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.

scholarly journals Obesity risk is associated with altered cerebral glucose metabolism and decreased μ-opioid and CB1 receptor availability

2021 ◽  
Author(s):  
Tatu Kantonen ◽  
Laura Pekkarinen ◽  
Tomi Karjalainen ◽  
Marco Bucci ◽  
Kari Kalliokoski ◽  
...  
Keyword(s):  
Risk Factors ◽  
Glucose Uptake ◽  
Familial Risk ◽  
Health Concern ◽  
Obesity Risk ◽  
Brain Glucose ◽  
Positron Emission ◽  
The Central Nervous System ◽  
Familial Obesity ◽  
The Brain

Abstract Background Obesity is a pressing public health concern worldwide. Novel pharmacological means are urgently needed to combat the increase of obesity and accompanying type 2 diabetes (T2D). Although fully established obesity is associated with neuromolecular alterations and insulin resistance in the brain, potential obesity-promoting mechanisms in the central nervous system have remained elusive. In this triple-tracer positron emission tomography study, we investigated whether brain insulin signaling, μ-opioid receptors (MORs) and cannabinoid CB1 receptors (CB1Rs) are associated with risk for developing obesity. Methods Subjects were 41 young non-obese males with variable obesity risk profiles. Obesity risk was assessed by subjects’ physical exercise habits, body mass index and familial risk factors, including parental obesity and T2D. Brain glucose uptake was quantified with [18F]FDG during hyperinsulinemic euglycemic clamp, MORs were quantified with [11C]carfentanil and CB1Rs with [18F]FMPEP-d2. Results Subjects with higher obesity risk had globally increased insulin-stimulated brain glucose uptake (19 high-risk subjects versus 19 low-risk subjects), and familial obesity risk factors were associated with increased brain glucose uptake (38 subjects) but decreased availability of MORs (41 subjects) and CB1Rs (36 subjects). Conclusions These results suggest that the hereditary mechanisms promoting obesity may be partly mediated via insulin, opioid and endocannabinoid messaging systems in the brain.

scholarly journals Central GLP-1 contributes to improved cognitive function and brain glucose uptake after duodenum-jejunum bypass on obese and diabetic rats

2021 ◽  
Author(s):  
Rexiati Ruze ◽  
Qian Xu ◽  
Guoqin Liu ◽  
Yuekai Li ◽  
Weijie Chen ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Glucose Uptake ◽  
Diabetic Rats ◽  
Brain Glucose ◽  
Positron Emission ◽  
Myosin Va ◽  
Glucagon Like Peptide 1 ◽  
Underlying Mechanisms ◽  
Related Proteins

The improvement of cognitive function following bariatric surgery has been highlighted, yet its underlying mechanisms remain elusive. Finding the improved brain glucose uptake of patients after Roux-en-Y gastric bypass (RYGB), duodenum-jejunum bypass (DJB) and sham surgery (Sham) were performed on obese and diabetic Wistar rats, and intracerebroventricular (ICV) injection of glucagon-like peptide-1 (GLP-1) analog liraglutide (Lira), antagonist exendin-(9-39) (Exe-9), and the viral-mediated GLP-1 receptor (Glp-1r) knockdown (KD) were applied on both groups to elucidate the role of GLP-1 in mediating cognitive function and brain glucose uptake assessed with the Morris water maze (MWM) and positron emission tomography (PET). Insulin and GLP-1 in serum and cerebral spinal fluid (CSF) were measured, and the expression of glucose uptake-related proteins including GLUT-1, GLUTT-4, pAS160, AS160, Rab10, Myosin-Va as well as the c-fos marker in the brain were examined. Along with augmented glucose homeostasis following DJB, central GLP-1 was correlated with the improved cognitive function and ameliorated brain glucose uptake, which was further confirmed by the enhancive role of Lira on both groups while the Exe-9 and Glp-1r KD were opposite. Known to activate insulin signaling pathways, central GLP-1 contributes to improved cognitive function and brain glucose uptake after DJB.

scholarly journals The Effect of Sulphoraphane on Brain Glucose Uptake during Neonatal Hypoxic-Ischemic Encephalopathy in Newborn Rats

2021 ◽  
Vol 68 (1) ◽  
pp. 136-138
Author(s):  
S. Kapoor ◽  
D. Kala ◽  
J. Svoboda ◽  
Z. Brnoliakova ◽  
J. Otahal
Keyword(s):  
Glucose Uptake ◽  
Newborn Rats ◽  
Time Intervals ◽  
Brain Glucose ◽  
Positron Emission ◽  
Socioeconomic Burden ◽  
18F Fdg ◽  
Ischemic Encephalopathy ◽  
Present Pilot Study

Abstract Neonatal hypoxic-ischemic insult (HII) is one of the leading causes of morbidity and mortality in newborns. It has long-term consequences and represents a socioeconomic burden. It is an urgent issue in current neonatology. The aim of the present pilot study was to evaluate the possible effect of sulforaphane on brain glucose uptake expressed as 18F-fluorodeoxyglucose (18F-FDG) activity at the acute, subacute, and subchronic time intervals after the experimental perinatal HII in rats. Significant protection has been observed in the hippocampus 5 weeks after the insult as represented by normalisations of interhemispheric ratio of measured 18F-FDG activity. In conclusion, positron emission tomography (PET) with 18F-FDG revealed a protective effect of SFN on glucose metabolism in the subchronic phase after HII. Further research within the field of neonatal HII in newborn rats will be necessary.

scholarly journals Brain Glucose Overexposure and Lack of Acute Metabolic Flexibility in Obesity and Type 2 Diabetes: A PET-[18F]FDG Study in Zucker and ZDF Rats

2010 ◽  
Vol 30 (5) ◽  
pp. 895-899 ◽  
Author(s):  
Tiziana Liistro ◽  
Letizia Guiducci ◽  
Silvia Burchielli ◽  
Daniele Panetta ◽  
Nicola Belcari ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Study Data ◽  
Mass Action ◽  
Glucose Disposal ◽  
Brain Glucose ◽  
Positron Emission ◽  
Obesity And Diabetes ◽  
Glucose Intake ◽  
High Fasting Glucose ◽  
And Control

Brain glucose exposure may complicate diabetes and obesity. We used positron emission tomography with 18F-fluorodeoxyglucose in Zucker obese, diabetic, and control rats to determine the contributions of blood glucose mass action versus local mechanisms in regulating central glucose disposal in fasted and acutely glucose-stimulated states, and their adaptations in obesity and diabetes. Our study data indicate that brain glucose uptake is dependent on both local and mass action components, and is stimulated by acute glucose intake in healthy rats. In diseased animals, the organ was chronically overexposed to glucose, due to high fasting glucose uptake, almost abolishing the physiologic response to glucose loading.

scholarly journals Peptide VSAK maintains tissue glucose uptake and attenuates pro-inflammatory responses caused by LPS in an experimental model of the systemic inflammatory response syndrome: a PET study

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ismael Luna-Reyes ◽  
Eréndira G. Pérez-Hernández ◽  
Blanca Delgado-Coello ◽  
Miguel Ángel Ávila-Rodríguez ◽  
Jaime Mas-Oliva
Keyword(s):  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Glucose Uptake ◽  
Inflammatory Responses ◽  
Serum Levels ◽  
Systemic Inflammatory Response ◽  
Positron Emission ◽  
Inflammatory Molecules ◽  
Circulating Levels ◽  
Lps Treatment

AbstractThe present investigation using Positron Emission Tomography shows how peptide VSAK can reduce the detrimental effects produced by lipopolysaccharides in Dutch dwarf rabbits, used to develop the Systemic Inflammatory Response Syndrome (SIRS). Animals concomitantly treated with lipopolysaccharides (LPS) and peptide VSAK show important protection in the loss of radiolabeled-glucose uptake observed in diverse organs when animals are exclusively treated with LPS. Treatment with peptide VSAK prevented the onset of changes in serum levels of glucose and insulin associated with the establishment of SIRS and the insulin resistance-like syndrome. Treatment with peptide VSAK also allowed an important attenuation in the circulating levels of pro-inflammatory molecules in LPS-treated animals. As a whole, our data suggest that peptide VSAK might be considered as a candidate in the development of new therapeutic possibilities focused on mitigating the harmful effects produced by lipopolysaccharides during the course of SIRS.

Neural Mechanism of Propofol Anesthesia in Severe Depression

2003 ◽  
Vol 98 (5) ◽  
pp. 1101-1111 ◽  
Author(s):  
Kenichi Ogawa ◽  
Takeshi Uema ◽  
Nobutaka Motohashi ◽  
Masami Nishikawa ◽  
Harumasa Takano ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Statistical Parametric Mapping ◽  
Severe Depression ◽  
Dose Effect ◽  
Emission Tomography ◽  
Association Cortex ◽  
Depressed Patients ◽  
Positron Emission

Background The precise neural mechanisms of propofol anesthesia in humans are still unknown. The authors examined the acute effects of propofol on regional cerebral blood flow (rCBF) using positron emission tomography in patients with severe depression. Methods In six severely depressed patients (mean age, 55.0 yr) scheduled for electroconvulsive therapy, anesthetic levels were monitored by electroencephalography, and rCBF was serially quantified in the awake, sedated, and anesthetized states. The authors used high-resolution positron emission tomography with 15O-labeled water and statistical parametric mapping 99 for imaging and analysis of the data. Results Global cerebral blood flow showed sharp decreases from the awake level during the administration of propofol, decreasing 26.8% in the sedated state and 54.4% in the anesthetized state. Moreover, a dose effect was seen in both parietal cortices and the left lateral prefrontal region with larger regions of relative decrease in rCBF at higher propofol doses. At the higher dose, the values of rCBF in the pulvinar nucleus of the thalamus, the pontine tegmentum, and the cerebellar cortex were also affected. Meanwhile, there were few changes of relative rCBF in the basal frontal lobes during both sedated and anesthetized states. Conclusions As in earlier studies using normal subjects, pronounced suppression in rCBF in the brain stem reticular formation, the thalamus, and the parietal association cortex occurred even in severely depressed patients. However, previously reported decreases in rCBF in the basal frontal lobe were absent in depressed patients.

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