scholarly journals Nutrient sensing; transcriptomic response and regulation of gut motility in an agastric vertebrate

2019 ◽  
Author(s):  
Hoang T. M. D. Le ◽  
Kai K. Lie ◽  
Angela Etayo ◽  
Ivar Rønnestad ◽  
Øystein Sæle
Keyword(s):  
Digestive Tract ◽  
Genetic Regulation ◽  
Nutrient Sensing ◽  
Transcriptomic Response ◽  
Gut Motility ◽  
Gut Evacuation ◽  
Vitro Model ◽  
Transcriptomic Changes ◽  
Upregulated Genes

AbstractThe transcriptome of nutrient sensing and the regulation of gut motility by nutrients in a stomachless fish with a short digestive tract; the ballan wrasse (Labrus berggylta) were investigated. Using an in vitro model, we differentiate how signals initiated by physical stretch and nutrients modulate the gut evacuation rate and motility patterns, and transcriptomic changes. Stretch on the intestine by inert cellulose initiated fast evacuation out of the anterior intestine compared to the digestible protein and lipid. Stretch on the intestine upregulated genes associated with increased muscle activity, whereas nutrients stimulated pathways related to ribosomal activity and the increase in the expression of several neuropeptides which are directly involved in gut motility regulation. Our findings show that physical pressure in the intestine initiate contractions propelling the matter towards the exit, whereas the sensing of nutrients modulates the motility to prolong the residence of digesta in the digestive tract for optimal digestion.Summary statementPressure by food speed up peristalsis in the intestine, but the intestines ability to sense nutrients slow down peristalsis for better digestion. This is partly controlled by genetic regulation.

scholarly journals Physical and nutrient stimuli differentially modulate gut motility patterns, gut transit rate, and transcriptome in an agastric fish, the ballan wrasse

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247076
Author(s):  
Hoang T. M. D. Le ◽  
Kai K. Lie ◽  
Angela Etayo ◽  
Ivar Rønnestad ◽  
Øystein Sæle
Keyword(s):  
Digestive Tract ◽  
Gut Motility ◽  
Lower Vertebrates ◽  
Motility Regulation ◽  
Protein Group ◽  
Anterior Intestine ◽  
Gut Evacuation ◽  
Upregulated Genes ◽  
Mechanical Sensing

The effects of nutrient and mechanical sensing on gut motility and intestinal metabolism in lower vertebrates remains largely unknown. Here we present the transcriptome response to luminal stimulation by nutrients and an inert bolus on nutrient response pathways and also the response on gut motility in a stomachless fish with a short digestive tract; the ballan wrasse (Labrus berggylta). Using an in vitro model, we differentiate how signals initiated by physical stretch (cellulose and plastic beads) and nutrients (lipid and protein) modulate the gut evacuation rate, motility patterns and the transcriptome. Intestinal stretch generated by inert cellulose initiated a faster evacuation of digesta out of the anterior intestine compared to digestible protein and lipid. Stretch on the intestine upregulated genes associated with increased muscle activity, whereas nutrients stimulated increased expression of several neuropeptides and receptors which are directly involved in gut motility regulation. Although administration of protein and lipid resulted in similar bulbous evacuation times, differences in intestinal motility, transit between the segments and gene expression between the two were observed. Lipid induced increased frequency of ripples and standing contraction in the middle section of the intestine compared to the protein group. We suggest that this difference in motility was modulated by factors [prepronociceptin (pnoca), prodynorphin (pdyn) and neuromedin U (nmu), opioid neurotransmitters and peptides] that are known to inhibit gastrointestinal motility and were upregulated by protein and not lipid. Our findings show that physical pressure in the intestine initiate contractions propelling the bolus distally, directly towards the exit, whereas the stimuli from nutrients modulates the motility to prolong the residence time of digesta in the digestive tract for optimal digestion.

scholarly journals Models and Tools for Studying Enteroendocrine Cells

Endocrinology ◽  
2018 ◽  
Vol 159 (12) ◽  
pp. 3874-3884 ◽  
Author(s):  
Deborah A Goldspink ◽  
Frank Reimann ◽  
Fiona M Gribble
Keyword(s):  
Molecular Mechanisms ◽  
Ex Vivo ◽  
Gut Hormones ◽  
Nutrient Sensing ◽  
Enteroendocrine Cells ◽  
Model Systems ◽  
Hormone Production ◽  
Obesity And Diabetes ◽  
Vitro Model

Abstract Gut hormones produced by gastrointestinal enteroendocrine cells modulate key physiological processes including glucose homeostasis and food intake, making them potential therapeutic candidates to treat obesity and diabetes. Understanding the function of enteroendocrine cells and the molecular mechanisms driving hormone production is a key step toward mobilizing endogenous hormone reserves in the gut as a therapeutic strategy. In this review, we will discuss the variety of ex vivo and in vitro model systems driving this research and their contributions to our current understanding of nutrient-sensing mechanisms in enteroendocrine cells.

scholarly journals α-Tocopherol Modulates Non-Amyloidogenic Pathway and Autophagy in an In Vitro Model of Alzheimer’s Disease: A Transcriptional Study

2019 ◽  
Vol 9 (8) ◽  
pp. 196 ◽  
Author(s):  
Agnese Gugliandolo ◽  
Luigi Chiricosta ◽  
Serena Silvestro ◽  
Placido Bramanti ◽  
Emanuela Mazzon
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neuroblastoma Cells ◽  
Amyloid Β ◽  
Amyloidogenic Processing ◽  
Model Of Alzheimer’S Disease ◽  
Thiazolyl Blue Tetrazolium Bromide ◽  
Vitro Model ◽  
Upregulated Genes

Alzheimer’s disease (AD) is the most common form of dementia worldwide. The hallmarks of AD are the extracellular amyloid plaques, which are formed by amyloid β (Aβ) aggregates derived from the processing of the amyloid precursor protein (APP), and the intraneuronal neurofibrillary tangles, which are formed by the hyperphosphorylated tau protein. The aim of this work was to study the effects of α-tocopherol in retinoic acid differentiated SH-SY5Y neuroblastoma cells exposed to Aβ1-42 evaluating the transcriptional profile by next-generation sequencing. We observed that α-tocopherol was able to reduce the cytotoxicity induced by Aβ treatment, as demonstrated by Thiazolyl Blue Tetrazolium Bromide (MTT) assay. Moreover, the transcriptomic analysis evidenced that α-tocopherol treatment upregulated genes involved in the non-amyloidogenic processing of APP, while it downregulated the amyloidogenic pathway. Moreover, α-tocopherol modulated the expression of the genes involved in autophagy and the cell cycle, which are both known to be altered in AD. The treatment with α-tocopherol was also able to reduce oxidative stress, restoring nuclear factor erythroid-derived 2-like 2 (Nrf2) and decreasing inducible nitric oxide synthase (iNOS) levels, as demonstrated by immunocytochemistry.

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

A new in vitro model for pre-transplantation diagnosis of frozen/thawed human ovarian tissue

2011 ◽  
Vol 71 (05) ◽  
Author(s):  
M Salama ◽  
K Winkler ◽  
KF Murach ◽  
S Hofer ◽  
L Wildt ◽  
...  
Keyword(s):  
In Vitro Model ◽  
Ovarian Tissue ◽  
Human Ovarian Tissue ◽  
Vitro Model
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