Gut T Cells Feast on GLP-1 to Modulate Cardiometabolic Disease

Tsai, Sue; Winer, Shawn; Winer, Daniel A.

doi:10.1016/j.cmet.2019.03.002

Cited by 7 publications

(4 citation statements)

References 11 publications

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“…A recent study in mice showed that the products generated by the intestinal microbiota such as SCFAs, secondary bile acids, endotoxins and tryptophan metabolites, are often altered in diets rich in fat (coconut oil and soybean oil) and low in fiber and would then impact L-cell glucagon-like peptide (GLP)-1 secretion [115].…”

Section: Diet Gut Microbiota and Cardiovascular Diseasesmentioning

confidence: 99%

The Gut Microbiota and Its Implication in the Development of Atherosclerosis and Related Cardiovascular Diseases

et al. 2020

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The importance of gut microbiota in health and disease is being highlighted by numerous research groups worldwide. Atherosclerosis, the leading cause of heart disease and stroke, is responsible for about 50% of all cardiovascular deaths. Recently, gut dysbiosis has been identified as a remarkable factor to be considered in the pathogenesis of cardiovascular diseases (CVDs). In this review, we briefly discuss how external factors such as dietary and physical activity habits influence host-microbiota and atherogenesis, the potential mechanisms of the influence of gut microbiota in host blood pressure and the alterations in the prevalence of those bacterial genera affecting vascular tone and the development of hypertension. We will also be examining the microbiota as a therapeutic target in the prevention of CVDs and the beneficial mechanisms of probiotic administration related to cardiovascular risks. All these new insights might lead to novel analysis and CVD therapeutics based on the microbiota.

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Section: Diet Gut Microbiota and Cardiovascular Diseasesmentioning

confidence: 99%

The Gut Microbiota and Its Implication in the Development of Atherosclerosis and Related Cardiovascular Diseases

et al. 2020

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“…Dysfunctional gut immune cells can promote the impaired bioavailability of gastrointestinal hormones such as GLP-1, which has important metabolic effects (as incretin that enhances the secretion of insulin to reduce blood glucose levels) and, in turn, is involved in the maintenance of barrier integrity acting on TJs and gut intraepithelial lymphocytes, which express the glucagon-like peptide 1 receptor (GLP1R) and have anti-inflammatory activity cytokines [ 462 ]. Additional mechanisms driven by obesity include gut epithelial lymphocytes sequestering GLP-1, decreased availability of GLP1-secreting enteroendocrine L cells, or lymphocyte-driven upregulation of the expression of molecules (dipeptidyl peptidase 4 (DPP4)) degrading GLP1 [ 91 , 463 ]. Lastly, gut immune cells such as anti-inflammatory IgA+ antibody-secreting cells (ASCs) can leave the barrier, decreasing the local protection (IL-10 and IgA), and migrate to other inflamed tissues (liver, visceral fat) [ 439 ].…”

Section: Intestinal Barrier Features In Obesitymentioning

confidence: 99%

Intestinal Barrier and Permeability in Health, Obesity and NAFLD

et al. 2021

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The largest surface of the human body exposed to the external environment is the gut. At this level, the intestinal barrier includes luminal microbes, the mucin layer, gastrointestinal motility and secretion, enterocytes, immune cells, gut vascular barrier, and liver barrier. A healthy intestinal barrier is characterized by the selective permeability of nutrients, metabolites, water, and bacterial products, and processes are governed by cellular, neural, immune, and hormonal factors. Disrupted gut permeability (leaky gut syndrome) can represent a predisposing or aggravating condition in obesity and the metabolically associated liver steatosis (nonalcoholic fatty liver disease, NAFLD). In what follows, we describe the morphological-functional features of the intestinal barrier, the role of major modifiers of the intestinal barrier, and discuss the recent evidence pointing to the key role of intestinal permeability in obesity/NAFLD.

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“…Interestingly, the GLP-1R receptor is expressed at a high density (and here the localization has been supported by in vivo ligand binding studies [Grunddal et al, Endocrinology, under revision]) in intestinal intraepithelial lymphocytes (iIELs). The iIELs express abundant levels of the full-length GLP-1R [130,131], and stimulation of isolated iIELs with Ex-4 directly increased dose-dependent cAMP accumulation in the iIELs and suppressed pro-inflammatory cytokines' expression [131]. It has also been reported that GLP-1R knock out (KO) mice are more susceptible to intestinal injury [131].…”

Section: The Immune System and Inflammationmentioning

confidence: 99%