Trefoil factor family member 2 (Tff2 ) KO mice are protected from high-fat diet-induced obesity

Obesity ◽  
2013 ◽  
Vol 21 (7) ◽  
pp. 1389-1395 ◽  
Author(s):  
Maria Rita De Giorgio ◽  
Mayumi Yoshioka ◽  
Isabelle Riedl ◽  
Olivier Moreault ◽  
Rose-Guerline Cherizol ◽  
...  
Life Sciences ◽  
2018 ◽  
Vol 215 ◽  
pp. 190-197 ◽  
Author(s):  
Abdelaziz Ghanemi ◽  
Aicha Melouane ◽  
Octave Mucunguzi ◽  
Mayumi Yoshioka ◽  
Jonny St-Amand

Genes ◽  
2021 ◽  
Vol 12 (10) ◽  
pp. 1505
Author(s):  
Abdelaziz Ghanemi ◽  
Mayumi Yoshioka ◽  
Jonny St-Amand

Trefoil Factor Family Member 2 (TFF2) belongs to TFF family peptides that includes TFF1, TFF2, TFF3. TFF2 is mainly known for its roles in the mucosal protection. In the context of obesity and high fat diet (HFD), Tff2 has been characterized as a HFD-induced gene. The knock-out of Tff2 in mice lead to the protection from HFD-induced obesity with a metabolic profile towards a negative energy balance. Such HFD-specific expression gives Tff2 a pattern worth exploring in biomedical research. Indeed, measuring TFF2/TFF2/Tff2 expression in biological samples following the ingestion of high-fat diet reflects the biological “responsiveness” to the lipids ingestion and would reflect the severity of obesity establishment afterwards. Such property could be explored for instance to screen animal models, evaluate the predisposition to HFD-induced obesity as well as in biomedical and clinical applications. Results might advance obesity research especially in terms of understanding lipid-induced signals, appetite control and adiposity storage.


Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 258
Author(s):  
Abdelaziz Ghanemi ◽  
Mayumi Yoshioka ◽  
Jonny St-Amand

Physiological homeostasis requires a balance between the immunological functions and the resulting damage/side effects of the immunological reactions including those related to high-fat (HF) diet. Within this context, whereas HF diet, through diverse mechanisms (such as inflammation), leads to immune-mediated damage, trefoil factor family member 2 (Tff2) represents a HF diet-induced gene. On the other hand, TFF2 both promotes tissue repair and reduces inflammation. These properties are towards counteracting the immune-mediated damage resulting from the HF diet. These observations suggest that the HF diet-induction of Tff2 could be a regulatory pathway aiming to counteract the immune-mediated damage resulting from the HF diet. Interestingly, since Tff2 expression increases with HF diet and with Tff2 also expressed in the brain, we also hypothesize that TFF2 could be a HF diet-induced food intake-control signal that reduces appetite. This hypothesis fits with counteracting the immune damage since reducing the food intake will reduce the HF intake and therefore, reduces the HF diet-induced tissue damage. Such food intake signaling would be an indirect mechanism by which TFF2 promotes tissue repair as well as a pathway worth exploring for potential obesity management pharmacotherapies.


Metabolites ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 536
Author(s):  
Abdelaziz Ghanemi ◽  
Mayumi Yoshioka ◽  
Jonny St-Amand

Obesity has its epidemiological patterns continuously increasing. With controlling both diet and exercise being the main approaches to manage the energy metabolism balance, a high-fat (HF) diet is of particular importance. Indeed, lipids have a low satiety potential but a high caloric density. Thus, focusing on pharmacologically targetable pathways remains an approach with promising therapeutic potential. Within this context, trefoil factor family member 2 (Tff2) has been characterized as specifically induced by HF diet rather than low-fat diet. TFF2 has also been linked to diverse neurological mechanisms and metabolic patterns suggesting its role in energy balance. The hypothesis is that TFF2 would be a HF diet-induced signal that regulates metabolism with a focus on lipids. Within this review, we put the spotlight on key findings highlighting this line of thought. Importantly, the hypothetical mechanisms pointed highlight TFF2 as an important contributor to obesity development via increasing lipids intestinal absorption and anabolism. Therefore, an outlook for future experimental activities and evaluation of the therapeutic potential of TFF2 inhibition is given. Indeed, its knockdown or downregulation would contribute to an antiobesity phenotype. We believe this work represents an addition to our understanding of the lipidic molecular implications in obesity, which will contribute to develop therapies aiming to manage the lipidic metabolic pathways including the absorption, storage and metabolism via targeting TFF2-related pathways. We briefly discuss important relevant concepts for both basic and clinical researchers.


Author(s):  
LC Bollheimer ◽  
H Wobser ◽  
CE Wrede ◽  
A Schäffler ◽  
J Schölmerich ◽  
...  

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