scholarly journals Microbiota and Diabetes Mellitus: Role of Lipid Mediators

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3039
Author(s):  
Juan Salazar ◽  
Lissé Angarita ◽  
Valery Morillo ◽  
Carla Navarro ◽  
María Sofía Martínez ◽  
...  

Diabetes Mellitus (DM) is an inflammatory clinical entity with different mechanisms involved in its physiopathology. Among these, the dysfunction of the gut microbiota stands out. Currently, it is understood that lipid products derived from the gut microbiota are capable of interacting with cells from the immune system and have an immunomodulatory effect. In the presence of dysbiosis, the concentration of lipopolysaccharides (LPS) increases, favoring damage to the intestinal barrier. Furthermore, a pro-inflammatory environment prevails, and a state of insulin resistance and hyperglycemia is present. Conversely, during eubiosis, the production of short-chain fatty acids (SCFA) is fundamental for the maintenance of the integrity of the intestinal barrier as well as for immunogenic tolerance and appetite/satiety perception, leading to a protective effect. Additionally, it has been demonstrated that alterations or dysregulation of the gut microbiota can be reversed by modifying the eating habits of the patients or with the administration of prebiotics, probiotics, and symbiotics. Similarly, different studies have demonstrated that drugs like Metformin are capable of modifying the composition of the gut microbiota, promoting changes in the biosynthesis of LPS, and the metabolism of SCFA.

2018 ◽  
Vol 2 ◽  
Author(s):  
Akram Abolbaghaei ◽  
B. Dave Oomah ◽  
Hamed Tavakoli ◽  
Farah Hosseinian

Circulating levels of branched chain amino acids (BCAAs) correlate strongly with type 2 diabetes (T2D). The correlation may be associated with insulin-resistance factors independent of glycemic markers currently used in the diagnosis and monitoring of diabetes. This can revolutionize the thought process and methodology not only in diabetes treatment, but also in its advance screening and prevention with BCAAs used as biomarkers and targets for treatment. Whether insulin resistance is the cause or result of BCAAs imbalances requires further investigation. Although the overall diet is important, the role of specific diets targeting the gut microbiome composition and hormone secretion affecting BCAA absorption and metabolism will be explored. Generic diet modifications apparently induce only negligible changes in the intrinsic genetic make-up of the gut and BCAA levels but influence specific modulation of the gut microbiome. This genetic make-up is indeed similar among T2D patients independent of numerous variables including obesity. Short-chain fatty acids (SCFAs), the primary end-products of non-digestible carbohydrates (NDC) fermentation, mediate metabolic imbalances through gut microbiota and gut hormone secretion. This review focuses on extensive evidence gathered using diverse methodologies on the strong parallel correlation between BCAA levels and insulin resistance. Furthermore, the role of specific diets particularly SCFAs as mediators of the stubbornly fixed intrinsic genetic make-up of gut microbiota will be scrutinized to delineate BCAA levels and insulin resistance in T2D.


2020 ◽  
Vol 21 (8) ◽  
pp. 785-798 ◽  
Author(s):  
Abedin Abdallah ◽  
Evera Elemba ◽  
Qingzhen Zhong ◽  
Zewei Sun

The gastrointestinal tract (GIT) of humans and animals is host to a complex community of different microorganisms whose activities significantly influence host nutrition and health through enhanced metabolic capabilities, protection against pathogens, and regulation of the gastrointestinal development and immune system. New molecular technologies and concepts have revealed distinct interactions between the gut microbiota and dietary amino acids (AAs) especially in relation to AA metabolism and utilization in resident bacteria in the digestive tract, and these interactions may play significant roles in host nutrition and health as well as the efficiency of dietary AA supplementation. After the protein is digested and AAs and peptides are absorbed in the small intestine, significant levels of endogenous and exogenous nitrogenous compounds enter the large intestine through the ileocaecal junction. Once they move in the colonic lumen, these compounds are not markedly absorbed by the large intestinal mucosa, but undergo intense proteolysis by colonic microbiota leading to the release of peptides and AAs and result in the production of numerous bacterial metabolites such as ammonia, amines, short-chain fatty acids (SCFAs), branched-chain fatty acids (BCFAs), hydrogen sulfide, organic acids, and phenols. These metabolites influence various signaling pathways in epithelial cells, regulate the mucosal immune system in the host, and modulate gene expression of bacteria which results in the synthesis of enzymes associated with AA metabolism. This review aims to summarize the current literature relating to how the interactions between dietary amino acids and gut microbiota may promote host nutrition and health.


PLoS ONE ◽  
2019 ◽  
Vol 14 (8) ◽  
pp. e0220642 ◽  
Author(s):  
Yuliia Holota ◽  
Taisa Dovbynchuk ◽  
Izumi Kaji ◽  
Igor Vareniuk ◽  
Natalia Dzyubenko ◽  
...  

Author(s):  
Lin Xiao ◽  
Qin Liu ◽  
Mei Luo ◽  
Lishou Xiong

Irritable bowel syndrome (IBS) is the most common functional bowel disorder worldwide and is associated with visceral hypersensitivity, gut motility, immunomodulation, gut microbiota alterations, and dysfunction of the brain-gut axis; however, its pathophysiology remains poorly understood. Gut microbiota and its metabolites are proposed as possible etiological factors of IBS. The aim of our study was to investigate specific types of microbiota-derived metabolites, especially bile acids, short-chain fatty acids, vitamins, amino acids, serotonin and hypoxanthine, which are all implicated in the pathogenesis of IBS. Metabolites-focused research has identified multiple microbial targets relevant to IBS patients, important roles of microbiota-derived metabolites in the development of IBS symptoms have been established. Thus, we provide an overview of gut microbiota and their metabolites on the different subtypes of IBS (constipation-predominant IBS-C, diarrhea-predominant IBS-D) and present controversial views regarding the role of microbiota in IBS.


2014 ◽  
Vol 11 (2) ◽  
pp. 8-12 ◽  
Author(s):  
F R Abdulkadirova ◽  
A S Ametov ◽  
E V Doskina ◽  
R A Pokrovskaya

Obesity is a major risk factor for diabetes mellitus type 2, cardiovascular diseases and associated comorbid conditions. It is traditionally considered that insulin resistance is dependent on glucose metabolism. However, in recent years more and more attention is devoted to the fatty acids metabolism, the increase in concentrations of which plays a significant role in the pathophysiological mechanisms associated with insulin resistance.


F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 738 ◽  
Author(s):  
Joe Alcock ◽  
Henry C. Lin

A high-fat diet and elevated levels of free fatty acids are known risk factors for metabolic syndrome, insulin resistance, and visceral obesity. Although these disease associations are well established, it is unclear how different dietary fats change the risk of insulin resistance and metabolic syndrome. Here, we review emerging evidence that insulin resistance and fat storage are linked to changes in the gut microbiota. The gut microbiota and intestinal barrier function, in turn, are highly influenced by the composition of fat in the diet. We review findings that certain fats (for example, long-chain saturated fatty acids) are associated with dysbiosis, impairment of intestinal barrier function, and metabolic endotoxemia. In contrast, other fatty acids, including short-chain and certain unsaturated fatty acids, protect against dysbiosis and impairment of barrier function caused by other dietary fats. These fats may promote insulin sensitivity by inhibiting metabolic endotoxemia and dysbiosis-driven inflammation. During dysbiosis, the modulation of metabolism by diet and microbiota may represent an adaptive process that compensates for the increased fuel demands of an activated immune system.


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