scholarly journals Astrocytic Insulin Signaling Couples Brain Glucose Uptake with Nutrient Availability

Cell ◽  
2016 ◽  
Vol 166 (4) ◽  
pp. 867-880 ◽  
Author(s):  
Cristina García-Cáceres ◽  
Carmelo Quarta ◽  
Luis Varela ◽  
Yuanqing Gao ◽  
Tim Gruber ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Nutrient Availability ◽  
Insulin Signaling ◽  
Brain Glucose

Green Tea Polyphenol Extract Regulates the Expression of Genes Involved in Glucose Uptake and Insulin Signaling in Rats Fed a High Fructose Diet

2007 ◽  
Vol 55 (15) ◽  
pp. 6372-6378 ◽  
Author(s):  
Heping Cao ◽  
Isabelle Hininger-Favier ◽  
Meghan A. Kelly ◽  
Rachida Benaraba ◽  
Harry D. Dawson ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Green Tea ◽  
Insulin Signaling ◽  
Tea Polyphenol ◽  
High Fructose Diet ◽  
Expression Of Genes ◽  
High Fructose ◽  
Green Tea Polyphenol

scholarly journals The Obesity Risk SNP (rs17782313) near the MC4R Gene Is Not Associated with Brain Glucose Uptake during Insulin Clamp—A Study in Finns

2021 ◽  
Vol 10 (6) ◽  
pp. 1312
Author(s):  
Eleni Rebelos ◽  
Miikka-Juhani Honka ◽  
Laura Ekblad ◽  
Marco Bucci ◽  
Jarna C. Hannukainen ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Statistical Parametric Mapping ◽  
Obesity Risk ◽  
Melanocortin System ◽  
Single Nucleotide ◽  
Brain Glucose ◽  
Mc4r Gene ◽  
Insulin Clamp ◽  
Positron Emission ◽  
Fractional Uptake

The melanocortin system is involved in the control of adiposity through modulation of food intake and energy expenditure. The single nucleotide polymorphism (SNP) rs17782313 near the MC4R gene has been linked to obesity, and a previous study using magnetoencephalography has shown that carriers of the mutant allele have decreased cerebrocortical response to insulin. Thus, in this study, we addressed whether rs17782313 associates with brain glucose uptake (BGU). Here, [18F]-fluorodeoxyglucose positron emission tomography (PET) data from 113 Finnish subjects scanned under insulin clamp conditions who also had the rs17782313 determined were compiled from a single-center cohort. BGU was quantified by the fractional uptake rate. Statistical analysis was performed with statistical parametric mapping. There was no difference in age, BMI, and insulin sensitivity as indexed by the M value between the rs17782313-C allele carriers and non-carriers. Brain glucose uptake during insulin clamp was not different by gene allele, and it correlated with the M value, in both the rs17782313-C allele carriers and non-carriers. The obesity risk SNP rs17782313 near the MC4R gene is not associated with brain glucose uptake during insulin clamp in humans, and this frequent mutation cannot explain the enhanced brain glucose metabolic rates in insulin resistance.

Does impaired mitochondrial function affect insulin signaling and action in cultured human skeletal muscle cells?

2008 ◽  
Vol 294 (1) ◽  
pp. E97-E102 ◽  
Author(s):  
Audrey E. Brown ◽  
Matthias Elstner ◽  
Stephen J. Yeaman ◽  
Douglass M. Turnbull ◽  
Mark Walker
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Insulin Signaling ◽  
Mitochondrial Respiration ◽  
Respiratory Function ◽  
Insulin Action ◽  
Human Skeletal Muscle ◽  
Human Skeletal Muscle Cells ◽  
Basal Glucose Uptake

Insulin-resistant type 2 diabetic patients have been reported to have impaired skeletal muscle mitochondrial respiratory function. A key question is whether decreased mitochondrial respiration contributes directly to the decreased insulin action. To address this, a model of impaired cellular respiratory function was established by incubating human skeletal muscle cell cultures with the mitochondrial inhibitor sodium azide and examining the effects on insulin action. Incubation of human skeletal muscle cells with 50 and 75 μM azide resulted in 48 ± 3% and 56 ± 1% decreases, respectively, in respiration compared with untreated cells mimicking the level of impairment seen in type 2 diabetes. Under conditions of decreased respiratory chain function, insulin-independent (basal) glucose uptake was significantly increased. Basal glucose uptake was 325 ± 39 pmol/min/mg (mean ± SE) in untreated cells. This increased to 669 ± 69 and 823 ± 83 pmol/min/mg in cells treated with 50 and 75 μM azide, respectively (vs. untreated, both P < 0.0001). Azide treatment was also accompanied by an increase in basal glycogen synthesis and phosphorylation of AMP-activated protein kinase. However, there was no decrease in glucose uptake following insulin exposure, and insulin-stimulated phosphorylation of Akt was normal under these conditions. GLUT1 mRNA expression remained unchanged, whereas GLUT4 mRNA expression increased following azide treatment. In conclusion, under conditions of impaired mitochondrial respiration there was no evidence of impaired insulin signaling or glucose uptake following insulin exposure in this model system.

scholarly journals Adaptation in brain glucose uptake following recurrent hypoglycemia.

1994 ◽  
Vol 91 (20) ◽  
pp. 9352-9356 ◽  
Author(s):  
P. J. Boyle ◽  
R. J. Nagy ◽  
A. M. O'Connor ◽  
S. F. Kempers ◽  
R. A. Yeo ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Brain Glucose ◽  
Recurrent Hypoglycemia

scholarly journals Imaging of brain glucose uptake by PET in obesity and cognitive dysfunction: life-course perspective

2019 ◽  
Vol 8 (11) ◽  
pp. R169-R183 ◽  
Author(s):  
Patricia Iozzo ◽  
Maria Angela Guzzardi
Keyword(s):  
Insulin Resistance ◽  
Life Course ◽  
Glucose Uptake ◽  
Cognitive Dysfunction ◽  
Brain Metabolism ◽  
Life Course Perspective ◽  
Whole Body ◽  
Current Evidence ◽  
Brain Glucose

The prevalence of obesity has reached epidemic proportions and keeps growing. Obesity seems implicated in the pathogenesis of cognitive dysfunction, Alzheimer’s disease and dementia, and vice versa. Growing scientific efforts are being devoted to the identification of central mechanisms underlying the frequent association between obesity and cognitive dysfunction. Glucose brain handling undergoes dynamic changes during the life-course, suggesting that its alterations might precede and contribute to degenerative changes or signaling abnormalities. Imaging of the glucose analog 18F-labeled fluorodeoxyglucose (18FDG) by positron emission tomography (PET) is the gold-standard for the assessment of cerebral glucose metabolism in vivo. This review summarizes the current literature addressing brain glucose uptake measured by PET imaging, and the effect of insulin on brain metabolism, trying to embrace a life-course vision in the identification of patterns that may explain (and contribute to) the frequent association between obesity and cognitive dysfunction. The current evidence supports that brain hypermetabolism and brain insulin resistance occur in selected high-risk conditions as a transient phenomenon, eventually evolving toward normal or low values during life or disease progression. Associative studies suggest that brain hypermetabolism predicts low BDNF levels, hepatic and whole body insulin resistance, food desire and an unfavorable balance between anticipated reward from food and cognitive inhibitory control. Emerging mechanistic links involve the microbiota and the metabolome, which correlate with brain metabolism and cognition, deserving attention as potential future prevention targets.

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