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Parenteral and Enteral Nutrition in Critical Illness
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
Unlike cells in the rest of the body, enterocytes get much of their nutrition from the flow of food particles in the gut lumen itself (Miron and Cristea 2012). This is somewhat analogous to the vascular endothelium which gets some of its oxygen supply from direct contact with the RBCs in the vessel lumen. The vascular endothelium doesn’t have to rely on penetrating vaso vasorum to provide oxygen. The vessel lumen is filled with oxygenated RBCs. Similarly, the enterocytes don’t have to rely on glucose, amino acids and lipids to be delivered through the mesenteric vascular system. They can take nutrients that they are already in contact with. Similarly, it is believed that the gut microbiome gets its entire nutritional intake from the gut luminar nutrient flow (Rowland et al. 2018).
The Gut and Heart Connection
Published in Mark C Houston, The Truth About Heart Disease, 2023
Alterations in the gut or intestinal barrier or lining (called the “enterocytes”) lead to dysfunction and increased intestinal leakage Certain types of bacteria called gram-negative bacteria may enter the blood to produce severe inflammation and damage to the arteries. The medical term for this is endotoxemia (internal toxins), which means that the bacteria, the components of the bacteria, the types of food that we eat, and the health of the gut may allow toxins to enter the blood and cause arterial damage. The chronic dietary intake of long-chain saturated fatty acids (SFAs) with refined carbohydrates and starches increases the gram-negative bacterial concentration by 70%. On the other hand, a vegetable intake, fiber, and probiotics decrease gram-negative gut concentration.
The Silver Lining
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Mark R Frey, Misty Good, Steven J. McElroy
Absorptive enterocytes make up the majority of the cells of the epithelial monolayer (9, 63). They are polarized simple columnar epithelial cells with a well-ordered luminal brush border consisting of microvilli and an associated glycocalyx (64). The brush border serves as a second-order multiplier of surface area (the first being the folded crypt villus structure of the epithelium overall) and is a storage and release site for secreted material such as digestive enzymes (65–67). Enterocytes participate in a variety of critical functions for the host, including nutrient absorption, innate immune surveillance (68, 69), regulation of water and ion/salt balance, and maintenance of the physical barrier between the body proper and the lumen of the gut, which is topologically “outside” the organism.
Dietary vitamin K is remodeled by gut microbiota and influences community composition
Published in Gut Microbes, 2021
Jessie L. Ellis, J. Philip Karl, Angela M. Oliverio, Xueyan Fu, Jason W. Soares, Benjamin E. Wolfe, Christopher J. Hernandez, Joel B. Mason, Sarah L. Booth
In vitro, only 2H8MD, but not full VK quinones, were remodeled to 2H7MKn. These results suggest that human gut bacteria cannot remove the sidechain of VK quinones, but can add a sidechain to a vitamin K precursor. A comparison of in vitro and in vivo models here suggests that there may be a keystone species in the murine, but not human, gut microbiota that can cleave the naphthoquinone ring from the sidechain, or that the host may generate a necessary intermediate in the remodeling of dietary vitamin K forms. MD is one possible candidate, as it is generated in intestinal tissue during the enzymatic conversion of dietary VK to MK4. The reaction is independent of the gut microbiota,23 and involves prenylation of MD by the mammalian enzyme UBIAD1.24,25 As enterocytes are routinely sloughed off every 2–3 days,26 host-generated MD may become available to the gut microbiota upon enterocyte shedding. MenA is a prenyltransferase in one of the two de novo bacterial synthesis pathways of MKn,10 and is the bacterial homolog of UBIAD1. Therefore, MenA is a likely candidate for the prenyltransferase involved in the remodeling of dietary vitamin K quinones. Although we have demonstrated in vitro the capability of human gut microbiota to prenylate MD to form menaquinones, further experiments are needed to confirm if MD serves as an intermediate in vivo.
Gut microbes in neurocognitive and mental health disorders
Published in Annals of Medicine, 2020
Tyler Halverson, Kannayiram Alagiakrishnan
Under normal physiological and homeostatic conditions there exists a healthy resting inflammatory state where the GM stimulate the release of cytokines and chemokines which allows for the regulation of the bacterial populations in the gut [7]. The bacteria colonised in the gut need to be controlled to prevent spread throughout the host. Primarily, the epithelial layer of our gut secretes a mucus layer creating a luminal-mucosal interface; the majority of the host-microbiota interactions occur here [29]. This interaction is dependent on the innate immune response. Enterocytes within the gut have innate immune receptors and release chemokines and cytokines and can influence local immune cells [29]. The host immune system can also monitor the GM, through Toll-like receptors (TLR), as many of the GI bacteria express a polysaccharide coating, thus identifying potential pathogens if exposed [30].
Glucose-6-phosphate dehydrogenase deficiency reduces susceptibility to cancer of endodermal origin
Published in Acta Oncologica, 2019
Giovanni Mario Pes, Alessandra Errigo, Sara Soro, Nunzio Pio Longo, Maria Pina Dore
The finding that lung cancer, in our study, seems to be an exception as its development is not affected by G6PD deficiency, as already reported [35], may be due to several causes: this cancer may originate from distinct types of cells but mostly from ciliated airway epithelial cells that are probably a terminally differentiated lineage [36]. As a consequence, their proliferative rate was estimated as a half-life of 6 months in the trachea and 17 months in the lungs, much longer than the three days estimated for mature enterocytes in the villi tips [37]. This suggests that the proliferative stimuli capable to amplify the hypothetical genotoxic damage induced by G6PD deficiency may be greater for enteric cells than for cell derived from the respiratory tract. Moreover, lung cancer cells as well as cancer cells of ectodermal origin may be less dependent from NADPH compared to gastric, colonic and liver tumor cells, thus overcoming the energy restriction induced by the G6PD enzyme deficiency. In any case, the protective effect of G6PD against cancers of endodermal origin would hardly influence significantly the survivorship curve of the population [38] since deaths from these tumors represent a near-negligible proportion of the overall mortality in the general population.