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Synergistic Effects of the Jackfruit Seed Sourced Resistant Starch and Bifidobacterium pseudolongum subsp. globosum on Suppression of Hyperlipidemia in Mice.

ABSTRACT: Approximately 17 million people suffer from cardiovascular diseases caused by hyperlipidemia, making it a serious global health concern. Among others, resistant starch (RS) has been widely used as a prebiotic in managing hyperlipidemia conditions. However, some studies have reported limited effects of RS on body weight and blood lipid profile of the host, suggesting further investigation on the synergistic effects of RS in combination with probiotics as gut microbes plays a role in lipid metabolism. This study evaluated the effects of jackfruit seed sourced resistant starch (JSRS) as a novel RS on mice gut microbes and hyperlipidemia by performing 16s rRNA and shotgun metagenomic sequencing. The results showed that 10% JSRS had a limited preventive effect on bodyweight and serum lipid levels. However, the JSRS promoted the growth of Bifidobacterium pseudolongum, which indicated the ability of B. pseudolongum for JSRS utilization. In the validation experiment, B. pseudolongum interacted with JSRS to significantly reduce bodyweight and serum lipid levels and had a therapeutic effect on hepatic steatosis in mice. Collectively, this study revealed the improvements of hyperlipidemia in mice by the synergistic effects of JSRS and B. pseudolongum, which will help in the development of "synbiotics" for the treatment of hyperlipidemia in the future.

SUBMITTER: Zhang Z

PROVIDER: S-EPMC8235523 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Starches resistant to mammalian digestion are present in foods and pass to the large bowel, where they may be degraded and fermented by the microbiota. Increases in relative abundances of bifidobacteria (blooms) have been reported in rats whose diet was supplemented with Hi-Maize resistant starch. We determined that the bifidobacterial species present in the rat cecum under these circumstances mostly belonged to Bifidobacterium animalis However, cultures of B. animalis isolated from the rats failed to degrade Hi-Maize starch to any extent. In contrast, Bifidobacterium pseudolongum also detected in the rat microbiota had high starch-degrading ability. Transcriptional comparisons showed increased expression of a type 1 pullulanase, alpha-amylase, and glycogen debranching enzyme by B. pseudolongum when cultured in medium containing Hi-Maize starch. Maltose was released into the culture medium, and B. animalis cultures had shorter doubling times in maltose medium than did B. pseudolongum Thus, B. pseudolongum, which was present at a consistently low abundance in the microbiota, but which has extensive enzymatic capacity to degrade resistant starch, showed the attributes of a keystone species associated with the bifidobacterial bloom.IMPORTANCE This study addresses the microbiology and function of a natural ecosystem (the rat gut) using DNA-based observations and in vitro experimentation. The microbial community of the large bowel of animals, including humans, has been studied extensively through the use of high-throughput DNA sequencing methods and advanced bioinformatics analysis. These studies reveal the compositions and genetic capacities of microbiotas but not the intricacies of how microbial communities function. Our work, combining DNA sequence analysis and laboratory experiments with cultured strains of bacteria, revealed that the increased abundance of bifidobacteria in the rat gut, induced by feeding indigestible starch, involved a species that cannot itself degrade the starch (Bifidobacterium animalis) but cohabits with a species that can (Bifidobacterium pseudolongum). B. pseudolongum has the characteristics of a keystone species in the community because it had low abundance but high ability to perform a critical function, the hydrolysis of resistant starch.

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Synergistic Effects of the Jackfruit Seed Sourced Resistant Starch and Bifidobacterium pseudolongum subsp. globosum on Suppression of Hyperlipidemia in Mice.

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