies of cardiac remodeling were investigated. Our study demonstrated that chronic MI rats had increased oxidative stress levels, depressed HRV, and adverse cardiac remodeling indicated by cardiac fibrosis, and LV dysfunction. Treatment with vildagliptin and enalapril both significantly decreased oxidative stress, attenuated cardiac fibrosis, and improved HRV and LV function. We conclude that vildagliptin exerts similar cardioprotective effects as enalapril in attenuating oxidative stress and cardiac fibrosis and improving cardiac function in chronic MI rats. Metformin does not provide these benefits in this model. Moreover, addition of either metformin or vildagliptin to enalapril does not provide additional benefit in attenuating cardiac remodeling or improving LV function, compared to enalapril alone. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Experimental physiology 03/2015; 100(6). DOI:10.1113/EP085108 · 2.87 Impact Factor
  • Journal of the American College of Cardiology 03/2015; 65(10):A799. DOI:10.1016/S0735-1097(15)60799-9 · 15.34 Impact Factor
  • Journal of the American College of Cardiology 03/2015; 65(10):A905. DOI:10.1016/S0735-1097(15)60905-6 · 15.34 Impact Factor
  • Sirinart Kumfu · Siriporn Chattipakorn · Suthat Fucharoen · Nipon Chattipakorn
    Journal of the American College of Cardiology 03/2015; 65(10):A901. DOI:10.1016/S0735-1097(15)60901-9 · 15.34 Impact Factor
  • Hiranya Pintana · Nipon Chattipakorn · Siriporn Chattipakorn
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    ABSTRACT: Testosterone is an androgenic steroid hormone, which plays an important role in the regulation of male reproduction and behaviors, as well as in the maintenance of insulin sensitivity. Several studies showed that testosterone exerted beneficial effects in brain function, including preventing neuronal cell death, balancing brain oxidative stress and antioxidant activity, improving synaptic plasticity and involving cognitive formation. Although previous studies showed that testosterone deficiency is positively correlated with cognitive impairment and insulin-resistant obesity, several studies demonstrated contradictory findings. Thus, this review comprehensively summarizes the current evidence from in vitro, in vivo and clinical studies of the relationship between testosterone deficiency and insulin-resistant obesity as well as the correlation between either insulin-resistant obesity or testosterone deficiency and cognitive impairment. Controversial reports and the mechanistic insights regarding the roles of testosterone in insulin-resistant obesity and cognitive function are also presented and discussed.
    Metabolic Brain Disease 02/2015; 30(4). DOI:10.1007/s11011-015-9655-3 · 2.40 Impact Factor
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    ABSTRACT: This paper reviews the reported pharmacological properties of protocatechuic acid (PCA, 3,4-dihydroxy benzoic acid), a type of phenolic acid found in many food plants such as olives and white grapes. PCA is a major metabolite of anthocyanin. The pharmacological actions of PCA have been shown to include strong in vitro and in vivo antioxidant activity. In in vivo experiments using rats and mice, PCA has been shown to exert anti-inflammatory as well as antihyperglycemic and antiapoptotic activities. Furthermore, PCA has been shown to inhibit chemical carcinogenesis and exert proapoptotic and antiproliferative effects in different cancerous tissues. Moreover, in vitro studies have shown PCA to have antimicrobial activities and also to exert synergistic interaction with some antibiotics against resistant pathogens. This review aims to comprehensively summarize the pharmacological properties of PCA reported to date with an emphasis on its biological properties and mechanisms of action which could be therapeutically useful in a clinical setting.
    Evidence-based Complementary and Alternative Medicine 02/2015; 2015:1-11. DOI:10.1155/2015/593902 · 1.88 Impact Factor
  • Karn Wijarnpreecha · Sirinart Kumfu · Siriporn C Chattipakorn · Nipon Chattipakorn
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    ABSTRACT: Abstract Iron overload cardiomyopathy is one of the most common causes of death in thalassemia patients. Although new iron chelating agents have been developed, the mortality rate from heart failure remains elevated as a result of iron overload. This could be due to the fact that our understanding of the underlying mechanism of iron uptake into cardiomyocytes is still unclear, thus impeding the discovery and refinement of more effective therapy for thalassemia therapeutic strategies in thalassemic iron overload cardiomyopathy. Growing evidence indicates that multiple routes of iron entry into cardiomyocytes exist under iron overload conditions. These include both L-type (LTCC) and T-type (TTCC) calcium channels, divalent metal transporter 1 (DMT1) and transferrin receptors (TfRs). In this review, the routes of iron uptake into cardiomyocytes under iron overload conditions are presented. Evidence from pharmacological interventions in support or against the possible route of iron entry of each portal in cardiomyocytes are also comprehensively summarized and discussed.
    Hemoglobin 01/2015; 39(1):1-9. DOI:10.3109/03630269.2014.987869 · 0.96 Impact Factor
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    ABSTRACT: Oxidative stress in the obese-insulin resistant condition has been shown to affect cognitive as well as brain mitochondrial functions. Garlic extract has exerted a potent antioxidant effect. However, the effects of garlic extract on the brain of obese-insulin resistant rats have never been investigated. We hypothesized that garlic extract improves cognitive function and brain mitochondrial function in obese-insulin resistant rats induced by long-term high-fat diet (HFD) consumption. Male Wistar rats were fed either normal diet or HFD for 16 weeks (n = 24/group). At week 12, rats in each dietary group received either vehicle or garlic extract (250 and 500 mg·kg(-1)·day(-1)) for 28 days. Learning and memory behaviors, metabolic parameters, and brain mitochondrial function were determined at the end of treatment. HFD led to increased body weight, visceral fat, plasma insulin, cholesterol, and malondialdehyde (MDA) levels, indicating the development of insulin resistance. Furthermore, HFD rats had cognitive deficit and brain mitochondrial dysfunction. HFD rats treated with both doses of garlic extract had decreased body weight, visceral fat, plasma cholesterol, and MDA levels. Garlic extract also improved cognitive function and brain mitochondrial function, which were impaired in obese-insulin resistant rats caused by HFD consumption.
    Journal of Applied Statistics 10/2014; 39(12):1-7. DOI:10.1139/apnm-2014-0255 · 0.45 Impact Factor
  • Nattayaporn Apaijai · Siriporn C Chattipakorn · Nipon Chattipakorn
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    ABSTRACT: The incidence of obesity with insulin resistance is increasing worldwide. This condition is also known as a risk factor of coronary artery disease and associated with increased arrhythmias, impaired left ventricular function, and increased infarct size during cardiac ischemia-reperfusion (I/R) injury. The proposed mechanisms are due to impaired glucose utilization and pro-survival signaling molecules, and increased inflammatory cytokines, which have been demonstrated in the I/R hearts in various models of obese-insulin resistance. However, the cardiac effects of diets in the I/R heart are still unsettled since several studies reported that high-caloric diet consumption might protect the heart from I/R injury. Although several therapeutic strategies such as anti-diabetic drugs, natural compounds as well as treadmill exercise have been proposed to exert cardioprotection in the I/R heart in obese-insulin resistant animals, some interventions including ischemic post-conditioning failed to protect the heart from I/R injury. In this comprehensive review, reports from both genetic deletion and dietary-induced obese-insulin resistant animal models regarding the effects of obese-insulin resistance on metabolic parameters, cardiac function, infarct size, and molecular mechanisms under I/R injury are summarized. Moreover, the effects of anti-diabetic drugs and other pharmacological interventions on these parameters in an obese-insulin resistant model under I/R injury are also comprehensively summarized and discussed.
    Cardiovascular Drugs and Therapy 10/2014; 28(6). DOI:10.1007/s10557-014-6553-6 · 2.95 Impact Factor
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    ABSTRACT: Background and Aims Obesity induced by high-fat diet (HFD) impaired brain insulin receptor function, caused cognitive decline well as reduced dendritic spine density. Previous studies suggested that dipeptidyl peptidase IV (DPP-4) inhibitor and peroxisome proliferator-activated receptor-gamma (PPARγ) agonist exerted the neuroprotective effects in obese insulin-resistant rats. However, the effects of these drugs on dendritic spines in obese insulin-resistant rats have not yet been investigated. In the present study, we determined the effects of DPP-4 inhibitor and PPARγ agonist on dendritic spines density of obese insulin-resistant rats caused by HFD. Methods Male Wistar Rats were divided into two groups. Animals in each group were fed with normal diet (ND) or HFD for 12 weeks. After then, rats in each group were subdivided into three subgroups to receive either vehicle or vildagliptin (3 mg/kg/day) or pioglitazone (10 mg/kg/day) for 3–4 weeks. At the end of the experiment, the metabolic parameters and density of dendritic spines in CA1 hippocampus were determined. Results We found that HFD-fed rats caused peripheral insulin resistance as well as the reduction of the density of dendritic spines in CA1 hippocampus. Treatment with both DPP-4 inhibitor and PPARγ agonist in HFD-fed rats improved insulin sensitivity as well as increased the number of dendritic spines in CA1 hippocampus. Moreover, both drugs have equally improved this deterioration. Conclusion Our findings indicate that DPP-4 inhibitor and PPARγ agonist restored the reduction of dendritic spines caused by HFD, suggesting the beneficial roles of DPP-4 inhibitors and PPARγ agonists in neurodegenerative disorders.
    Archives of Medical Research 09/2014; 45(7). DOI:10.1016/j.arcmed.2014.09.002 · 2.41 Impact Factor
  • International Journal of Cardiology 08/2014; 176(3). DOI:10.1016/j.ijcard.2014.07.302 · 6.18 Impact Factor

Publication Stats

947 Citations
411.62 Total Impact Points

Institutions

  • 2004–2015
    • Chiang Mai University
      • • Faculty of Medicine
      • • Faculty of Dentistry
      • • Department of Physiology
      • • Department of Pathology
      Amphoe Muang Chiang Mai, Chiang Mai, Thailand
  • 2003
    • University of Alabama at Birmingham
      • Department of Medicine
      Birmingham, Alabama, United States