Obesity accelerates cognitive decline by aggravating mitochondrial dysfunction, insulin resistance and synaptic dysfunction under estrogen-deprived conditions

Pratchayasakul, Wasana; Sa‐nguanmoo, Piangkwan; Sivasinprasasn, Sivaporn; Pintana, Hiranya; Tawinvisan, Rungroj; Sripetchwandee, Jirapas; Kumfu, Sirinart; Chattipakorn, Nipon; Chattipakorn, Siriporn C.

doi:10.1016/j.yhbeh.2015.04.023

Cited by 84 publications

(62 citation statements)

References 46 publications

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“…We found in recent literature some studies involving female rats that evaluate obesity effects [71,38,17,81] and stress [4,78] in a dissociated form, or in younger models [24,47,91], which differs from our work.…”

Section: Resultscontrasting

confidence: 72%

“…However, only a limited number of studies have been conducted in female rodents. In relation to obesity, although some work has been conducted using female rats [71,17,38,81,82], the neurobehavioral aspects that can indicate neuropsychiatric disorders, such as locomotors alterations, anxiety and depression have not been the focus of these studies.…”

Section: Introductionmentioning

confidence: 99%

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Predictive behaviors for anxiety and depression in female Wistar rats subjected to cafeteria diet and stress

Estrela

Silva

Guimarães

et al. 2015

Physiology & Behavior

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Obesity and chronic stress have been considered important public health problems that affect millions of people worldwide. Our aim was to analyze the effect of obesity associated with chronic stress on neurobehavioral parameters in female rats, considering that the association of these syndromes can enhance the negative effects on homeostasis. The animals were distributed into standard diet (Std), standard diet+stress (Std+stress), cafeteria diet (Cafe), and cafeteria diet+stress (Cafe+stress) groups. The animals of groups Std and Std+stress were fed with rodent standard feed. Groups Cafe and Cafe+stress, additionally to the standard feed, were offered palatable and calorie-rich processed food and cola-type soft drink ad libitum. From the eighth experimental week, groups Std+stress and Cafe+stress were subjected to restraint chronic stress model (50 days). After the stress protocol, predictive anxiety (open-field and elevated plus-maze tests) and depression (forced swim) were applied. The cafeteria diet was effective in inducing obesity. The ratio locomotion in the central quadrants/total locomotion evaluated during the open field test was not indicative of anxiogenic or anxiolytic effect in the animal's behavior. However, the elevated plus maze test showed that obese and stressed animals were prone to higher anxiety levels. In addition, the obese and stressed animals display less climbing behavior than all the other groups, which can be considered an indicator of depression-like behavior. Nevertheless, it is suggested that the mechanisms involved in effects of obesity associated with chronic stress be better investigated in female rats, considering the organic complexity related to these modern illnesses.

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Section: Resultscontrasting

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Predictive behaviors for anxiety and depression in female Wistar rats subjected to cafeteria diet and stress

Estrela

Silva

Guimarães

et al. 2015

Physiology & Behavior

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show abstract

“…Plasma glucose and triglyceride levels were determined by colorimetric assay from a commercially available kit (Biotech, Bangkok, Thailand). Fasting plasma HDL and LDL were determined using commercially available kits (ERBA diagnostic, Mannheim, Germany)59. Plasma lactate dehydrogenase (LDH) was determined by the clinical chemistry laboratory of the central diagnostic laboratory, Maharajnakorn Chiang Mai hospital, Chiang Mai University, Thailand.…”

Section: Methodsmentioning

confidence: 99%

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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“…[3][4][5][6][7] It has been shown that microglia play important roles in normal and pathological brain, such as the excessive synaptic pruning in the brains of patients with Alzheimer's disease, and excessive brain inflammation in obesity. [3][4][5][6][7] It has been shown that microglia play important roles in normal and pathological brain, such as the excessive synaptic pruning in the brains of patients with Alzheimer's disease, and excessive brain inflammation in obesity.…”

mentioning

confidence: 99%

Testosterone deprivation intensifies cognitive decline in obese male rats via glial hyperactivity, increased oxidative stress, and apoptosis in both hippocampus and cortex

et al. 2018

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Aim:The study hypothesized that testosterone deprivation aggravates cognitive decline in obesity through increasing oxidative stress, glial activation, and apoptosis. Methods: Male Wistar rats (n = 24) were fed with either normal-diet (ND) or high-fat diet (HFD) for 24 weeks. At week 13, ND-fed rats and HFD-fed rats were randomly assigned to two subgroups to receive either a sham-operation or bilateral-orchiectomy (ORX). Rats were evaluated for metabolic parameters and cognition at 4, 8, and 12 weeks after the operation. At the end of protocol, the reactive oxygen species (ROS), glial morphology, and cell apoptosis were determined in hippocampus and cortex. Results: Both HFD-fed groups developed obese-insulin resistance, but ND-fed rats did not. HFD-fed rats with sham-operation showed cognitive decline, when compared to ND-fed rats with sham-operation at all time points. At 4-and 8-week after ORX, the cognitive impairment of ND-fed rats and both HFD-fed groups was not different. However, 12-week after ORX, cognitive decline and of glial hyperactivity of HFD-fed rats had the greatest increase among all groups. Hippocampal ROS levels and apoptotic cells in both HFD-fed groups were equally increased, but the cortical ROS levels and apoptotic cells of HFD-fed rats with ORX were the highest ones. Conclusions: These findings suggest that testosterone deprivation aggravates cognitive decline in obesity via increasing oxidative stress, glial activity and apoptosis. K E Y W O R D Sapoptosis, cognitive function, glia function, obesity, reactive oxygen species, testosterone deprivation

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Obesity accelerates cognitive decline by aggravating mitochondrial dysfunction, insulin resistance and synaptic dysfunction under estrogen-deprived conditions

Cited by 84 publications

References 46 publications

Predictive behaviors for anxiety and depression in female Wistar rats subjected to cafeteria diet and stress

Predictive behaviors for anxiety and depression in female Wistar rats subjected to cafeteria diet and stress

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

Testosterone deprivation intensifies cognitive decline in obese male rats via glial hyperactivity, increased oxidative stress, and apoptosis in both hippocampus and cortex

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