| 1. |
- Charmpilas, Nikolaos, et al.
(författare)
-
Acyl-CoA-binding protein (ACBP) : a phylogenetically conserved appetite stimulator
- 2020
-
Ingår i: Cell Death and Disease. - : Springer Science and Business Media LLC. - 2041-4889. ; 11:1
-
Tidskriftsartikel (refereegranskat)abstract
- Recently, we reported that, in mice, hunger causes the autophagy-dependent release of a protein called acyl-CoA-binding protein or diazepam binding inhibitor (ACBP/DBI) from cells, resulting in an increase in plasma ACBP concentrations. Administration of extra ACBP is orexigenic and obesogenic, while its neutralization is anorexigenic in mice, suggesting that ACBP is a major stimulator of appetite and lipo-anabolism. Accordingly, obese persons have higher circulating ACBP levels than lean individuals, and anorexia nervosa is associated with subnormal ACBP plasma concentrations. Here, we investigated whether ACBP might play a phylogenetically conserved role in appetite stimulation. We found that extracellular ACBP favors sporulation in Saccharomyces cerevisiae, knowing that sporulation is a strategy for yeast to seek new food sources. Moreover, in the nematode Caenorhabditis elegans, ACBP increased the ingestion of bacteria as well as the frequency pharyngeal pumping. These observations indicate that ACBP has a phylogenetically ancient role as a 'hunger factor' that favors food intake.
|
|
| 2. |
- Mangu, Jagadish, 1986-
(författare)
-
Influence of gut microbiota on xenobiotic toxicity in a Caenorhabditis elegans model with a focus on arsenic and PFAS
- 2023
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Exposure to environmental toxins presents a hazard to humans. Inorganic metalloid- arsenic (As), organic chemicals- per and poly-fluoroalkyl substances (PFAS) are frequently detected in the environment. Exposure to As and PFAS is associated with multiple adverse effects in humans and animals. However, little attention has been given to the interaction between host microbiota and pollutants. Gut microbiota interactions with the host and xenobiotics, is hy-pothesized to decrease xenobiotic toxicity. However, the role of microbiota on host responses during these exposure scenarios is poorly understood. Therefore, the aim was to study the influence of gut microbes on Caenorhabditis elegans responses using As and PFAS as environmental toxins. Specific objectives were to study the role of single microbes, and simple three microbe combinations with tractable diversity in nematode responses to As and PFAS. The study examined C. elegans physiological responses to As in the presence of single As resistant microbe Lysinibacillus sphaericus (Paper I) and simple 3-bacteria combinations (Paper IV). These studies showed that gut microbes decrease As toxicity and increase nematode survival through mediating host stress responses and fat metabolism. Combinations of microbes with toxins in microbiota also affect lifespan (Paper III). Furthermore, effects of PFAS mixtures were also analyzed on C. elegans and pathogen Staphylococcus aureus (Paper II); and role of gut microbe combinations during exposures to PFOS (Paper V). Exposure to PFAS/ PFOS increased virulence of pathogens and decreased host immunity, stress response and survival with opportunists; with non-pathogens C. elegans showed increased stress response and lived longer. These results emphasized that gut microbes contribute to alter xenobiotic toxicity in the host. Finally, this thesis presents novel insights into the role of gut microbes in modulating host physiological responses during As and PFAS exposures.
|
|
