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Li, B.-H.

Publications and source records attributed to Li, B.-H..

2 recordsLinked to original sources

Characterization of dynamic age-dependent changes and driver microbes in primate gut microbiota during host's development and healthy aging via captive crab-eating macaque model

Recent population studies have significantly advanced our understanding of how age shapes the gut microbiota. However, the actual role of age could be inevitably confounded due to varying environmental factors in human populations. A well-controlled environment is thus necessary to reduce undesirable cofounding effects, and recapitulate age-dependent taxonomic and functional changes in the healthy primate gut microbiota. Herein we performed 16S rRNA gene sequencing, characterized age-associated gut microbial profiles from infant to elderly crab-eating macaques reared in captivity, and systemically revealed lifelong dynamic changes of primate gut microbiota in the model. While the most significantly age-associated gut microbial taxa were mainly found in commensals such as Faecalibacterium, a set of suspicious pathogens such as Helicobacter were exclusively enriched in infants, pointing to their potential role in host development. Importantly, topology analysis indicated that the connectivity of gut microbial network was even more age-dependent than taxonomic diversity, with its tremendous decline probably linked to the hosts healthy aging. NetShift analysis identified Prevotella 9, Rikenellaceae RC9 gut group and Megasphaera as key drivers during gut microbiota maturation and development, actively involved in age-dependent changes in phenotypes and functions of the gut microbial community. The current study demonstrates lifelong age-dependent changes in healthy primate gut microbiota. Our findings indicate potential importance of appropriate exposure to suspicious pathogens in infant development. The age-associated baseline profiles and driver microbes of primate gut microbiota in the current study could provide new insight into its role in the hosts development and healthy aging.

microbiology

Low-protein/high-carbohydrate diet induces AMPK-dependent canonical and non-canonical thermogenic response in subcutaneous adipose tissue

Low-protein/high-carbohydrate (LPHC) diet promotes metabolic health and longevity in adult humans and animal models. However, the complex molecular underpinnings of how LPHC diet leads to metabolic benefits remain elusive. Through a multi-layered approach, here we observed that LPHC diet promotes an energy-dissipating response consisting in the parallel recruitment of canonical and non-canonical (muscular) thermogenic systems in subcutaneous white adipose tissue (sWAT). In particular, we measured Ucp1 induction in association with up-regulation of actomyosin components and several Serca (Serca1, Serca2a, Serca2b) ATPases. In beige adipocytes, we observed that AMPK activation is responsible for transducing the amino acid lowering in an enhanced fat catabolism, which sustains both Ucp1- and Serca-dependent energy dissipation. Limiting AMPK activation counteracts the expression of brown fat and muscular genes, including Ucp1 and Serca, as well as mitochondrial oxidative genes. We observed that mitochondrial reactive oxygen species are the upstream molecules controlling AMPK-mediated metabolic rewiring in amino acid-restricted beige adipocytes. Our findings delineate a novel metabolic phenotype of responses to amino acid shortage, which recapitulates some of the benefits of cool temperature in sWAT. In conclusion, this highlights LPHC diet as a valuable and practicable strategy to prevent metabolic diseases through the enhancement of mitochondrial oxidative metabolism and the recruitment of different energy dissipating routes in beige adipocytes.

physiology