scholarly journals Diet Impact on Obesity beyond Calories and Trefoil Factor Family 2 (TFF2) as an Illustration: Metabolic Implications and Potential Applications

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1830
Author(s):  
Abdelaziz Ghanemi ◽  
Mayumi Yoshioka ◽  
Jonny St-Amand
Keyword(s):  
Energy Balance ◽  
High Fat Diet ◽  
Social Life ◽  
Caloric Intake ◽  
Metabolic Effects ◽  
Health Economy ◽  
Trefoil Factor ◽  
Potential Applications ◽  
Trefoil Factor Family ◽  
Pharmacologically Active

Obesity is a health problem with increasing impacts on public health, economy and even social life. In order to reestablish the energy balance, obesity management focuses mainly on two pillars; exercise and diet. Beyond the contribution to the caloric intake, the diet nutrients and composition govern a variety of properties. This includes the energy balance-independent properties and the indirect metabolic effects. Whereas the energy balance-independent properties are close to “pharmacological” effects and include effects such as antioxidant and anti-inflammatory, the indirect metabolic effects represent the contribution a diet can have on energy metabolism beyond the caloric contribution itself, which include the food intake control and metabolic changes. As an illustration, we also described the metabolic implication and hypothetical pathways of the high-fat diet-induced gene Trefoil Factor Family 2. The properties the diet has can have a variety of applications mainly in pharmacology and nutrition and further explore the “pharmacologically” active food towards potential therapeutic applications.

scholarly journals Moderate Aerobic Exercise Training Prevents the Augmented Hepatic Glucocorticoid Response Induced by High-Fat Diet in Mice

2020 ◽  
Vol 21 (20) ◽  
pp. 7582
Author(s):  
Jonatan Dassonvalle ◽  
Francisco Díaz-Castro ◽  
Camila Donoso-Barraza ◽  
Carlos Sepúlveda ◽  
Francisco Pino-de la Fuente ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Energy Balance ◽  
Aerobic Exercise ◽  
High Fat Diet ◽  
Aerobic Exercise Training ◽  
Metabolic Effects ◽  
Obese Mice ◽  
High Fat ◽  
Epididymal Fat ◽  
Glucocorticoid Response

Glucocorticoids (GCs) are critical regulators of energy balance. Their deregulation is associated with the development of obesity and metabolic syndrome. However, it is not understood if obesity alters the tissue glucocorticoid receptor (GR) response, and moreover whether a moderate aerobic exercise prevents the alteration in GR response induced by obesity. Methods: To evaluate the GR response in obese mice, we fed C57BL6J mice with a high-fat diet (HFD) for 12 weeks. Before mice were sacrificed, we injected them with dexamethasone. To assess the exercise role in GR response, we fed mice an HFD and subjected them to moderate aerobic exercise three times a week. Results: We found that mice fed a high-fat diet for 12 weeks developed hepatic GC hypersensitivity without changes in the gastrocnemius or epididymal fat GR response. Therefore, moderate aerobic exercise improved glucose tolerance, increased the corticosterone plasma levels, and prevented hepatic GR hypersensitivity with an increase in epididymal fat GR response. Conclusion: Collectively, our results suggest that mice with HFD-induced obesity develop hepatic GR sensitivity, which could enhance the metabolic effects of HFD in the liver. Moreover, exercise was found to be a feasible non-pharmacological strategy to prevent the deregulation of GR response in obesity.

scholarly journals DEPTOR in POMC neurons affects liver metabolism but is dispensable for the regulation of energy balance

2016 ◽  
Vol 310 (11) ◽  
pp. R1322-R1331 ◽  
Author(s):  
Alexandre Caron ◽  
Sébastien M. Labbé ◽  
Mathilde Mouchiroud ◽  
Renaud Huard ◽  
Denis Richard ◽  
...  
Keyword(s):  
Energy Balance ◽  
High Fat Diet ◽  
Fasting Blood Glucose ◽  
Metabolic Effects ◽  
High Fat ◽  
Interacting Protein ◽  
Neuronal Populations ◽  
Diet Induced Obesity ◽  
Glucose And Lipid Homeostasis ◽  
Locomotion Activity

We have recently demonstrated that specific overexpression of DEP-domain containing mTOR-interacting protein (DEPTOR) in the mediobasal hypothalamus (MBH) protects mice against high-fat diet-induced obesity, revealing DEPTOR as a significant contributor to energy balance regulation. On the basis of evidence that DEPTOR is expressed in the proopiomelanocortin (POMC) neurons of the MBH, the present study aimed to investigate whether these neurons mediate the metabolic effects of DEPTOR. Here, we report that specific DEPTOR overexpression in POMC neurons does not recapitulate any of the phenotypes observed when the protein was overexpressed in the MBH. Unlike the previous model, mice overexpressing DEPTOR only in POMC neurons 1) did not show differences in feeding behavior, 2) did not exhibit changes in locomotion activity and oxygen consumption, 3) did not show an improvement in systemic glucose metabolism, and 4) were not resistant to high-fat diet-induced obesity. These results support the idea that other neuronal populations are responsible for these phenotypes. Nonetheless, we observed a mild elevation in fasting blood glucose, insulin resistance, and alterations in liver glucose and lipid homeostasis in mice overexpressing DEPTOR in POMC neurons. Taken together, these results show that DEPTOR overexpression in POMC neurons does not affect energy balance regulation but could modulate metabolism through a brain-liver connection.

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

Life Sciences ◽  
2018 ◽  
Vol 215 ◽  
pp. 190-197 ◽  
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

Detrimental metabolic effects of combining long-term cigarette smoke exposure and high-fat diet in mice

2007 ◽  
Vol 293 (6) ◽  
pp. E1564-E1571 ◽  
Author(s):  
Hui Chen ◽  
Michelle J. Hansen ◽  
Jessica E. Jones ◽  
Ross Vlahos ◽  
Gary P. Anderson ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Caloric Intake ◽  
Fold Increase ◽  
Smoke Exposure ◽  
Metabolic Effects ◽  
Cigarette Smoke Exposure ◽  
High Fat ◽  
Fat Accumulation ◽  
Reduced Body ◽  
Plasma Leptin

Obesity and cigarette smoking are both important risk factors for insulin resistance, cardiovascular disease, and cancer. Smoking reduces appetite, which makes many people reluctant to quit. Few studies have documented the metabolic impact of combined smoke exposure (se) and high-fat-diet (HFD). Neuropeptide Y (NPY) is a powerful hypothalamic feeding stimulator that promotes obesity. We investigated how chronic se affects caloric intake, adiposity, plasma hormones, inflammatory mediators, and hypothalamic NPY peptide in animals fed a palatable HFD. Balb/c mice (5 wk old, male) were exposed to smoke (2 cigarettes, twice/day, 6 days/wk, for 7 wk) with or without HFD. Sham-exposed mice were handled similarly without se. Plasma leptin, hypothalamic NPY, and adipose triglyceride lipase (ATGL) mRNA were measured. HFD induced a 2.3-fold increase in caloric intake, increased adiposity, and glucose in both sham and se cohorts. Smoke exposure decreased caloric intake by 23%, with reduced body weight in both dietary groups. Fat mass and glucose were reduced only by se in the chow-fed animals. ATGL mRNA was reduced by HFD in se animals. Total hypothalamic NPY was reduced by HFD, but only in sham-exposed animals; se increased arcuate NPY. We conclude that although se ameliorated hyperphagia and reversed the weight gain associated with HFD, it failed to reverse fat accumulation and hyperglycemia. The reduced ATGL mRNA expression induced by combined HFD and se may contribute to fat retention. Our data support a powerful health message that smoking in the presence of an unhealthy Western diet increases metabolic disorders and fat accumulation.

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 ◽  
...  
Keyword(s):  
Family Member ◽  
High Fat Diet ◽  
Trefoil Factor ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Trefoil Factor Family

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

Genes ◽  
2021 ◽  
Vol 12 (10) ◽  
pp. 1505
Author(s):  
Abdelaziz Ghanemi ◽  
Mayumi Yoshioka ◽  
Jonny St-Amand
Keyword(s):  
Family Member ◽  
High Fat Diet ◽  
Negative Energy ◽  
Trefoil Factor ◽  
High Fat ◽  
Appetite Control ◽  
Specific Expression ◽  
Knock Out ◽  
Diet Induced Obesity ◽  
Trefoil Factor Family

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.

scholarly journals Effect of selective expression of dominant-negative PPARγ in pro-opiomelanocortin neurons on the control of energy balance

2016 ◽  
Vol 48 (7) ◽  
pp. 491-501 ◽  
Author(s):  
Madeliene Stump ◽  
Deng-Fu Guo ◽  
Ko-Ting Lu ◽  
Masashi Mukohda ◽  
Xuebo Liu ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Balance ◽  
High Fat Diet ◽  
Control Diet ◽  
Cre Recombinase ◽  
Dominant Negative ◽  
High Fat ◽  
Pparγ Agonist ◽  
The Brain

Peroxisome proliferator-activated receptor-γ (PPARγ), a master regulator of adipogenesis, was recently shown to affect energy homeostasis through its actions in the brain. Deletion of PPARγ in mouse brain, and specifically in the pro-opiomelanocortin (POMC) neurons, results in resistance to diet-induced obesity. To study the mechanisms by which PPARγ in POMC neurons controls energy balance, we constructed a Cre-recombinase-dependent conditionally activatable transgene expressing either wild-type (WT) or dominant-negative (P467L) PPARγ and the tdTomato reporter. Inducible expression of both forms of PPARγ was validated in cells in culture, in liver of mice infected with an adenovirus expressing Cre-recombinase (AdCre), and in the brain of mice expressing Cre-recombinase either in all neurons (NESCre/PPARγ-P467L) or selectively in POMC neurons (POMCCre/PPARγ-P467L). Whereas POMCCre/PPARγ-P467L mice exhibited a normal pattern of weight gain when fed 60% high-fat diet, they exhibited increased weight gain and fat mass accumulation in response to a 10% fat isocaloric-matched control diet. POMCCre/PPARγ-P467L mice were leptin sensitive on control diet but became leptin resistant when fed 60% high-fat diet. There was no difference in body weight between POMCCre/PPARγ-WT mice and controls in response to 60% high-fat diet. However, POMCCre/PPARγ-WT, but not POMCCre/PPARγ-P467L, mice increased body weight in response to rosiglitazone, a PPARγ agonist. These observations support the concept that alterations in PPARγ-driven mechanisms in POMC neurons can play a role in the regulation of metabolic homeostasis under certain dietary conditions.

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