Effects of lactic acid bacteria on cardiac apoptosis are mediated by activation of the phosphatidylinositol-3 kinase/AKT survival-signalling pathway in rats fed a high-fat diet

Abstract

Through a high-fat diet, obesity leads to cardiomyocyte dysfunction and apoptosis. In addition, there is no evidence that probiotics have potential health effects associated with cardiac apoptosis in obese rats. The present study aimed to explore the effects of probiotics on obesity and cardiac apoptosis in rats fed a high-fat diet (HF). Eight‑week‑old male Wistar rats were separated randomly into five equally sized experimental groups: Normal diet (NC) and high-fat diet (HFC) groups, and high-fat diet supplemented with low (HFL), medium (HFM) or high (HFH) doses of multi‑strain probiotics groups. The rats were subsequently studied for 8 weeks. Food intake and body weights were recorded following sacrifice, and food utilization rates, body fat and serum cholesterol levels were analysed. The myocardial architecture of the left ventricle was evaluated by hematoxylin‑eosin staining, and key apoptotic‑related pathway molecules were analysed by western blotting. Rat weights and triglyceride levels were decreased with oral administration of high doses of probiotics (HFH) compared to the HFC group. Abnormal myocardial architecture and enlarged interstitial spaces were observed in HFC hearts, but were significantly decreased in groups that were provided multi‑strain probiotics compared with NC hearts. Western blot analysis demonstrated that key components of the Fas receptor‑ and mitochondrial‑dependent apoptotic pathways were significantly suppressed in multi‑strain probiotic treated groups compared to the HF group. Additionally, cardiac insulin, such as the insulin‑like growth factor I receptor (IGFIR)‑dependent survival signalling components, were highly induced in left ventricles from rats administered probiotics. Together, these findings strongly suggest that oral administration of probiotics may attenuate cardiomyocyte apoptosis by activation of the phosphatidylinositol‑3 kinase/AKT survival‑signalling pathway in obese rats.

Exposure to a chronic high-fat diet promotes atrial structure and gap junction remodeling in rats

“…Apart from the AF-promoting conditions mentioned above, apoptosis cell death may be another potential mechanism contributing to AF by participating in atrial remodeling (34,35). The effect of HFD-induced obesity on apoptosis in ventricles has been well documented (20,21,36). In accordance with these results, we found a robust increase in cell death in both HFD-OB and HFD-NOB rat atria as detected by TUNEL assay (Fig.…”

“…In the present study, 6-to 8-week-old female SD rats were fed an HFD for 12 weeks, and subsequent atrial fibrosis and gap junction remodeling were analyzed. Large numbers of previous studies have reported significant increases in the body weight of HFD-fed rats (20,21). However, our findings showed that only approximately 3/5 of the HFD-fed rats were more susceptible to HFD-induced obesity, while the other 2/5 were not (Fig.…”

Heat Killed Lactobacillus reuteri GMNL-263 Reduces Fibrosis Effects on the Liver and Heart in High Fat Diet-Hamsters via TGF-β Suppression

“…Recently, certain reports have revealed the effects of certain probiotic strains on cholesterol and hypertension reduction, and these data suggest that probiotics could be more widely applied for cardiovascular health [ 19 , 20 , 21 ]. Reports show that Lactobacillus reuteri is a probiotic species with a serum cholesterol-lowering ability in humans [ 22 ].…”

“…Previous studies show that heat-killed Lr263 potentially improved in heart function against the effects of HFD [ 29 ]. In our previous research, a high-fat diet treatment caused obesity and cardiac fibrosis in an animal model [ 21 , 26 , 28 ]. In this work, a high-fat diet was employed to induce obesity and cardiac fibrosis in hamsters; the protective effects exerted by different doses of heat-killed Lr263 on the heart and liver were also investigated in hamsters with high-fat diet-induced obesity.…”

The Heart Protection Effect of Alcalase Potato Protein Hydrolysate Is through IGF1R-PI3K-Akt Compensatory Reactivation in Aging Rats on High Fat Diets

“…In our previous research discovered, HFD treatment will increase FAS expression and cause FAS-induced cardiac apoptosis [ 31 ]. The expression of Fas-induced apoptosis signaling pathway proteins in the heart tissues of each group after four weeks of the indicated treatments were analyzed by Western blotting assay ( Figure 3 ).…”