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Obese-insulin resistance accelerates and aggravates cardiometabolic disorders and cardiac mitochondrial dysfunction in estrogen-deprived female rats.Testosterone replacement attenuates cognitive decline in testosterone-deprived lean rats, but not in obese rats, by mitigating brain oxidative stress.DPP-4 Inhibitor and Estrogen Share Similar Efficacy Against Cardiac Ischemic-Reperfusion Injury in Obese-Insulin Resistant and Estrogen-Deprived Female Rats.Hyperglycemia induced the Alzheimer's proteins and promoted loss of synaptic proteins in advanced-age female Goto-Kakizaki (GK) rats.SGLT2-inhibitor and DPP-4 inhibitor improve brain function via attenuating mitochondrial dysfunction, insulin resistance, inflammation, and apoptosis in HFD-induced obese rats.Energy restriction combined with dipeptidyl peptidase-4 inhibitor exerts neuroprotection in obese male rats.Dipeptidyl peptidase 4 inhibitor improves brain insulin sensitivity, but fails to prevent cognitive impairment in orchiectomy obese rats.Estrogen deprivation aggravates cardiometabolic dysfunction in obese-insulin resistant rats through the impairment of cardiac mitochondrial dynamics.Role of D-galactose-induced brain aging and its potential used for therapeutic interventions.Atorvastatin and insulin equally mitigate brain pathology in diabetic rats.Decreased microglial activation through gut-brain axis by prebiotics, probiotics, or synbiotics effectively restored cognitive function in obese-insulin resistant rats.Obesity accelerates cognitive decline by aggravating mitochondrial dysfunction, insulin resistance and synaptic dysfunction under estrogen-deprived conditions.DPP4-inhibitor improves neuronal insulin receptor function, brain mitochondrial function and cognitive function in rats with insulin resistance induced by high-fat diet consumption.Estrogen and DPP-4 inhibitor share similar efficacy in reducing brain pathology caused by cardiac ischemia-reperfusion injury in both lean and obese estrogen-deprived rats.Effects of metformin on learning and memory behaviors and brain mitochondrial functions in high fat diet induced insulin resistant rats.Tabernaemontana divaricata extract inhibits neuronal acetylcholinesterase activity in rats.DPP-4 inhibitor and PPARγ agonist restore the loss of CA1 dendritic spines in obese insulin-resistant rats.FGF21 improves cognition by restored synaptic plasticity, dendritic spine density, brain mitochondrial function and cell apoptosis in obese-insulin resistant male rats.Effects of estrogen in preventing neuronal insulin resistance in hippocampus of obese rats are different between genders.Effects of high-fat diet on insulin receptor function in rat hippocampus and the level of neuronal corticosterone.Testosterone deprivation has neither additive nor synergistic effects with obesity on the cognitive impairment in orchiectomized and/or obese male rats.Estrogen and DPP4 inhibitor, but not metformin, exert cardioprotection via attenuating cardiac mitochondrial dysfunction in obese insulin-resistant and estrogen-deprived female rats.Estrogen restores brain insulin sensitivity in ovariectomized non-obese rats, but not in ovariectomized obese rats.Both oophorectomy and obesity impaired solely hippocampal-dependent memory via increased hippocampal dysfunction.Chronic treatment with prebiotics, probiotics and synbiotics attenuated cardiac dysfunction by improving cardiac mitochondrial dysfunction in male obese insulin-resistant rats.
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description
researcher
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wetenschapper
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հետազոտող
@hy
name
Wasana Pratchayasakul
@ast
Wasana Pratchayasakul
@en
Wasana Pratchayasakul
@es
Wasana Pratchayasakul
@nl
type
label
Wasana Pratchayasakul
@ast
Wasana Pratchayasakul
@en
Wasana Pratchayasakul
@es
Wasana Pratchayasakul
@nl
prefLabel
Wasana Pratchayasakul
@ast
Wasana Pratchayasakul
@en
Wasana Pratchayasakul
@es
Wasana Pratchayasakul
@nl
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P1153
15840445800
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0000-0003-3970-4323