scholarly journals Alisol A attenuates high‐fat‐diet‐induced obesity and metabolic disorders via the AMPK/ACC/SREBP‐1c pathway

2019 ◽  
Vol 23 (8) ◽  
pp. 5108-5118 ◽  
Author(s):  
Chiakang Ho ◽  
Ya Gao ◽  
Danning Zheng ◽  
Yanjun Liu ◽  
Shengzhou Shan ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Metabolic Disorders ◽  
High Fat ◽  
Diet Induced Obesity

scholarly journals Effect of Supplementation with Hydroethanolic Extract of Campomanesia xanthocarpa (Berg.) Leaves and Two Isolated Substances from the Extract on Metabolic Parameters of Mice Fed a High-Fat Diet

Molecules ◽  
2020 ◽  
Vol 25 (11) ◽  
pp. 2693 ◽  
Author(s):  
Carla Maiara Lopes Cardozo ◽  
Aline Carla Inada ◽  
Claudia Andrea Lima Cardoso ◽  
Wander Fernando de Oliveira Filiú ◽  
Bernardo Barcelar de Farias ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Metabolic Disorders ◽  
Brazilian Cerrado ◽  
American Institute ◽  
High Fat ◽  
Beneficial Effects ◽  
Diet Induced Obesity ◽  
Protein Expressions ◽  
Hydroethanolic Extract ◽  
Lipid Parameters

There are still controversies regarding the correlation between the beneficial effects for health and the administration of isolated compounds or crude extracts in therapeutic applications. Campomanesia xanthocarpa, found in the Brazilian Cerrado, demonstrated beneficial effects in metabolic disorders associated with obesity. We investigated the effects of Campomanesia xanthocarpa hydroethanolic extract and two isolated substances from the extract (S1 and S2) in a diet-induced obesity (DIO) model. Male Swiss mice were divided into five groups: (1) American Institute of Nutrition (AIN-93M) diet, (2) high-fat diet (HF), (3) HF supplemented with C. xanthocarpa hydroethanolic leaf extract at 100 mg/kg (HFE), (4) HF supplemented with S1 at 1 mg/kg (HFS1) and (5) HF supplemented with S2 at 1 mg/kg (HFS2). The HFS1, HFS2 and HFE groups did not present decreasing body weight or visceral adiposity gain. No differences in glycemic and lipid parameters, or in the expression of protein content in two cytokines, interleukin-6 (IL-6) and anti-inflammatory (IL-10), were observed. Only the HFS1 group displayed decreased food intake. Even though substantial effects such as an improvement in obesity features or the metabolic and histological parameters promoted by S1, S2 and the extract were not observed, further investigations are necessary to evaluate the principal genes and protein expressions involved in regulating food behavior promoted by S1.

Leopoldia comosa prevents metabolic disorders in rats with high-fat diet-induced obesity

2018 ◽  
Vol 58 (3) ◽  
pp. 965-979 ◽  
Author(s):  
T. Casacchia ◽  
F. Scavello ◽  
C. Rocca ◽  
M. C. Granieri ◽  
G. Beretta ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Metabolic Disorders ◽  
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).

scholarly journals Deficiency of Oncostatin M Receptor β (OSMRβ) Exacerbates High-fat Diet-induced Obesity and Related Metabolic Disorders in Mice

2014 ◽  
Vol 289 (20) ◽  
pp. 13821-13837 ◽  
Author(s):  
Tadasuke Komori ◽  
Minoru Tanaka ◽  
Emiko Senba ◽  
Atsushi Miyajima ◽  
Yoshihiro Morikawa
Keyword(s):  
High Fat Diet ◽  
Metabolic Disorders ◽  
Oncostatin M ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Oncostatin M Receptor

scholarly journals Enteric glial cells respond to a dietary change in the lamina propria in a MyD88-dependent manner

2020 ◽  
Author(s):  
Zhuanzhuan Liu ◽  
Hongxiang Sun ◽  
Ming Liang ◽  
Jing Gao ◽  
Liyuan Meng ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Nervous System ◽  
Glial Cells ◽  
High Fat Diet ◽  
Metabolic Disorders ◽  
Neuronal System ◽  
High Fat ◽  
Dietary Shift ◽  
Diet Induced Obesity ◽  
Enteric Glial Cells

AbstractImmune and nervous system sensing are two important ways of detecting inner and outer environmental changes. Immune cell activation in the gut can promote metabolic disorders. However, whether enteric nervous system sensing and activities are also important in metabolic syndromes is not clear. Enteric glial cells (EGCs) are thought to have sensing ability, but little is known about the potential connections between EGC and metabolic disorders. Consuming a modern Western-type high-fat low-fiber diet increases the risk of obesity. Here, we reported that dietary shift from a normal chow diet to a high-fat diet in wild-type (WT) C57BL/6 mice induced a transient emergence of glial fibrillary acidic protein (GFAP)-positive EGC network in the ileal lamina propria, accompanied by an increase of glial-derived neurotrophic factors production. Inhibition of EGC metabolic activity via gliotoxin fluorocitrate or glial-intrinsic deletion of myeloid differentiation factor 88 (Myd88) in mice blocked this dietary change-induced activity. Furthermore, we found a different role of MYD88 in glial cells versus adipocyte in diet-induced obesity. The glial Myd88 knockout mice gained less body weight after HFD feeding compared to the littermate controls. In contrast, adipocyte deletion of Myd88 in mice had no impact on the weight gain but had exacerbated glucose metabolic disorders. Pharmacological interventions of glial activities by fluorocitrate prevented body weight gain in a dietary type- and glial MYD88-independent manner. Collectively, our data reveal a previously unappreciated function of EGC in sensing a dietary shift-induced perturbation and glial activities as a whole may play roles in diet-induced obesity.New & NoteworthyIt is known that obesity and its related metabolic syndrome can damage the neuronal system. However, whether the neuronal system also participates in the development of obesity is unclear. Diet is an important contributing factor to obesity. Our study reveals that consuming a high-fat diet can induce a transient enteric glial cell response via its intrinsic sensing molecule(s). Inhibiting overall glial cell activities may have an impact on the development of the metabolic syndrome.

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