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. 2016 Jul 5;13(8):569-77.
doi: 10.7150/ijms.15597. eCollection 2016.

Heat-killed Lactobacillus Reuteri GMNL-263 Prevents Epididymal Fat Accumulation and Cardiac Injury in High-Calorie Diet-Fed Rats

Po-Hsiang Liao  1 , Wei-Wen Kuo  2 , Dennis Jine-Yuan Hsieh  3 , Yu-Lan Yeh  4 , Cecilia-Hsuan Day  5 , Ya-Hui Chen  6 , Sheng-Huang Chang  7 , V Vijaya Padma  8 , Yi-Hsing Chen  9 , Chih-Yang Huang  10
Affiliations

Heat-killed Lactobacillus Reuteri GMNL-263 Prevents Epididymal Fat Accumulation and Cardiac Injury in High-Calorie Diet-Fed Rats

Po-Hsiang Liao et al. Int J Med Sci. .

Abstract

High-calorie diet-induced obesity leads to cardiomyocyte dysfunction and apoptosis. Impaired regulation of epididymal fat content in obese patients has been known to increase the risk of cardiac injury. In our study, a lactic acid bacteria, Lactobacillus reuteri GMNL-263, was evaluated for its potential to reduce body weight and body fat ratio and to prevent heart injury in rats with high-fat diet-induced obesity. Lactic acid bacteria supplementation restored the cardiac function and decreased the physiological changes in the heart of the obese rats. In addition, the Fas/Fas-associated protein pathway-induced caspase 3/e Poly polymerase mediated apoptosis in the cardiomyocytes of the obese rats was reversed in the Lr263-treated rats. These results reveal that fed with Lr-263 reduces body fat ratio, inhibits caspase 3-mediated apoptosis and restores cardiac function in obese rats through recovery of ejection fraction and fractional shortening. Our results indicated that the administration of Lr263 lactic acid bacteria can significantly down-regulate body fat and prevent cardiomyocyte injury in obese rats.

Keywords: Cardiac dysfunction; Functional food; High-calorie diet; Obesity.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

Figures

Figure 1
Figure 1
Hematoxylin and eosin staining of cardiac tissue sections. Histopathological analysis of cardiac tissue sections of the left ventricles of the control rats (N), high-calorie-induced obesity rats without treatment (sham) (HC), high-calorie-induced obesity rats treated with a low dose of Lr263 (HCL) and high-calorie-induced obesity rats treated with a high dose of Lr263 (HCH). Cellular disorder area (White arrows).
Figure 2
Figure 2
Protein expression analysis by Western blotting. The level of apoptosis marker proteins increased and survival marker proteins decreased in the left ventricles of the rats with high-calorie-induced obesity, whereas treatment with low dose and high dose of Lr263 reduced the expression of apoptotic proteins and increased survival proteins. (A) Western blots of caspase 3/PARP and p-Akt/Bcl2 proteins. (B-E) The densitometry of the Western blots shown in (A). Quantitative analysis of the expression levels of (B) p-Akt, (C) Bcl2, (D) caspase 3 and (E) PARP was performed by normalization using GAPDH as the internal control. Data represent the results of four animal models; the samples from two rats were pooled together, and therefore, four independent experiments were conducted. Mean values were significantly different from those of the N group: *P<0.05, **P<0.01 and ***P<0.001. Mean values were significantly different from those of the HC group: #P<0.05, ##P<0.01 and ###P<0.001.
Figure 3
Figure 3
TUNEL and DAPI staining to detect cardioapoptosis. (A) DAPI- and TUNEL-stained heart tissue sections of the control rats, high-calorie induced-obesity rats and rats treated with low and high doses of Lr263. The nuclei were stained blue by DAPI staining, and the DNA fragments were stained green by the TUNEL assay. (B) Quantitative analysis of the percentage of apoptosis as detected by the TUNEL assay. Mean values were significantly different from those of the N group: *P<0.05, **P<0.01 and ***P<0.001. Mean values were significantly different from those of the HC group: #P<0.05, ##P<0.01 and ###P<0.001.
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