Beneficial metabolic effects of selected probiotics on diet-induced obesity and insulin resistance in mice are associated with improvement of dysbiotic gut microbiota

2016 ◽  
Vol 18 (5) ◽  
pp. 1484-1497 ◽  
Author(s):  
Jeanne Alard ◽  
Véronique Lehrter ◽  
Moez Rhimi ◽  
Irène Mangin ◽  
Véronique Peucelle ◽  
...  
2021 ◽  
Author(s):  
Haizhao Song ◽  
Xinchun Shen ◽  
Yang Zhou ◽  
Xiaodong Zheng

Supplementation of black rice anthocyanins (BRAN) alleviated high fat diet-induced obesity, insulin resistance and hepatic steatosis by improvement of lipid metabolism and modification of the gut microbiota.


2016 ◽  
Vol 29 (2) ◽  
pp. 234-248 ◽  
Author(s):  
Katherine Gil-Cardoso ◽  
Iris Ginés ◽  
Montserrat Pinent ◽  
Anna Ardévol ◽  
Mayte Blay ◽  
...  

AbstractDiet-induced obesity is associated with low-grade inflammation, which, in most cases, leads to the development of metabolic disorders, primarily insulin resistance and type 2 diabetes. Although prior studies have implicated the adipose tissue as being primarily responsible for obesity-associated inflammation, the latest discoveries have correlated impairments in intestinal immune homeostasis and the mucosal barrier with increased activation of the inflammatory pathways and the development of insulin resistance. Therefore, it is essential to define the mechanisms underlying the obesity-associated gut alterations to develop therapies to prevent and treat obesity and its associated diseases. Flavonoids appear to be promising candidates among the natural preventive treatments that have been identified to date. They have been shown to protect against several diseases, including CVD and various cancers. Furthermore, they have clear anti-inflammatory properties, which have primarily been evaluated in non-intestinal models. At present, a growing body of evidence suggests that flavonoids could exert a protective role against obesity-associated pathologies by modulating inflammatory-related cellular events in the intestine and/or the composition of the microbiota populations. The present paper will review the literature to date that has described the protective effects of flavonoids on intestinal inflammation, barrier integrity and gut microbiota in studies conducted using in vivo and in vitro models.


2020 ◽  
Vol 34 (9) ◽  
pp. 12289-12307
Author(s):  
Ilavenil Soundharrajan ◽  
Palaniselvam Kuppusamy ◽  
Srigopalram Srisesharam ◽  
Jeong Chae Lee ◽  
Ravikumar Sivanesan ◽  
...  

Gut ◽  
2014 ◽  
Vol 64 (6) ◽  
pp. 872-883 ◽  
Author(s):  
Fernando F Anhê ◽  
Denis Roy ◽  
Geneviève Pilon ◽  
Stéphanie Dudonné ◽  
Sébastien Matamoros ◽  
...  

2015 ◽  
Vol 29 (6) ◽  
pp. 2397-2411 ◽  
Author(s):  
Injae Hwang ◽  
Yoon Jeong Park ◽  
Yeon‐Ran Kim ◽  
Yo Na Kim ◽  
Sojeong Ka ◽  
...  

2016 ◽  
Vol 397 (8) ◽  
pp. 753-764 ◽  
Author(s):  
Opeolu O. Ojo ◽  
Dinesh K. Srinivasan ◽  
Bosede O. Owolabi ◽  
Mary K. McGahon ◽  
R. Charlotte Moffett ◽  
...  

Abstract The frog skin host-defense peptide tigerinin-1R stimulates insulin release in vitro and improves glucose tolerance and insulin sensitivity in animal models of type 2 diabetes. This study extends these observations by investigating the molecular mechanisms of action underlying the beneficial metabolic effects of the analogue [Arg4]tigerinin-1R in mice with diet-induced obesity, glucose intolerance and insulin resistance. The study also investigates the electrophysiological effects of the peptide on KATP and L-type Ca2+ channels in BRIN-BD11 clonal β cells. Non-fasting plasma glucose and glucagon concentrations were significantly (p<0.05) decreased and plasma insulin increased by twice daily treatment with [Arg4]tigerinin-1R (75 nmol/kg body weight) for 28 days. Oral and intraperitoneal glucose tolerance were significantly (p<0.05) improved accompanied by enhanced secretion and action of insulin. The peptide blocked KATP channels and, consistent with this, improved beta cell responses of isolated islets to a range of secretagogues. Peptide administration resulted in up-regulation of key functional genes in islets involved insulin secretion (Abcc8, Kcnj11, Cacna1c and Slc2a2) and in skeletal muscle involved with insulin action (Insr, Irs1, Pdk1, Pik3ca, and Slc2a4). These observations encourage further development of tigerinin-1R analogues for the treatment of patients with type 2 diabetes.


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