Trefoil Factor Family Member 2 Expression as an Indicator of the Severity of the High-Fat Diet-Induced Obesity

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.

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Energy and metabolic pathways in trefoil factor family member 2 (Tff2) KO mice beyond the protection from high-fat diet-induced obesity

Life Sciences ◽

10.1016/j.lfs.2018.11.006 ◽

2018 ◽

Vol 215 ◽

pp. 190-197 ◽

Cited By ~ 5

Author(s):

Abdelaziz Ghanemi ◽

Aicha Melouane ◽

Octave Mucunguzi ◽

Mayumi Yoshioka ◽

Jonny St-Amand

Keyword(s):

Family Member ◽

Metabolic Pathways ◽

High Fat Diet ◽

Trefoil Factor ◽

High Fat ◽

Diet Induced Obesity ◽

Trefoil Factor Family

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

Obesity ◽

10.1002/oby.20165 ◽

2013 ◽

Vol 21 (7) ◽

pp. 1389-1395 ◽

Cited By ~ 10

Author(s):

Maria Rita De Giorgio ◽

Mayumi Yoshioka ◽

Isabelle Riedl ◽

Olivier Moreault ◽

Rose-Guerline Cherizol ◽

...

Keyword(s):

Family Member ◽

High Fat Diet ◽

Trefoil Factor ◽

High Fat ◽

Diet Induced Obesity ◽

Trefoil Factor Family

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Diet-Induced Obesity Causes Ghrelin Resistance in Arcuate NPY/AgRP Neurons

Endocrinology ◽

10.1210/en.2010-0556 ◽

2010 ◽

Vol 151 (10) ◽

pp. 4745-4755 ◽

Cited By ~ 180

Author(s):

Dana I. Briggs ◽

Pablo J. Enriori ◽

Moyra B. Lemus ◽

Michael A. Cowley ◽

Zane B. Andrews

Keyword(s):

Food Intake ◽

High Fat Diet ◽

Healthy Aging ◽

Hormone Secretion ◽

Growth Hormone Secretion ◽

High Fat ◽

Appetite Control ◽

Diet Induced Obesity ◽

Therapeutic Outcomes ◽

The Brain

Circulating ghrelin is decreased in obesity, and peripheral ghrelin does not induce food intake in obese mice. We investigated whether ghrelin resistance was a centrally mediated phenomenon involving dysregulated neuropeptide Y (NPY) and agouti-related peptide (AgRP) circuits. We show that diet-induced obesity (DIO) (12 wk) suppresses the neuroendocrine ghrelin system by decreasing acylated and total plasma ghrelin, decreasing ghrelin and Goat mRNA in the stomach, and decreasing expression of hypothalamic GHSR. Peripheral (ip) or central (intracerebroventricular) ghrelin injection was able to induce food intake and arcuate nucleus Fos immunoreactivity in chow-fed but not high-fat diet-fed mice. DIO decreased expression of Npy and Agrp mRNA, and central ghrelin was unable to promote expression of these genes. Ghrelin did not induce AgRP or NPY secretion in hypothalamic explants from DIO mice. Injection of NPY intracerebroventricularly increased food intake in both chow-fed and high-fat diet-fed mice, indicating that downstream NPY/AgRP neural targets are intact and that defective NPY/AgRP function is a primary cause of ghrelin resistance. Ghrelin resistance in DIO is not confined to the NPY/AgRP neurons, because ghrelin did not stimulate growth hormone secretion in DIO mice. Collectively, our data suggests that DIO causes ghrelin resistance by reducing NPY/AgRP responsiveness to plasma ghrelin and suppressing the neuroendocrine ghrelin axis to limit further food intake. Ghrelin has a number of functions in the brain aside from appetite control, including cognitive function, mood regulation, and protecting against neurodegenerative diseases. Thus, central ghrelin resistance may potentiate obesity-related cognitive decline, and restoring ghrelin sensitivity may provide therapeutic outcomes for maintaining healthy aging.

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High-Fat Diet-Induced Trefoil Factor Family Member 2 (TFF2) to Counteract the Immune-Mediated Damage in Mice

Animals ◽

10.3390/ani11020258 ◽

2021 ◽

Vol 11 (2) ◽

pp. 258

Author(s):

Abdelaziz Ghanemi ◽

Mayumi Yoshioka ◽

Jonny St-Amand

Keyword(s):

Food Intake ◽

Family Member ◽

Tissue Repair ◽

Trefoil Factor ◽

High Fat ◽

Immune Mediated ◽

Physiological Homeostasis ◽

Immunological Reactions ◽

Trefoil Factor Family ◽

The Brain

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.

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Trefoil Factor Family Member 2: From a High-Fat-Induced Gene to a Potential Obesity Therapy Target

Metabolites ◽

10.3390/metabo11080536 ◽

2021 ◽

Vol 11 (8) ◽

pp. 536

Author(s):

Abdelaziz Ghanemi ◽

Mayumi Yoshioka ◽

Jonny St-Amand

Keyword(s):

Family Member ◽

Therapeutic Potential ◽

Trefoil Factor ◽

High Fat ◽

Caloric Density ◽

Low Fat Diet ◽

Obesity Therapy ◽

Trefoil Factor Family ◽

Therapy Target ◽

Induced Signal

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.

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