Alterations in Gut Microbiota and Immunity by Dietary Fat.

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Term Occurence Count Dictionary
metabolic syndrome 33 endocrinologydiseases
metformin 7 endocrinologydiseasesdrugs
obesity 25 endocrinologydiseases
glucose intolerance 2 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
metformin 13554 Akkermansia has a protective effect against the development of atherosclerosis.[42]The metabolic action of metformin , the first-line anti-diabetic therapy recommended by the American Diabetes Association and the European
metformin 13926 Akkermansia, which is accompanied by an increase in mucin-producing goblet cells. Moreover, administration of metformin ameliorates metabolic inflammation and restores Treg cells in adipose tissue, similar to the effect
metformin 14096 in adipose tissue, similar to the effect of Akkermansia administration.[38][43] In a previous study, metformin action on gut microbiota of HFD-fed mice is analogous to the metformin action on gut microbiota of Caenorhabditis
metformin 14167 administration.[38][43] In a previous study, metformin action on gut microbiota of HFD-fed mice is analogous to the metformin action on gut microbiota of Caenorhabditis elegans, which results in alteration of folate and the methionine
metformin 14356 of folate and the methionine metabolism of E. coli in the intestine of the worm.[44] Intriguingly, metformin administration greatly increases the abundance of Akkermansia in patients with type 2 diabetes as well.[45][46]While
metformin 25548 also be employed to modulate gut microbiota or immunity. As discussed above, the anti-diabetic drug metformin can exert beneficial metabolic effects through modulation of gut microbiota in mice and human patients.[38][43][46]
metformin 25688 effects through modulation of gut microbiota in mice and human patients.[38][43][46] The action of metformin as an anti-aging or pro-longevity agent[38][43] may also be related to its effect on gut microbiota.[44]
Select Disease Character Offset Disease Term Instance
glucose intolerance 5556 obesity and diabetes: germ-free (GF) mice are resistant to high-fat diet (HFD)-induced obesity and glucose intolerance due to de-repressed expression of fasting-induced adipose factor (Fiaf) in the intestinal epithelium.[16][17]
glucose intolerance 22104 of Th17 cells, unlike that of Th1 cells, was shown to alleviate weight gain, increased fat mass, and glucose intolerance of HFD-fed Rag1-knockout mice. However, Th17 cells from integrin β7-knockout mice had no such metabolic
metabolic syndrome 1004 with dietary fats. Interestingly, excessive dietary fat has been incriminated as a primary culprit of metabolic syndrome and obesity. After intake of high-fat diet or Western diet, extensive changes in gut microbiota have
metabolic syndrome 1400 microbiota and immunity associated with dietary fat, as well as their relationships with the pathogenesis of metabolic syndrome . These findings may provide insight into the understanding of the complex pathophysiology related to
metabolic syndrome 2383 diseases. Metabolic inflammation consequently causes insulin resistance, contributing to the development of metabolic syndrome .[2] However, the underlying mechanisms of low-grade tissue inflammation inducing metabolic symptoms
metabolic syndrome 5165 increased food intake and obesity.[14] In addition to these effects, SCFAs can contribute to improvement of metabolic syndrome by promoting secretions of peptide hormones, such as peptide YY and glucagon-like peptide-1, that decrease
metabolic syndrome 6236 nutrient homeostasis and also a possible etiological role of altered gut microbiota in the development of metabolic syndrome .Phylum level changes and enterotypeTo investigate the role of microbiota in nutrient uptake or in the
metabolic syndrome 6372 changes and enterotypeTo investigate the role of microbiota in nutrient uptake or in the development of metabolic syndrome , identification of individual microorganism is crucial. However, identification of gut microbiota has
metabolic syndrome 10855 be also novel therapeutic targets in the management of obesity or diabetes.Changes in Akkermansia in metabolic syndrome One of the prominent changes in gut microbiota associated with metabolic syndrome is that of Akkermansia
metabolic syndrome 10936 in Akkermansia in metabolic syndromeOne of the prominent changes in gut microbiota associated with metabolic syndrome is that of Akkermansia muciniphila. Akkermansia muciniphila has recently been identified as a Gram-negative
metabolic syndrome 14594 results suggest potential therapeutic value of Akkermansia or its components as a drug candidate against metabolic syndrome , such prospects have been hampered by the sensitivity of Akkermansia to oxygen, the presence of animal-derived
metabolic syndrome 15265 pasteurization was identified, brightening the prospect for the development of novel therapeutics against metabolic syndrome and diabetes.[47]CHANGES IN INNATE IMMUNITY OF THE INTESTINE IN METABOLIC SYNDROMERole of gut innate
metabolic syndrome 15405 diabetes.[47]CHANGES IN INNATE IMMUNITY OF THE INTESTINE IN METABOLIC SYNDROMERole of gut innate immune receptors in metabolic syndrome Several recent studies have suggested that disruption of the gut barrier function and the gut microbiota-derived
metabolic syndrome 15580 the gut barrier function and the gut microbiota-derived LPS could contribute to the pathogenesis of metabolic syndrome and diabetes. HFD increases gut permeability and reduces the expression of tight junction proteins,
metabolic syndrome 16235 family, plays a crucial role in inflammasome activation and metabolic inflammation associated with metabolic syndrome and diabetes.[50][51] Increased systemic LPS due to disrupted gut barrier function can activate not
metabolic syndrome 16477 NLRP3, together with palmitic acid or other inflammasome activators that can be increased in obesity or metabolic syndrome .[51] However, it is not clear whether such metabolic inflammation is associated with changes of innate
metabolic syndrome 16814 intestine,[52][53] it is likely that these innate immune receptors in the intestine contribute to the development of metabolic syndrome . A direct role of intestinal TLR in metabolic syndrome has been demonstrated using mice with targeted
metabolic syndrome 16869 the intestine contribute to the development of metabolic syndrome. A direct role of intestinal TLR in metabolic syndrome has been demonstrated using mice with targeted disruption of MyD88, specifically in gut epithelial cells
metabolic syndrome 17316 innate immune receptors in intestinal epithelial cells than in myeloid cells in the development of metabolic syndrome .An intriguing model of metabolic syndrome associated with the activation of innate immune receptors
metabolic syndrome 17358 epithelial cells than in myeloid cells in the development of metabolic syndrome.An intriguing model of metabolic syndrome associated with the activation of innate immune receptors in the intestine is the occurrence of metabolic
metabolic syndrome 17473 syndrome associated with the activation of innate immune receptors in the intestine is the occurrence of metabolic syndrome in TLR5-knockout mice. The development of metabolic syndrome in TLR5-knockout mice appears to be due
metabolic syndrome 17534 in the intestine is the occurrence of metabolic syndrome in TLR5-knockout mice. The development of metabolic syndrome in TLR5-knockout mice appears to be due to changes in gut microbiota associated with the absence of
metabolic syndrome 17933 of TLR5 in intestinal epithelial cells, but not that in dendritic cells (DCs), in the development of metabolic syndrome .[56] Altered gut microbiota in TLR5-knockout mice can increase hepatic lipogenesis mediated by stearoyl
metabolic syndrome 18154 stearoyl CoA desaturase through production of cecal SCFAs.[57]Changes in innate immune cells in the gut of metabolic syndrome At the cell level, several changes were noted in obese subjects or HFD-fed mice. Recent investigations
metabolic syndrome 18438 are derived from common lymphoid progenitors, but devoid of antigen receptors, in the development of metabolic syndrome . In adipose tissue, group 2 ILCs (ILC2s) producing Th2 cytokines, such as interleukin (IL)-4 and IL-13,
metabolic syndrome 19152 inflammation, and regulates lipid metabolism in liver and adipose tissues,[61] NKp46+ ILC3s seem to alleviate metabolic syndrome via IL-22 production.Macrophages and DCs are crucial members of innate immune cells belonging to antigen-presenting
metabolic syndrome 19613 there are only few reports studying the changes of APCs in the intestine of experimental animals with metabolic syndrome . One study showed that expressions of ICAM1, CD86 costimulatory molecule and certain cytokines (IL-6
metabolic syndrome 20730 investigations have shown a significant change in the adaptive immunity of the intestine in association with metabolic syndrome : Th1 cell increases and Treg cell decreases in the intestinal lamina propria of HFD-fed mice.[60] In
metabolic syndrome 22672 metabolic effects.[64] Given that Th17 cells produce IL-22, as well as IL-17, Th17 cells may also improve metabolic syndrome via IL-22 production.[61] Moreover, since Th17 cell transfer leads to expansion of microbiota associated
metabolic syndrome 23534 Th17 in metabolic regulation and the potential of guttrophic Th17 cell transfer as a new therapy for metabolic syndrome or diabetes.MODULATION OF GUT MICROBIOTA OR IMMUNITY AS A NOVEL THERAPEUTIC STRATEGY AGAINST METABOLIC
metabolic syndrome 24283 inflammation in adipose tissue.[33] In addition, a fiber-rich diet may contribute to amelioration of metabolic syndrome by inhibiting expansion and activity of mucus-degrading bacteria that are harmful to the intestinal
metabolic syndrome 25861 related to its effect on gut microbiota.[44] Anti-inflammatory agent 5-aminosalicylic acid can improve metabolic syndrome through suppression of inflammation as well.[60] Active components of Akkermansia, such as Amuc_1100,
metabolic syndrome 26198 intestine, may also be able to open a new horizon in the development of next-generation therapies against metabolic syndrome or diabetes.CONCLUSIONChanges in the gut microbiota and immunity are being accepted as important elements
metabolic syndrome 26345 diabetes.CONCLUSIONChanges in the gut microbiota and immunity are being accepted as important elements in the development of metabolic syndrome and diabetes. However, still numerous questions need to be elucidated to clearly understand the interaction
metabolic syndrome 26786 pathological context will pave the way for the development of innovative therapeutic agents against metabolic syndrome and diabetes.Fig. 1Regulation of host metabolism and immunity by gut microbiota. Under a fiber-rich
obesity 1027 Interestingly, excessive dietary fat has been incriminated as a primary culprit of metabolic syndrome and obesity . After intake of high-fat diet or Western diet, extensive changes in gut microbiota have been observed,
obesity 1890 change in dietary preferences has contributed to a dramatic increase in metabolic diseases, such as obesity and type 2 diabetes, over the last decade, and these diseases now are a significant threat to the public
obesity 2017 diabetes, over the last decade, and these diseases now are a significant threat to the public health.[1] In obesity and type 2 diabetes, inflammatory cells infiltrate adipose tissues, the liver, and pancreatic islets
obesity 2927 influence systemic immunity and local intestinal immunity. Moreover, gut microbiota are changed by obesity , which is followed by the altered intestinal immunity, contributing substantially to the pathogenesis
obesity 3191 recent findings on changes in gut microbiota and intestinal immunity in association with diet-induced obesity and insulin resistance.CHANGES IN GUT MICROBIOTA ASSOCIATED WITH METABOLIC SYNDROMEHow does intestinal
obesity 3323 resistance.CHANGES IN GUT MICROBIOTA ASSOCIATED WITH METABOLIC SYNDROMEHow does intestinal microbiota influence obesity and diabetes?The gut microbiota in humans consist of 10-100 trillion microorganisms and outnumber all
obesity 5083 secretion and ghrelin secretion via parasympathetic activation, leading to increased food intake and obesity .[14] In addition to these effects, SCFAs can contribute to improvement of metabolic syndrome by promoting
obesity 5457 1).[15]Recently, many studies have shown that change in the gut microbiota is related to the development of obesity and diabetes: germ-free (GF) mice are resistant to high-fat diet (HFD)-induced obesity and glucose intolerance
obesity 5544 development of obesity and diabetes: germ-free (GF) mice are resistant to high-fat diet (HFD)-induced obesity and glucose intolerance due to de-repressed expression of fasting-induced adipose factor (Fiaf) in the
obesity 7398 abundance of Firmicutes.[21] Further studies have confirmed similar changes in mice with diet-induced obesity , a more physiological model of obesity than ob/ob mice, while overall diversity among Firmicutes is
obesity 7437 studies have confirmed similar changes in mice with diet-induced obesity, a more physiological model of obesity than ob/ob mice, while overall diversity among Firmicutes is different from that of ob/ob mice.[18]
obesity 7699 observed in humans.[19] Furthermore, there seems to be a causality between changes in gut microbiota and obesity , since transfer of gut microbiota from obese mice to recipient GF mice promotes fat deposition.[18]
obesity 7858 to recipient GF mice promotes fat deposition.[18] The mechanism of increased Firmicutes abundance in obesity might be related to an enrichment of homoacetogens belonging to Firmicutes in obesity, which facilitates
obesity 7944 abundance in obesity might be related to an enrichment of homoacetogens belonging to Firmicutes in obesity , which facilitates disposal of H2 produced by anaerobic bacteria during fermentation of nutrients.[22]
obesity 8153 nutrients.[22] Among Bacteroidetes, a role for Bacteroides thetaiotaomicron, a glutamate-fermenting bacteria, in obesity was addressed in a recent study. Administration of Bacteroides thetaiotaomicron, the abundance of which
obesity 8568 generally accepted that the abundance of Bacteroidetes is decreased and that of Firmicutes are increased in obesity , it does not necessarily mean that the abundances of all bacteria belonging to Firmicutes phylum increase
obesity 10605 enterotypes (Prevotella, Bacteroides, and Ruminococcus).[30]These changes in microbiota composition in obesity may be able to work as early diagnostic markers in the clinic to better identify obese subjects who
obesity 10809 who are prone to develop diabetes, and could be also novel therapeutic targets in the management of obesity or diabetes.Changes in Akkermansia in metabolic syndromeOne of the prominent changes in gut microbiota
obesity 12236 systemic metabolism was demonstrated by oral administration of Akkermansia to mice with diet-induced obesity . Akkermansia administration improves glucose profiles and insulin sensitivity.[37][38] Although the
obesity 16466 but also NLRP3, together with palmitic acid or other inflammasome activators that can be increased in obesity or metabolic syndrome.[51] However, it is not clear whether such metabolic inflammation is associated
obesity 17040 disruption of MyD88, specifically in gut epithelial cells that are partially protected from diet-induced obesity and metabolic inflammation.[54] In contrast, MyD88 deletion in myeloid cells does not improve the metabolic
obesity 20919 propria of HFD-fed mice.[60] In humans, CD8αβ+ intraepithelial lymphocytes (IELs) are increased by obesity , and these IELs impair insulin sensitivity of epithelial cells.[65] In addition to cells traditionally
obesity 24543 enriched with inulin may have protective effects against gut injury associated with HFD and diet-induced obesity , since deficiency of inulin in HFD has been reported to a vital element in the loss of cecal and colonic
obesity 24907 especially those of the genera Lactobacillus and Bifiodobacterium, have been reported to ameliorate obesity and improve metabolic parameters. The suggested mechanisms thereof include inhibition of pathogen adherence
obesity 27566 secretion of ghrelin, a hunger hormone, and increases food intake, consequently causing hyperphagia and obesity . Nevertheless, acetate has anti-inflammatory function like butyrate. Butyrate enhances gut barrier function

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