Does gut microbiota regulate brooding in geese?

2021 ◽  
pp. 1-13
Author(s):  
Guojun Liu ◽  
Zhenhua Guo ◽  
Di Liu ◽  
He Meng ◽  
Yuming Zheng ◽  
...  

Abstract Domestic geese can reduce the amount of food intake when brooding. Because of the reduction in food intake, the total number of microorganisms in the gut is also reduced. Will this affect the goose’s thinking and make the goose stop brooding and eat food? We hypothesize that gut microbiota affects the brain through a brain–gut peptide and further regulates the breeding behavior of geese. In this study, we evaluated the microbiome related to the goose and transcription groups of brooding and egg production periods. The changes and differences in gut microbiota and gene expression of female geese in different reproduction periods were analyzed, and the possible interaction between them was explored. The results showed that the relative abundance of Faecalibacterium with a growth-promoting effect in the cecum was higher in the egg production group than in the brooding group. Microbial metabolic pathways with significant differences between the two groups were also enriched in the secondary functional groups with different gut microbiota metabolism. The downregulated genes in the egg production group were mainly related to energy metabolism, such as ATP synthesis-related genes. These results suggest that the brooding group’s gut microbiota can make relevant changes according to the reproduction stage of the goose. Since the amount of food taken in is reduced, it can promote the decomposition of the host’s fat. Simultaneously, insulin is also used to deliver messages to the brain; it is necessary to end the brooding behavior at an appropriate time and for eating to start.

Author(s):  
Ana Agustí ◽  
Isabel Campillo ◽  
Tiziano Balzano ◽  
Alfonso Benítez-Páez ◽  
Inmaculada López-Almela ◽  
...  

AbstractFood addiction (FA) is characterized by behavioral and neurochemical changes linked to loss of food intake control. Gut microbiota may influence appetite and food intake via endocrine and neural routes. The gut microbiota is known to impact homeostatic energy mechanisms, but its role in regulating the reward system is less certain. We show that the administration of Bacteroides uniformis CECT 7771 (B. uniformis) in a rat FA model impacts on the brain reward response, ameliorating binge eating and decreasing anxiety-like behavior. These effects are mediated, at least in part, by changes in the levels of dopamine, serotonin, and noradrenaline in the nucleus accumbens and in the expression of dopamine D1 and D2 receptors in the prefrontal cortex and intestine. B. uniformis reverses the fasting-induced microbiota changes and increases the abundance of species linked to healthy metabolotypes. Our data indicate that microbiota-based interventions might help to control compulsive overeating by modulating the reward response.


2021 ◽  
Vol 22 (11) ◽  
pp. 5830
Author(s):  
Marina Romaní-Pérez ◽  
Clara Bullich-Vilarrubias ◽  
Inmaculada López-Almela ◽  
Rebeca Liébana-García ◽  
Marta Olivares ◽  
...  

Obesity currently represents a major societal and health challenge worldwide. Its prevalence has reached epidemic proportions and trends continue to rise, reflecting the need for more effective preventive measures. Hypothalamic circuits that control energy homeostasis in response to food intake are interesting targets for body-weight management, for example, through interventions that reinforce the gut-to-brain nutrient signalling, whose malfunction contributes to obesity. Gut microbiota–diet interactions might interfere in nutrient sensing and signalling from the gut to the brain, where the information is processed to control energy homeostasis. This gut microbiota–brain crosstalk is mediated by metabolites, mainly short chain fatty acids, secondary bile acids or amino acids-derived metabolites and subcellular bacterial components. These activate gut–endocrine and/or neural-mediated pathways or pass to systemic circulation and then reach the brain. Feeding time and dietary composition are the main drivers of the gut microbiota structure and function. Therefore, aberrant feeding patterns or unhealthy diets might alter gut microbiota–diet interactions and modify nutrient availability and/or microbial ligands transmitting information from the gut to the brain in response to food intake, thus impairing energy homeostasis. Herein, we update the scientific evidence supporting that gut microbiota is a source of novel dietary and non-dietary biological products that may beneficially regulate gut-to-brain communication and, thus, improve metabolic health. Additionally, we evaluate how the feeding time and dietary composition modulate the gut microbiota and, thereby, the intraluminal availability of these biological products with potential effects on energy homeostasis. The review also identifies knowledge gaps and the advances required to clinically apply microbiome-based strategies to improve the gut–brain axis function and, thus, combat obesity.


1990 ◽  
Vol 80 (1) ◽  
pp. 109-113 ◽  
Author(s):  
Ester P. Lorences ◽  
Gordon J. McDougall ◽  
Stephen C. Fry

2020 ◽  
Vol 57 (12) ◽  
pp. 5026-5043 ◽  
Author(s):  
Shan Liu ◽  
Jiguo Gao ◽  
Mingqin Zhu ◽  
Kangding Liu ◽  
Hong-Liang Zhang

Abstract Understanding how gut flora influences gut-brain communications has been the subject of significant research over the past decade. The broadening of the term “microbiota-gut-brain axis” from “gut-brain axis” underscores a bidirectional communication system between the gut and the brain. The microbiota-gut-brain axis involves metabolic, endocrine, neural, and immune pathways which are crucial for the maintenance of brain homeostasis. Alterations in the composition of gut microbiota are associated with multiple neuropsychiatric disorders. Although a causal relationship between gut dysbiosis and neural dysfunction remains elusive, emerging evidence indicates that gut dysbiosis may promote amyloid-beta aggregation, neuroinflammation, oxidative stress, and insulin resistance in the pathogenesis of Alzheimer’s disease (AD). Illustration of the mechanisms underlying the regulation by gut microbiota may pave the way for developing novel therapeutic strategies for AD. In this narrative review, we provide an overview of gut microbiota and their dysregulation in the pathogenesis of AD. Novel insights into the modification of gut microbiota composition as a preventive or therapeutic approach for AD are highlighted.


Zygote ◽  
2008 ◽  
Vol 16 (3) ◽  
pp. 239-247 ◽  
Author(s):  
T. Metoki ◽  
H. Iwata ◽  
M. Itoh ◽  
M. Kasai ◽  
A. Takajyo ◽  
...  

SummaryWe examined the effect of supplementing the culture medium with follicular fluid (FF) on the growth of porcine preantral follicles and oocytes. Firstly, preantral follicles were retrieved from ovaries and then FF was collected from all antral follicles that were 2–7 mm in diameter (AFF), which included large follicles of 4–7 mm in diameter (LFF) and small follicles of 2–3 mm in diameter (SFF). When preantral follicles with a diameter of 250 μm were cultured in medium containing AFF, the growth of follicles and oocytes was greater than when follicles were cultured in medium containing fetal calf serum (FCS). When this growth-promoting effect in AFF was compared for LFF and SFF, the LFF were shown to be significantly more effective than SFF. This LFF effect was lost, however, when the concentration of LFF in the medium was decreased from 5% to 0.5% or when LFF were heat treated (60 °C for 30 min) or trypsin was added. In contrast, a decrease in SFF concentration from 5% to 0.5% and heat treatment of the SFF enhanced preantral follicle growth. Furthermore, proteins obtained from LFF that had molecular weights greater than 10 kDa (LFF > 10 kDa) had similar, but relatively reduced, growth-promoting properties. The remaining three LFF protein fractions (<10 kDa or <100 kDa or >100 kDa), however, did not have these growth-promoting properties. In conclusion, the supplementation of medium with LFF, rather than serum, enhanced preantral follicle and oocyte growth. Factors that enhanced follicle development in LFF and factors that suppressed follicle development in SFF were proteins and these LFF factors ranged in size from 10 kDa to over 100 kDa.


2011 ◽  
Vol 301 (2) ◽  
pp. R448-R455 ◽  
Author(s):  
Jason Wright ◽  
Carlos Campos ◽  
Thiebaut Herzog ◽  
Mihai Covasa ◽  
Krzysztof Czaja ◽  
...  

Intraperitoneal injection of CCK reduces food intake and triggers a behavioral pattern similar to natural satiation. Reduction of food intake by CCK is mediated by vagal afferents that innervate the stomach and small intestine. These afferents synapse in the hindbrain nucleus of the solitary tract (NTS) where gastrointestinal satiation signals are processed. Previously, we demonstrated that intraperitoneal (IP) administration of either competitive or noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonists attenuates reduction of food intake by CCK. However, because vagal afferents themselves express NMDA receptors at both central and peripheral endings, our results did not speak to the question of whether NMDA receptors in the brain play an essential role in reduction of feeding by CCK. We hypothesized that activation of NMDA receptors in the NTS is necessary for reduction of food intake by CCK. To test this hypothesis, we measured food intake following IP CCK, subsequent to NMDA receptor antagonist injections into the fourth ventricle, directly into the NTS or subcutaneously. We found that either fourth-ventricle or NTS injection of the noncompetitive NMDA receptor antagonist MK-801 was sufficient to inhibit CCK-induced reduction of feeding, while the same antagonist doses injected subcutaneously did not. Similarly fourth ventricle injection of d-3-(2-carboxypiperazin-4-yl)-1-propenyl-1-phosphoric acid (d-CPPene), a competitive NMDA receptor antagonist, also blocked reduction of food intake following IP CCK. Finally, d-CPPene injected into the fourth ventricle attenuated CCK-induced expression of nuclear c-Fos immunoreactivity in the dorsal vagal complex. We conclude that activation of NMDA receptors in the hindbrain is necessary for the reduction of food intake by CCK. Hindbrain NMDA receptors could comprise a critical avenue for control and modulation of satiation signals to influence food intake and energy balance.


Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 880
Author(s):  
Karine Mandon ◽  
Fanny Nazaret ◽  
Davoud Farajzadeh ◽  
Geneviève Alloing ◽  
Pierre Frendo

Plants interact with a large number of microorganisms that greatly influence their growth and health. Among the beneficial microorganisms, rhizosphere bacteria known as Plant Growth Promoting Bacteria increase plant fitness by producing compounds such as phytohormones or by carrying out symbioses that enhance nutrient acquisition. Nitrogen-fixing bacteria, either as endophytes or as endosymbionts, specifically improve the growth and development of plants by supplying them with nitrogen, a key macro-element. Survival and proliferation of these bacteria require their adaptation to the rhizosphere and host plant, which are particular ecological environments. This adaptation highly depends on bacteria response to the Reactive Oxygen Species (ROS), associated to abiotic stresses or produced by host plants, which determine the outcome of the plant-bacteria interaction. This paper reviews the different antioxidant defense mechanisms identified in diazotrophic bacteria, focusing on their involvement in coping with the changing conditions encountered during interaction with plant partners.


2000 ◽  
Vol 118 (4) ◽  
pp. A602
Author(s):  
Shigeo Takaishi ◽  
Mitsutaka Sawada ◽  
Yukari Morita ◽  
Hiroaki Fukuzawa ◽  
Hiroshi Seno ◽  
...  

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