Beyond gut microbiota: understanding obesity and type 2 diabetes

Lau, Eva; Carvalho, Davide; Pina-Vaz, Cidália; Barbosa, J.T; Freitas, Paula

doi:10.14310/horm.2002.1571

Cited by 30 publications

(39 citation statements)

References 93 publications

(105 reference statements)

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“…The pathogenic association of gut microbiota in the development of obesity-related diseases have suggested so that possible action to prevent and treat the consequences can be undertaken. Treatment of T1D has been suggested through probiotics based new therapeutics to resolve the changes in gut microbiota due to multiple factors [45,46].…”

Section: Discussionmentioning

confidence: 99%

Gut Microbiota and Diabetes Mellitus - An Interlinkage

Vijayasimha

Prabhakar

2018

Asian J Pharm Clin Res

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In recent years, the curiosity to investigate the relationship between gut microbiota and diabetes development has increased. Evidence from previous studies suggests that gut microbiota manipulation may assure to prevent diabetes development in future, primarily in susceptible individuals. Here, we reviewed special gut microbiota types proposing development of Type 1 (T1D) and Type 2 diabetes (T2D) in humans and laboratory animals. The available data we found are still inconclusive and required more attention in discriminating specific groups of gut microbiomes strongly indicating T1D and T2D development or prevention. Further, we suggested for the first time to study the gut microbiota in different ways to find the root cause of diabetes development.

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Section: Discussionmentioning

confidence: 99%

Gut Microbiota and Diabetes Mellitus - An Interlinkage

Vijayasimha

Prabhakar

2018

Asian J Pharm Clin Res

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“…Secreted by adipose tissue, intestines and liver, the angioproteina-like 4/(FIAF) antagonizes the activity of LPL, thereby preventing the storage of triglycerides as fat. The group of Bakhed et al showed that the intestinal microbiota suppresses the expression of the FIAF in response to a great quantity of food, thus increasing the LPL activity and finally the deposition of fat in adipocytes (16)(17)(18). • Suppression of adenosine monophosphateactivated protein kinase (AMPK): AMPK is a heterotrimeric enzyme that plays an active role in energy homeostasis.…”

Section: Obesity Promotionmentioning

confidence: 99%

Influence of non-steroidal anti-inflammatory drugs on intestinal permeability and non alcoholic fatty liver disease

Utzeri¹

2015

RGHN

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The incidence of non-alcoholic fatty liver disease (NAFLD) and its related conditions including obesity and metabolic syndrome has dramatically increased in Western countries. Gut microbiota contributes to body weight regulation and related disorders like NAFLD by influencing metabolic and immune host functions. High fat diet may induce small intestinal bacterial overgrowth (SIBO) and dysbiosis which determine a malfunction of tight junctions (TJ) playing a critical role in the increase of intestinal permeability and the translocation of bacteria and their products. The endotoxaemia induces an inflammatory response that determines the development of insulin resistance, body weight gain, lipogenesis, fibrogenesis and hepatic oxidative stress which contributes to the second hit mechanisms in the pathophysiology of non-alcoholic steatohepatitis. In these categories of predisposed patients these mechanisms may be exacerbated by the administration of non-steroidal anti-inflammatory drugs (NSAIDs) that causes an initial alteration of intestinal permeability up to more serious complications. NSAIDs enteropathy is due to enterohepatic recycling of drug resulting in a prolonged and repeated exposure of the intestinal mucosa to the compound and its metabolites leading to so called topical effects. The pathogenesis of NSAID enteropathy is less linked to their ability to suppress cyclooxygenase activity and to the presence of gastric acid, even if more and more emphasis is placed on co-administration of antisecretory agents which determine hypocloridia, associated with small intestinal bacterial overgrowth and bile acid dysmetabolism, responsible of exacerbation of NSAID-induced intestinal damage. Prevention and treatment of NSAID enteropathy and his systemic complication like NAFLD have become major priorities, consequently novel approaches directed toward other pathomechanisms and research of new therapeutic strategies are needed.

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“…The gut microbiota plays a crucial role in gastrointestinal mucosa permeability and regulates the fermentation and absorption of dietary polysaccharides, which may explain its importance in the regulation of fat accumulation and the resultant development of obesity-related diseases [14].…”

Section: Introductionmentioning

confidence: 99%