Obese-insulin resistance accelerates and aggravates cardiometabolic disorders and cardiac mitochondrial dysfunction in estrogen-deprived female rats

Sivasinprasasn, Sivaporn; Sa‐nguanmoo, Piangkwan; Pratchayasakul, Wasana; Kumfu, Sirinart; Chattipakorn, Nipon

doi:10.1007/s11357-015-9766-0

Cited by 34 publications

(44 citation statements)

References 27 publications

(40 reference statements)

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“…Our findings demonstrated that females had lower State 2 and ROS production while showed higher calcium retention capacity. The current findings suggest that female rats have a better mitochondrial coupling than male rats, possibly due to oestradiol effects, which is corroborated by previous observations in cell culture and heart studies (Jung et al., ; Lagranha, Deschamps, Aponte, Steenbergen, & Murphy, ; Rattanasopa, Phungphong, Wattanapermpool, & Bupha‐Intr, ; Sivasinprasasn et al., ). In addition, a study by Sandhir, Sethi, Aggarwal, and Khera () found that oestradiol withdrawal impairs mitochondrial function and increases oxidative stress in the brain (Sandhir et al., ).…”

Section: Discussionsupporting

confidence: 90%

Serotonin transporter inhibition during neonatal period induces sex‐dependent effects on mitochondrial bioenergetics in the rat brainstem

Silva

Freitas

et al. 2018

Eur J of Neuroscience

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The serotonin reuptake is mainly regulated by the serotonin transporters (SERTs), which are abundantly found in the raphe nuclei, located in the brainstem. Previous studies have shown that dysfunction in the SERT has been associated with several disorders, including depression and cardiovascular diseases. In this manuscript, we aimed to investigate how gender and the treatment with a serotonin selective reuptake inhibitor (SSRI) could affect mitochondrial bioenergetics and oxidative stress in the brainstem of male and female rats. Fluoxetine, our chosen SSRI, was used during the neonatal period (i.e., from postnatal Day 1 to postnatal Day 21-PND1 to PND21) in both male and female animals. Thereafter, experiments were conducted in adult rats (60 days old). Our results demonstrate that, during lactation, fluoxetine treatment modulates the mitochondrial bioenergetics in a sex-dependent manner, such as improving male mitochondrial function and female antioxidant capacity.

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Section: Discussionsupporting

confidence: 90%

Serotonin transporter inhibition during neonatal period induces sex‐dependent effects on mitochondrial bioenergetics in the rat brainstem

Silva

Freitas

et al. 2018

Eur J of Neuroscience

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“…We previously compared the effect of high-fat diet consumption (a high-fat diet sham group; HFS) and estrogen deprivation (normal-diet fed rats with ovariectomy; NDO) on plasma and cardiac oxidative stress, and our results indicated that both HFS and NDO had similar degree of oxidative stress and cardiometabolic dysfunction15. In that study, we also further demonstrated that plasma and cardiac oxidative stress levels were higher in high-fat fed rats with estrogen deprivation (HFO), compared to HFS and NDO rats15. In this study, we aimed to focus on the therapeutic strategy that could attenuate oxidative stress and cardiometabolic dysfunction only in estrogen deprived model subjected to ischemia/reperfusion injury.…”

Section: Methodsmentioning

confidence: 95%

DPP-4 Inhibitor and Estrogen Share Similar Efficacy Against Cardiac Ischemic-Reperfusion Injury in Obese-Insulin Resistant and Estrogen-Deprived Female Rats

Sivasinprasasn

Tanajak

Pongkan

et al. 2017

Sci Rep

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Estrogen deprivation aggravates cardiac injury after myocardial ischemia and reperfusion (I/R) injury. Although either estrogen or the dipeptidyl peptidase-4 (DPP-4) inhibitor, vildagliptin, reduces myocardial damage following cardiac I/R, their effects on the heart in obese-insulin resistant and estrogen deprived conditions remain unknown. Ovariectomized (O) rats (n = 36) were divided to receive either normal diet (NDO) or high-fat diet (HFO) for 12 weeks, followed by treatment with a vehicle, estrogen or vildagliptin for 4 weeks. The setting of in vivo cardiac I/R injury, 30-min ischemia and 120-min reperfusion, was performed. At 12 weeks after ovariectomy, both NDO and HFO rats exhibited an obese-insulin resistant condition. Both NDO and HFO rats treated with estrogen and vildagliptin showed reduced fasting plasma glucose, insulin and HOMA index. Both treatments improved cardiac function indicated by restoration of heart rate variability and increased %left ventricular ejection fraction (%LVEF). The treatments similarly protected cardiac mitochondrial function against I/R injury, leading to a reduction in the infarct size, oxidative stress and apoptosis in the ischemic myocardium. These findings demonstrate that vildagliptin effectively improves metabolic status, and shares similar efficacy to estrogen in reducing myocardial infarction and protecting cardiac mitochondrial function against I/R injury in estrogen-deprived obese-insulin resistant rats.

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“…Cardiac autonomic control has been shown to be mainly influenced by oxidative stress (Brook et al 2010). It has been shown that increased oxidative stress is associated with cardiac autonomic imbalance (Sivasinprasasn et al 2015). Moreover, cardiac mitochondrial function has been Table 4 Effect of obese insulin resistance in testosterone-deprived rats on cardiac function at 12 weeks (n = 6 per group).…”

Section: Discussionmentioning

confidence: 99%

Testosterone deprivation accelerates cardiac dysfunction in obese male rats

Pongkan

Pintana

Sivasinprasasn

et al. 2016

Journal of Endocrinology

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Low testosterone level is associated with increased risks of cardiovascular diseases. As obese-insulin-resistant condition could impair cardiac function and that the incidence of obesity is increased in aging men, a condition of testosterone deprivation could aggravate the cardiac dysfunction in obese-insulin-resistant subjects. However, the mechanism underlying this adverse effect is unclear. This study investigated the effects of obesity on metabolic parameters, heart rate variability (HRV), left ventricular (LV) function, and cardiac mitochondrial function in testosterone-deprived rats. Orchiectomized or sham-operated male Wistar rats (n=36per group) were randomly divided into groups and were given either a normal diet (ND, 19.77% of energy fat) or a high-fat diet (HFD, 57.60% of energy fat) for 12weeks. Metabolic parameters, HRV, LV function, and cardiac mitochondrial function were determined at 4, 8, and 12weeks after starting each feeding program. We found that insulin resistance was observed after 8weeks of the consumption of a HFD in both sham (HFS) and orchiectomized (HFO) rats. Neither the ND sham (NDS) group nor ND orchiectomized (NDO) rats developed insulin resistance. The development of depressed HRV, LV contractile dysfunction, and increased cardiac mitochondrial reactive oxygen species production was observed earlier in orchiectomized (NDO and HFO) rats at week 4, whereas HFS rats exhibited these impairments later at week 8. These findings suggest that testosterone deprivation accelerates the impairment of cardiac autonomic regulation and LV function via increased oxidative stress and impaired cardiac mitochondrial function in obese-orchiectomized male rats.

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Obese-insulin resistance accelerates and aggravates cardiometabolic disorders and cardiac mitochondrial dysfunction in estrogen-deprived female rats

Cited by 34 publications

References 27 publications

Serotonin transporter inhibition during neonatal period induces sex‐dependent effects on mitochondrial bioenergetics in the rat brainstem

Serotonin transporter inhibition during neonatal period induces sex‐dependent effects on mitochondrial bioenergetics in the rat brainstem

DPP-4 Inhibitor and Estrogen Share Similar Efficacy Against Cardiac Ischemic-Reperfusion Injury in Obese-Insulin Resistant and Estrogen-Deprived Female Rats

Testosterone deprivation accelerates cardiac dysfunction in obese male rats

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