scholarly journals Human intestinal glucosidases MGAM and SI: Roles in Health and Disease

2014 ◽  
Vol 70 (a1) ◽  
pp. C834-C834
Author(s):  
David Rose
Keyword(s):  
Indigenous Populations ◽  
Intestinal Microbiome ◽  
Intestinal Lumen ◽  
Gastrointestinal Cancers ◽  
Nutritional Disorder ◽  
Political Issues ◽  
Health And Disease ◽  
Small Intestinal ◽  
Intestinal Glucosidases ◽  
Shed Light

The way to a person's heart is through their stomach - not just their heart. All aspects of health are affected by sources of nutrition; not just health but social and political issues, too. The metabolism of starch into glucose is linked directly to the development of the human brain. There is considerable interest worldwide into the processing of starch and other foods by the intestinal microbiome. This talk will focus on the main mammalian intestinal enzymes that process starch, their structures, functions and potential roles in human health and disease. The alpha-glucosidases maltase-glucoamylase (MGAM) and sucrase-isomaltast (SI) are resident in the small-intestinal lumen and are responsible for generating glucose from a wide variety of starch structures. Their malfunction is responsible for many nutritional intolerances and diseases including diabetes, gastrointestinal cancers and obesity. A pediatric nutritional disorder directly associated with mutations in SI, Congenital Sucrase-Isomaltase Deficiency (CSID) has significant occurrence, especially in northern and indigenous populations. The structural analyses presented in this talk will shed light on the molecular basis for this disease, as well as the development of inhibitor analyses that are designed to investigate the roles of human intestinal glucosidases in health and disease.

scholarly journals The STING1 network regulates autophagy and cell death

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Ruoxi Zhang ◽  
Rui Kang ◽  
Daolin Tang
Keyword(s):  
Cell Death ◽  
Mitotic Cell ◽  
Therapeutic Interventions ◽  
Type I Interferons ◽  
Microbial Pathogens ◽  
Type I ◽  
Autophagic Degradation ◽  
Health And Disease ◽  
Shed Light ◽  
Pro Inflammatory Cytokines

AbstractCell death and immune response are at the core of life. In past decades, the endoplasmic reticulum (ER) protein STING1 (also known as STING or TMEM173) was found to play a fundamental role in the production of type I interferons (IFNs) and pro-inflammatory cytokines in response to DNA derived from invading microbial pathogens or damaged hosts by activating multiple transcription factors. In addition to this well-known function in infection, inflammation, and immunity, emerging evidence suggests that the STING1-dependent signaling network is implicated in health and disease by regulating autophagic degradation or various cell death modalities (e.g., apoptosis, necroptosis, pyroptosis, ferroptosis, mitotic cell death, and immunogenic cell death [ICD]). Here, we outline the latest advances in our understanding of the regulating mechanisms and signaling pathways of STING1 in autophagy and cell death, which may shed light on new targets for therapeutic interventions.

Use of shape-from-shading to estimate three-dimensional architecture in the small intestinal lumen of celiac and control patients

2013 ◽  
Vol 111 (3) ◽  
pp. 676-684 ◽  
Author(s):  
Edward J. Ciaccio ◽  
Christina A. Tennyson ◽  
Govind Bhagat ◽  
Suzanne K. Lewis ◽  
Peter H.R. Green
Keyword(s):  
Three Dimensional ◽  
Shape From Shading ◽  
Intestinal Lumen ◽  
Small Intestinal ◽  
And Control

Phytates reduce uptake of leucine and glutamate but not lysine and glucose from the intestinal lumen of chickens: Short communication

2008 ◽  
Vol 56 (4) ◽  
pp. 511-514 ◽  
Author(s):  
Edward Onyango ◽  
Elikplimi Asem ◽  
Olayiwola Adeola
Keyword(s):  
Amino Acids ◽  
Free Amino Acids ◽  
Free Amino ◽  
Short Communication ◽  
Intestinal Lumen ◽  
Depressive Effect ◽  
Leucine Uptake ◽  
Small Intestinal

An investigation into the influence of phytates on the in situ absorption of amino acids (lysine, glutamate and leucine) and glucose from the intestinal lumen of 3-week-old chickens was carried out. Birds were anaesthetised and the intestines exteriorised. Uptake of 5 mM of each nutrient over a 4-min period was measured in the presence of four phytate concentrations (0, 50, 250 and 500 mM). Five birds were used for each nutrient at each concentration of phytate tested. Leucine uptake decreased linearly (P < 0.001) and that of glutamate showed a tendency to decrease (P = 0.055) as the phytate concentration increased. Absorption of lysine and glucose were unaffected by the presence of phytate. In conclusion, phytate in the small intestinal lumen exerted a depressive effect on the absorption of specific free amino acids from the lumen. Its depressive effect was greatest for leucine followed by glutamate, and phytate had little effect on the absorption of lysine.

scholarly journals Gallbladder-derived surfactant protein D regulates gut commensal bacteria for maintaining intestinal homeostasis

2017 ◽  
Vol 114 (38) ◽  
pp. 10178-10183 ◽  
Author(s):  
Hana Sarashina-Kida ◽  
Hideo Negishi ◽  
Junko Nishio ◽  
Wataru Suda ◽  
Yuki Nakajima ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Local Environment ◽  
Surfactant Protein ◽  
Commensal Bacteria ◽  
Intestinal Lumen ◽  
Surfactant Protein D ◽  
Organ Systems ◽  
Notable Increase ◽  
Health And Disease ◽  
Deficient Mice

The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune–inflammatory diseases. Further, this immune regulation by gut microbiota is important systemically, impacting health and disease of organ systems beyond the local environment of the gut. What has not been explored is how distant organs might in turn shape the microbiota via microbe-targeted molecules. Here, we provide evidence that surfactant protein D (SP-D) synthesized in the gallbladder and delivered into intestinal lumen binds selectively to species of gut commensal bacteria. SP-D–deficient mice manifest intestinal dysbiosis and show a susceptibility to dextran sulfate sodium-induced colitis. Further, fecal transfer from SP-D–deficient mice to wild-type, germ-free mice conveyed colitis susceptibility. Interestingly, colitis caused a notable increase inSftpdgene expression in the gallbladder, but not in the lung, via the activity of glucocorticoids produced in the liver. These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy.

scholarly journals Change of Intestinal Microbiome in Patients with Coronavirus Infection

2021 ◽  
Vol 6 (5) ◽  
pp. 22-27
Author(s):  
M. M. Mishina ◽  
◽  
O. V. Kotsar ◽  
Pochernina M. H. ◽  
O. V. Kochnieva ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Intestinal Barrier ◽  
Multiple Organ ◽  
Infection Process ◽  
The Body ◽  
Intestinal Microbiome ◽  
Intestinal Lumen ◽  
Treatment Regimens ◽  
Analysis And Synthesis ◽  
Coronavirus Infection

The purpose of the study was to analyze modern literature on the problems of dysbiosis in patients with COVID-19, to study the main mechanisms of systemic interaction between the intestine and lungs, as well as changes in the microbiota that occur under the influence of coronavirus infection. Materials and methods. A comprehensive selection of research methods was used for the work: systematization of the material, the method of generalization, methods of analysis and synthesis. Scientific works in the field of microbiology, epidemiology and infectious diseases were studied. Literature data for the last 2 years (2019-2021) were considered. The results of bacteriological studies from patients with COVID infection were described. The data obtained were processed using information-analytical and statistical-analytical methods. Results and discussion. As a result of this work, a complex of connections between intestine and lungs, which is called the "intestinal-lung axis", was considered. It is known that the interaction between these two biotopes occurs with the participation of microflora and its metabolites. Dysfunction of the intestinal barrier is accompanied by bacterial translocation. Bacteria from the intestinal lumen enter the liver through the portal vein system. The lymphatic pathway of bacterial translocation from the intestine to the lungs is also possible, which causes multiple organ failure syndrome in coronavirus infection. The COVID-19 virus is able to reduce the number of ACE2 receptors in the gastrointestinal tract, which leads to an imbalance in the intestines. At the same time, the infection process in the lungs promotes the growth of bacteria of the Enterobacteriacae family in the intestine, which also leads to dysbiotic disorders. The use of probiotics is an effective tool in the complex treatment of this infection, which facilitates the general condition of patients. In the course of treatment, it is important not only to eliminate the virus from the body, but also to restore normal intestinal microbiota after an infection. Conclusion. Thus, the use of probiotic drugs for the treatment of patients with coronavirus infection can significantly reduce the risk of developing dysbiosis and improve the condition of patients. A perspective direction is the development of new treatment regimens for dysbiotic conditions using probiotics, eubiotics, synbiotics and postbiotics to prevent the development of severe complications in COVID infection

scholarly journals Dietary ascorbic acid lowers the concentration of soluble copper in the small intestinal lumen of rats

1994 ◽  
Vol 71 (5) ◽  
pp. 701-707 ◽  
Author(s):  
G. J. Van Den Berg ◽  
S. YU ◽  
A. G. Lemmens ◽  
A. C. Beynen
Keyword(s):  
Ascorbic Acid ◽  
Small Intestine ◽  
Liquid Phase ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Intestinal Lumen ◽  
Distal Intestine ◽  
Small Intestinal ◽  
Ascorbic Acid Supplementation

We tested the hypothesis that ascorbic acid in the diet of rats lowers the concentration of soluble Cu in the small intestine, causing a decrease in apparent Cu absorption. Male rats were fed on diets adequate in Cu (5 mg Cu/kg) without or with 10 g ascorbic acid/kg. The diet with ascorbic acid was fed for either 6 or 42 d. Ascorbic acid depressed tissue Cu concentrations after a feeding period of 42, but not after 6 d. Dietary ascorbic acid lowered apparent Cu absorption after 6, but not after 42 d. The lowering of tissue Cu concentrations after long-term ascorbic acid feeding may have increased the efficiency of Cu absorption, and thus counteracted the inhibitory effect of ascorbic acid. Dietary ascorbic acid caused a significant decrease in the Cu concentrations in the liquid phase of both the proximal and distal parts of the small intestinal lumen. This effect was due to both a decrease in the amount of Cu in the liquid digesta and an increase in the volume of the liquid phase; only the latter effect for the distal intestine was statistically significant. We conclude that ascorbic acid supplementation lowers Cu absorption by decreasing the concentration of soluble Cu in the small intestine.

scholarly journals The Gut Ecosystem: A Critical Player in Stroke

2020 ◽  
Author(s):  
Rosa Delgado Jiménez ◽  
Corinne Benakis
Keyword(s):  
Current Knowledge ◽  
Critical Factor ◽  
Intestinal Microbiome ◽  
Brain Disorders ◽  
Therapeutic Approaches ◽  
Health And Disease ◽  
Brain Stroke ◽  
The Brain ◽  
Improve Patient

AbstractThe intestinal microbiome is emerging as a critical factor in health and disease. The microbes, although spatially restricted to the gut, are communicating and modulating the function of distant organs such as the brain. Stroke and other neurological disorders are associated with a disrupted microbiota. In turn, stroke-induced dysbiosis has a major impact on the disease outcome by modulating the immune response. In this review, we present current knowledge on the role of the gut microbiome in stroke, one of the most devastating brain disorders worldwide with very limited therapeutic options, and we discuss novel insights into the gut-immune-brain axis after an ischemic insult. Understanding the nature of the gut bacteria-brain crosstalk may lead to microbiome-based therapeutic approaches that can improve patient recovery.

scholarly journals TMPRSS2 and TMPRSS4 promote SARS-CoV-2 infection of human small intestinal enterocytes

2020 ◽  
Vol 5 (47) ◽  
pp. eabc3582 ◽  
Author(s):  
Ruochen Zang ◽  
Maria Florencia Gomez Castro ◽  
Broc T. McCune ◽  
Qiru Zeng ◽  
Paul W. Rothlauf ◽  
...  
Keyword(s):  
Serine Proteases ◽  
Gastrointestinal Symptoms ◽  
Host Cells ◽  
Productive Infection ◽  
Intestinal Lumen ◽  
Fecal Shedding ◽  
Oral Transmission ◽  
Stool Specimens ◽  
Small Intestinal ◽  
Intestinal Enterocytes

Gastrointestinal symptoms and fecal shedding of SARS-CoV-2 RNA are frequently observed in COVID-19 patients. However, it is unclear whether SARS-CoV-2 replicates in the human intestine and contributes to possible fecal-oral transmission. Here, we report productive infection of SARS-CoV-2 in ACE2+ mature enterocytes in human small intestinal enteroids. Expression of two mucosa-specific serine proteases, TMPRSS2 and TMPRSS4, facilitated SARS-CoV-2 spike fusogenic activity and promoted virus entry into host cells. We also demonstrate that viruses released into the intestinal lumen were inactivated by simulated human colonic fluid, and infectious virus was not recovered from the stool specimens of COVID-19 patients. Our results highlight the intestine as a potential site of SARS-CoV-2 replication, which may contribute to local and systemic illness and overall disease progression.

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