scholarly journals Effects of Curcumin in a Mouse Model of Very High Fat Diet-Induced Obesity

Biomolecules ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1368
Author(s):  
Iurii Koboziev ◽  
Shane Scoggin ◽  
Xiaoxia Gong ◽  
Parvin Mirzaei ◽  
Masoud Zabet-Moghaddam ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Protective Effects ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Dietary Interventions ◽  
Experimental Conditions ◽  
White Adipocyte ◽  
Diet Induced Obesity ◽  
Invaluable Tool ◽  
Very High

Worldwide rates of Western-diet-induced obesity epidemics are growing dramatically. Being linked with numerous comorbidities and complications, including cardiovascular disease, type 2 diabetes, cancer, chronic inflammation, and osteoarthritis (OA), obesity represents one of the most threatening challenges for modern healthcare. Mouse models are an invaluable tool for investigating the effects of diets and their bioactive components against high fat diet (HFD)-induced obesity and its comorbidities. During recent years, very high fat diets (VHFDs), providing 58–60% kcal fat, have become a popular alternative to more traditional HFDs, providing 40–45% total kcal fat, due to the faster induction of obesity and stronger metabolic responses. This project aims to investigate if the 60% fat VHFD is suitable to evaluate the protective effects of curcumin in diet-induced obesity and osteoarthritis. B6 male mice, prone to diet-induced metabolic dysfunction, were supplemented with VHFD without or with curcumin for 13 weeks. Under these experimental conditions, feeding mice a VHFD for 13 weeks did not result in expected robust manifestations of the targeted pathophysiologic conditions. Supplementing the diet with curcumin, in turn, protected the animals against obesity without significant changes in white adipocyte size, glucose clearance, and knee cartilage integrity. Additional research is needed to optimize diet composition, curcumin dosage, and duration of dietary interventions to establish the VHFD-induced obesity for evaluating the effects of curcumin on metabolic dysfunctions related to obesity and osteoarthritis.

Leuconostoc mesenteroides subsp. mesenteroides SD23 Prevents Metabolic Dysfunction Associated with High-Fat Diet–Induced Obesity in Male Mice

2019 ◽  
Vol 12 (2) ◽  
pp. 505-516 ◽  
Author(s):  
Diana C. Castro-Rodríguez ◽  
Luis A. Reyes-Castro ◽  
Claudia C. Vega ◽  
Guadalupe L. Rodríguez-González ◽  
Jorge Yáñez-Fernández ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Leuconostoc Mesenteroides ◽  
Metabolic Dysfunction ◽  
Male Mice ◽  
High Fat ◽  
Diet Induced Obesity

scholarly journals Protective effects of selenium-enriched peptides from Cardamine violifolia against high-fat diet induced obesity and its associated metabolic disorders in mice

RSC Advances ◽  
2020 ◽  
Vol 10 (52) ◽  
pp. 31411-31424
Author(s):  
Tian Yu ◽  
Jia Guo ◽  
Song Zhu ◽  
Meng Li ◽  
Zhenzhou Zhu ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Metabolic Disorders ◽  
Protective Effects ◽  
High Fat ◽  
Diet Induced Obesity

Selenium-enriched peptides from Cardamine violifolia (CSP) have excellent antioxidant functions but little is known about their effects on obesity and associated metabolic disorders in mice fed with a high-fat diet (HFD).

Short-term moderate exercise provides long-lasting protective effects against metabolic dysfunction in rats fed a high-fat diet

2014 ◽  
Vol 54 (8) ◽  
pp. 1353-1362 ◽  
Author(s):  
Laize Peron Tófolo ◽  
Tatiane Aparecida da Silva Ribeiro ◽  
Ananda Malta ◽  
Rosiane Aparecida Miranda ◽  
Rodrigo Mello Gomes ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Protective Effects ◽  
Metabolic Dysfunction ◽  
Moderate Exercise ◽  
High Fat ◽  
Short Term

scholarly journals Ellagic acid promotes browning of white adipose tissues in high-fat diet-induced obesity in rats through suppressing white adipocyte maintaining genes

2019 ◽  
Vol 66 (10) ◽  
pp. 923-936 ◽  
Author(s):  
Lifeng Wang ◽  
Yuanyuan Wei ◽  
Chao Ning ◽  
Minfang Zhang ◽  
Ping Fan ◽  
...  
Keyword(s):  
Ellagic Acid ◽  
High Fat Diet ◽  
High Fat ◽  
Adipose Tissues ◽  
White Adipocyte ◽  
Diet Induced Obesity

scholarly journals Loss of macrophage fatty acid oxidation does not potentiate systemic metabolic dysfunction

2017 ◽  
Vol 312 (5) ◽  
pp. E381-E393 ◽  
Author(s):  
Elsie Gonzalez-Hurtado ◽  
Jieun Lee ◽  
Joseph Choi ◽  
Ebru S. Selen Alpergin ◽  
Samuel L. Collins ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
High Fat Diet ◽  
Macrophage Polarization ◽  
Acid Oxidation ◽  
Causative Role ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Diet Induced Obesity

Fatty acid oxidation in macrophages has been suggested to play a causative role in high-fat diet-induced metabolic dysfunction, particularly in the etiology of adipose-driven insulin resistance. To understand the contribution of macrophage fatty acid oxidation directly to metabolic dysfunction in high-fat diet-induced obesity, we generated mice with a myeloid-specific knockout of carnitine palmitoyltransferase II (CPT2 Mϕ-KO), an obligate step in mitochondrial long-chain fatty acid oxidation. While fatty acid oxidation was clearly induced upon IL-4 stimulation, fatty acid oxidation-deficient CPT2 Mϕ-KO bone marrow-derived macrophages displayed canonical markers of M2 polarization following IL-4 stimulation in vitro. In addition, loss of macrophage fatty acid oxidation in vivo did not alter the progression of high-fat diet-induced obesity, inflammation, macrophage polarization, oxidative stress, or glucose intolerance. These data suggest that although IL-4-stimulated alternatively activated macrophages upregulate fatty acid oxidation, fatty acid oxidation is dispensable for macrophage polarization and high-fat diet-induced metabolic dysfunction. Macrophage fatty acid oxidation likely plays a correlative, rather than causative, role in systemic metabolic dysfunction.

scholarly journals Acute vs chronic exposure to high fat diet leads to distinct regulation of PKA

2017 ◽  
Vol 59 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Edra London ◽  
Maria Nesterova ◽  
Constantine A Stratakis
Keyword(s):  
High Fat Diet ◽  
Energy Homeostasis ◽  
Critical Role ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Subunit Expression ◽  
Peripheral Effect ◽  
Dependent Protein ◽  
The Impact

The cAMP-dependent protein kinase (PKA) is an essential regulator of lipid and glucose metabolism that plays a critical role in energy homeostasis. The impact of diet on PKA signaling has not been defined, although perturbations in individual PKA subunits are associated with changes in adiposity, physical activity and energy intake in mice and humans. We hypothesized that a high fat diet (HFD) would elicit peripheral and central alterations in the PKA system that would differ depending on length of exposure to HFD; these differences could protect against or promote diet-induced obesity (DIO). 12-week-old C57Bl/6J mice were randomly assigned to a regular diet or HFD and weighed weekly throughout the feeding studies (4 days, 14 weeks; respectively), and during killing. PKA activity and subunit expression were measured in liver, gonadal adipose tissue (AT) and brain. Acute HFD-feeding suppressed basal hepatic PKA activity. In contrast, hepatic and hypothalamic PKA activities were significantly increased after chronic HFD-feeding. Changes in AT were more subtle, and overall, altered PKA regulation in response to chronic HFD exposure was more profound in female mice. The suppression of hepatic PKA activity after 4 day HFD-feeding was indicative of a protective peripheral effect against obesity in the context of overnutrition. In response to chronic HFD-feeding, and with the development of DIO, dysregulated hepatic and hypothalamic PKA signaling was a signature of obesity that is likely to promote further metabolic dysfunction in mice.

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