scholarly journals A high-fat diet changes astrocytic metabolism to enhance synaptic plasticity and promote exploratory behavior

2021 ◽  
Author(s):  
Alexander Popov ◽  
Nadezda Brazhe ◽  
Anna Fedotova ◽  
Alisa Tiaglik ◽  
Maxim Bychkov ◽  
...  

A high-fat diet (HFD) is generally considered to negatively influence the body, the brain, and cognitive abilities. On the other hand, fat and fatty acids are essential for nourishing and constructing brain tissue. Astrocytes are central for lipolysis and fatty acids metabolism. Here we show that exposure of young mice to one month of HFD elevates lipid content and increases the relative amount of reduced cytochromes in astrocytes but not in neurons. Metabolic changes were paralleled with an enlargement of astrocytic territorial domains due to an increased outgrowth of branches and leaflets. Astrocyte remodeling was associated with an increase in expression of ezrin and with no changes in glial fibrillary acidic protein (GFAP), glutamate transporter-1 (GLT-1), and glutamine synthetase (GS). Such physiological (non-reactive) enlargement of astrocytes in the brain active milieu promoted glutamate clearance and long-term potentiation. These changes translated into improved exploratory behavior. Thus, dietary fat intake is not invariably harmful and might exert beneficial effects depending on the biological context.

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Sung-Hui Tseng ◽  
Ting-Yi Chien ◽  
Jiun-Rong Chen ◽  
I-Hsin Lin ◽  
Ching-Chiung Wang

In traditional Chinese medicine (TCM), purgation is indicated when a person suffers an illness due to the accumulation of evil internal heat. Obese individuals with a large belly, red face, thick and yellow tongue fur, constipation, and avoidance of heat are thought accumulates of evil internal heat, and they are also treated with purgatives such asTa-Cheng-Chi-Tang(TCCT),Xiao-Chen-Chi-Tang(XCCT), andTiao-Wei-Chen-Chi-Tang(TWCCT) by TCM doctors. In previous studies, our group found that TCCT has potent anti-inflammatory activity, and that XCCT is an effective antioxidant. Since rhubarb is the principle herb in these three prescriptions, we will first present a thorough review of the literature on the demonstrated effect (or lack of effect) of rhubarb and rhubarb-containing polyherbal preparations on lipid and weight control. We will then continue our research with an investigation of the anti-obesity and lipid-lowering effect of TCCT, XCCT, TWCCT, and rhubarb extracts using two animal models. TWCCT lowered the serum triglyceride concentration as much as fenofibrate in Triton WR-1339-treated mice. Daily supplementation with XCCT and TWCCT significantly attenuated the high-fat-diet-induced hypercholesterolemia in rats. In addition, TWCCT also significantly lowered the high-fat-diet-induced hypertriglycemia. Although feeding high-fat diet rats with these extracts did not cause loose stools or diarrhea or other deleterious effects on renal or hepatic function. None of these extracts lowered the body weight of rats fed on high-fat diet. In conclusion, the results suggest that XCCT and TWCCT might exert beneficial effects in the treatment of hyperlipidemia.


2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Samra Vazirian ◽  
Anahita Dona Navab ◽  
Ladan Vakili ◽  
Sheila Safarpour ◽  
Maryam Haghnegahdar ◽  
...  

2021 ◽  
Vol 5 (2) ◽  
pp. 74
Author(s):  
Saut Horas Hatoguan Nababan ◽  
Seruni Tyas Khairunissa ◽  
Erni Erfan ◽  
Nafrialdi Nafrialdi ◽  
Ening Krisnuhoni ◽  
...  

Background: Non-alcoholic steatohepatitis (NASH) is an expanding cause of chronic liver disease worldwide, including Indonesia, with higher risk progression to cirrhosis and hepatocellular carcinoma. Preclinical experiments using several mice models have been conducted to clarify its complex pathogenesis. This study was designed to investigate whether BALB/c mice on a choline-deficient high-fat diet can be used as a model for NASH. Materials and Methods: BALB/c male mice were fed choline-deficient L-amino acid-defined high-fat diet (CDAHFD) or a standard diet for six weeks. The body and liver weights, liver histology, and plasma biochemistry were analyzed. The relative expression levels of tumor necrosis factor (TNF)α, transforming growth factor (TGF)β1, collagen-1α1 (COL1α1), glutathione peroxidase 1 (GPx1), and uncoupling protein 2 (UCP2) genes in the livers were analyzed using a two-step real time-polymerase chain reaction. Liver fatty acids composition was analyzed using gas chromatography with flame ionization detector (GC-FID). Results: CDAHFD induced steatohepatitis in BALB/c mice with increased plasma levels of alanine aminotransferase. The liver of CDAHFD-fed BALB/c mice showed upregulated relative expression levels of TNFα, TGFβ1, COL1α1, GPx1, and UCP2 genes. The liver fatty acid analysis showed a significant accumulation of saturated fatty acids (SFAs) and an increased ratio of n-6/n-3 polyunsaturated fatty acids (PUFAs) in the livers of CDAHFD-fed BALB/c mice. Conclusion: This study suggests that CDAHFD can induce steatohepatitis in BALB/c mice and therefore may be used as NASH mice model.Keywords: steatohepatitis, fatty liver, choline-deficient high fat diet, BALB/c 


2019 ◽  
Vol 97 (6) ◽  
pp. 693-701 ◽  
Author(s):  
Aline Haas de Mello ◽  
Rosiane de Bona Schraiber ◽  
Mariana Pereira de Souza Goldim ◽  
Khiany Mathias ◽  
Carolini Mendes ◽  
...  

This study evaluated the effects of omega-3 polyunsaturated fatty acids (PUFAs) on oxidative stress and energy metabolism parameters in the visceral fat of a high-fat-diet induced obesity model. Energy intake, body mass, and visceral fat mass were also evaluated. Male Swiss mice received either a control diet (control group) or a high-fat diet (obese group) for 6 weeks. After this period, the groups were divided into control + saline, control + omega-3, obese + saline, and obese + omega-3, and to these groups 400 mg·(kg body mass)−1·day−1 of fish oil (or saline) was administered orally, for 4 weeks. Energy intake and body mass were monitored throughout the experiment. In the 10th week, the animals were euthanized and the visceral fat (mesenteric) was removed. Treatment with omega-3 PUFAs did not affect energy intake or body mass, but it did reduced visceral fat mass. In visceral fat, omega-3 PUFAs reduced oxidative damage and alleviated changes to the antioxidant defense system and the Krebs cycle. The mitochondrial respiratory chain was neither altered by obesity nor by omega-3 PUFAs. In conclusion, omega-3 PUFAs have beneficial effects on the visceral fat of obese mice because they mitigate changes caused by the consumption of a high-fat diet.


2019 ◽  
Vol 10 (5) ◽  
pp. 2847-2860 ◽  
Author(s):  
Jianhui Liu ◽  
Wangjun Hao ◽  
Zouyan He ◽  
Erika Kwek ◽  
Yimin Zhao ◽  
...  

Anti-obesity activity of tea water extracts is partially mediated by altering intestinal microbiota via suppressing production of LPS and promoting production of SCFAs.


2021 ◽  
Vol 22 (7) ◽  
pp. 3746
Author(s):  
Ilaria Zuliani ◽  
Chiara Lanzillotta ◽  
Antonella Tramutola ◽  
Eugenio Barone ◽  
Marzia Perluigi ◽  
...  

The disturbance of protein O-GlcNAcylation is emerging as a possible link between altered brain metabolism and the progression of neurodegeneration. As observed in brains with Alzheimer’s disease (AD), flaws of the cerebral glucose uptake translate into reduced protein O-GlcNAcylation, which promote the formation of pathological hallmarks. A high-fat diet (HFD) is known to foster metabolic dysregulation and insulin resistance in the brain and such effects have been associated with the reduction of cognitive performances. Remarkably, a significant role in HFD-related cognitive decline might be played by aberrant protein O-GlcNAcylation by triggering the development of AD signature and mitochondrial impairment. Our data support the impairment of total protein O-GlcNAcylation profile both in the brain of mice subjected to a 6-week high-fat-diet (HFD) and in our in vitro transposition on SH-SY5Y cells. The reduction of protein O-GlcNAcylation was associated with the development of insulin resistance, induced by overfeeding (i.e., defective insulin signaling and reduced mitochondrial activity), which promoted the dysregulation of the hexosamine biosynthetic pathway (HBP) flux, through the AMPK-driven reduction of GFAT1 activation. Further, we observed that a HFD induced the selective impairment of O-GlcNAcylated-tau and of O-GlcNAcylated-Complex I subunit NDUFB8, thus resulting in tau toxicity and reduced respiratory chain functionality respectively, highlighting the involvement of this posttranslational modification in the neurodegenerative process.


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