Author + information
- Nattayaporn Apaijaia,b,
- Titikorn Chunchaia,b,
- Siripong Paleea,b,
- Thidarat Jaiwongkama,b,
- Siriporn Chattipakorna,b and
- Nipon Chattipakorna,b
Background: Obese-insulin resistance occurring in testosterone-deprived young-age rats has been shown to accelerate, but not aggravate, left ventricular (LV) dysfunction. However, in a clinical setting, whether testosterone deprivation occurring later at older age following obese-insulin resistance would show similar cardiometabolic dysfunction remains unclear. We hypothesized that testosterone deprivation aggravates LV dysfunction via impairing mitochondrial function, insulin receptor function and increased apoptosis in obese-insulin resistant rats.
Method: Obese-insulin resistant rats caused by 12-week high-fat feeding were divided into 2 groups to have either a sham operation (HFS) or orchidectomy (HFO). Lean rats with (NDO) or without (NDS) orchidectomy were used as controls. Metabolic parameters and LV function were determined at 1, 2, 4 and 8 weeks after operation. Cardiac mitochondrial function and apoptosis were determined.
Results: HFS rats had impaired insulin sensitivity and LV dysfunction. HFO rats had higher plasma insulin and glucose levels than HFS rats. At week 8 after ORX, the worsening LV function, markedly mitochondrial dysfunction, impaired insulin receptor function and decreased anti-apoptotic protein were found in HFO, compared to HFS rats (Figure).
Conclusions: Testosterone deprivation in old age aggravated the impairment of insulin receptor function and mitochondrial function, leading to the worsening LV dysfunction in obese-insulin resistant rats.
Poster Hall, Hall C
Friday, March 17, 2017, 3:45 p.m.-4:30 p.m.
Session Title: Diabetes and Endothelial Dysfucntion in Heart Failure
Abstract Category: 12. Heart Failure and Cardiomyopathies: Basic
Presentation Number: 1162-243
- 2017 American College of Cardiology Foundation