Disturbances in the glucose metabolism in the brain: the role of stress and high-fat diet

2018 ◽  
Author(s):  
Katarzyna Glombik
Keyword(s):  
Glucose Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
The Brain

Disturbances in the glucose metabolism in the brain: the role of stress and high-fat diet

2019 ◽  
Vol 29 ◽  
pp. S215-S216
Author(s):  
K. Glombik ◽  
J. Detka ◽  
A. Kurek ◽  
B. Budziszewska
Keyword(s):  
Glucose Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
The Brain

Abstract 224: Angiogenic Imbalance Causes Cerebrovascular Pathological Neovascularization in Diabetes: Role of Pericytes.

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Mohammed Abdelsaid ◽  
John Paul Valenzuel ◽  
Adviye Ergul
Keyword(s):  
High Fat Diet ◽  
Wistar Rats ◽  
Low Dose ◽  
High Fat ◽  
Migration Assay ◽  
Cerebrovascular Complications ◽  
Pericyte Coverage ◽  
The Brain

Diabetes increases cerebrovascular complications such as stroke and cognitive impairment. We have previously showed that diabetes causes dysfunctional cerebral neovascularization. Pericytes have a pivotal role in modulating microvascular physiology and pathology, yet its role in diabetes dysfunctional cerebral neovascularization is unknown. In the present study we testedthe hypothesis that pericytes play a crucial role in diabetes-mediated dysfunctional pathological cerebral neovascularization via dysregulation of antiangiogenic Slit-2/ROBO4 and the proangiogenic EphrinB2/EphB4 signaling. Methods: Diabetes was induced in Wistar rats using low dose of streptozotocin and high fat diet (STZ/HFD). Immunohistochemistry and immunoblotting were used to assess ROBO4 and EphrinB2 expression in the brain and human brain microvascular pericytes (HBMVP). HBMVP was exposed to glucose (25 mM) /palmitate (200 uM) to mimic diabetic conditions. Scratch migration assay was used to assess the effect of high glucose/palmitate (HG/Pal) on pericytes migration. Adenovirus was used to overexpress ROBO4 in the brain in vivo. Results: STZ/HFD caused a significant increase in HbA1C (10.8*). Diabetic brains and HBMVP exposed to HG/Pal showed reduced ROBO4 expression (66%* and 48%*) and increased EphrinB2 expression (1.9* and 1.6* folds). HG/Pal increased pericyte migration by 2* fold. Pericyte migration was increased by 2.5* fold with silencing ROBO4 but significantly reduced with silencing EphrinB2 (35%*) or ROBO4 overexpression (47%*) under HG/Pal. In vivo ROBO4 overexpression decreased pathological neovascularization indices and increased pericyte coverage. (n= 3-5, *P<0.05). Conclusion: Our findings emphasize the importance of balanced anti- and proangiogenic signaling for proper pericyte function in diabetes. Our results suggest that pericytes are involved in proangiogenic and barrier functions of endothelial cells and pericyte dysfunction may contribute to pathological neovascularization in diabetes. Thus, pericyte ROBO4 and EphrinB2 signaling are promising therapeutic targets to improve cerebrovascular integrity in diabetes.

scholarly journals TRPM2 Ca2+ channel regulates energy balance and glucose metabolism

2012 ◽  
Vol 302 (7) ◽  
pp. E807-E816 ◽  
Author(s):  
Zhiyou Zhang ◽  
Wenyi Zhang ◽  
Dae Young Jung ◽  
Hwi Jin Ko ◽  
Yongjin Lee ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Gsk 3Β ◽  
Fat Feeding

TRPM2 Ca2+-permeable cation channel is widely expressed and activated by markers of cellular stress. Since inflammation and stress play a major role in insulin resistance, we examined the role of TRPM2 Ca2+ channel in glucose metabolism. A 2-h hyperinsulinemic euglycemic clamp was performed in TRPM2-deficient (KO) and wild-type mice to assess insulin sensitivity. To examine the effects of diet-induced obesity, mice were fed a high-fat diet for 4–10 mo, and metabolic cage and clamp studies were conducted in conscious mice. TRPM2-KO mice were more insulin sensitive partly because of increased glucose metabolism in peripheral organs. After 4 mo of high-fat feeding, TRPM2-KO mice were resistant to diet-induced obesity, and this was associated with increased energy expenditure and elevated expressions of PGC-1α, PGC-1β, PPARα, ERRα, TFAM, and MCAD in white adipose tissue. Hyperinsulinemic euglycemic clamps showed that TRPM2-KO mice were more insulin sensitive, with increased Akt and GSK-3β phosphorylation in heart. Obesity-mediated inflammation in adipose tissue and liver was attenuated in TRPM2-KO mice. Overall, TRPM2 deletion protected mice from developing diet-induced obesity and insulin resistance. Our findings identify a novel role of TRPM2 Ca2+ channel in the regulation of energy expenditure, inflammation, and insulin resistance.

The role of rice bran extract on acetyl CoA carboxylase in liver of rats fed a high-fat diet

Planta Medica ◽  
2011 ◽  
Vol 77 (12) ◽  
Author(s):  
C Charkhonpunya ◽  
S Sireeratawong ◽  
S Komindr ◽  
N Lerdvuthisopon
Keyword(s):  
Rice Bran ◽  
High Fat Diet ◽  
Acetyl Coa Carboxylase ◽  
High Fat ◽  
Acetyl Coa ◽  
Rice Bran Extract

Altered bone metabolism after high fat diet and exercise: role of Wnt signaling and insulin resistance

2016 ◽  
Author(s):  
Ann-Kristin Picke ◽  
Lykke Sylow ◽  
Lisbeth L V Moller ◽  
Rasmus Kjobsted ◽  
Erik Richter ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Wnt Signaling ◽  
Bone Metabolism ◽  
High Fat Diet ◽  
High Fat ◽  
Diet And Exercise

scholarly journals Mechanistic role of antioxidants in rescuing delayed gastric emptying in high fat diet induced diabetic female mice

2021 ◽  
Vol 137 ◽  
pp. 111370
Author(s):  
Chethan Sampath ◽  
Derek Wilus ◽  
Mohammad Tabatabai ◽  
Michael L. Freeman ◽  
Pandu R. Gangula
Keyword(s):  
Gastric Emptying ◽  
High Fat Diet ◽  
Delayed Gastric Emptying ◽  
High Fat ◽  
Female Mice

scholarly journals High-Fat Diet Leads to Reduced Protein O-GlcNAcylation and Mitochondrial Defects Promoting the Development of Alzheimer’s Disease Signatures

2021 ◽  
Vol 22 (7) ◽  
pp. 3746
Author(s):  
Ilaria Zuliani ◽  
Chiara Lanzillotta ◽  
Antonella Tramutola ◽  
Eugenio Barone ◽  
Marzia Perluigi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Alzheimer's Disease ◽  
High Fat Diet ◽  
Mitochondrial Activity ◽  
High Fat ◽  
Hexosamine Biosynthetic Pathway ◽  
Neurodegenerative Process ◽  
The Brain

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.

scholarly journals High-fat diet-induced obesity and impairment of brain neurotransmitter pool

2020 ◽  
Vol 11 (1) ◽  
pp. 147-160
Author(s):  
Ranyah Shaker M. Labban ◽  
Hanan Alfawaz ◽  
Ahmed T. Almnaizel ◽  
Wail M. Hassan ◽  
Ramesa Shafi Bhat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Obese Group ◽  
Control Group ◽  
High Fat ◽  
Brain Neurotransmitter ◽  
The Brain ◽  
Lean Group

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

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