Abstract 3305: FDG PET Imaging in the PRKAG2 Cardiac Syndrome Demonstrates Altered Myocardial Glucose Uptake

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Andrew C Ha ◽  
Jennifer Renaud ◽  
Stephanie Thorn ◽  
Rob deKemp ◽  
Keiichiro Yoshinaga ◽  
...  

Background : The PRKAG2 gene encodes for the gamma-2 subunit of AMP-activated protein kinase (AMPK), a protein implicated in the regulation of myocardial glucose metabolism. In humans, mutations of the PRKAG2 gene result in a cardiomyopathy characterized by ventricular pre-excitation, atrioventricular conduction disease, and cardiac hypertrophy. It is recognized that altered cardiac glucose metabolism and abnormal glycogen stores are responsible for the clinical manifestations of this syndrome. Since myocardial glucose uptake can be measured with 2-[ 18 F]Fluoro-2-deoxyglucose dynamic positron emission tomography ([ 18 F]FDG PET), we examined whether adult patients with an identified Arg302Gln PRKAG2 mutation have altered myocardial glucose uptake using this imaging modality. Methods: [ 18 F]FDG PET was performed in 5 adult patients with the Arg302Gln PRKAG2 mutation (PRKAG2) and in 6 healthy volunteers (Control) with a hyperinsulinemic euglycemic clamp protocol. The fractional rate of radiotracer uptake (K) is derived from PATLAK analysis. The rate of myocardial glucose uptake (rMGU) of the left ventricle (LV) is calculated as (K / LC) x P glucose , where P glucose represents the mean plasma glucose level during imaging. LC (lump constant) corrects for the differences in the transport and phosphorylation of [ 18 F]FDG and glucose. Results are expressed as mean ± standard deviation and are analyzed with the student t-test. Results: The mean rMGU in the PRKAG2 group was significantly lower than the control group. There was no difference in the mean plasma glucose levels between the 2 groups. (Table ) Conclusion: Myocardial glucose uptake is reduced in adult patients with mutation of the PRKAG2 gene when compared to normal controls. Measurement of rMGU using [ 18 F]FDG PET imaging appears to be a useful tool to investigate the pathophysiology of the PRKAG2 cardiac syndrome and to potentially distinguish this metabolic cardiomyopathy from other etiolgies. Mean rate of myocardial glucose uptake between patients with the PRKAG2 mutation and normal controls

2021 ◽  
Vol 18 ◽  
Author(s):  
Amir Ashraf-Ganjouei ◽  
Kamyar Moradi ◽  
Shahriar Faghani ◽  
AmirHussein Abdolalizadeh ◽  
Mohammadreza Khomeijani-Farahani ◽  
...  

Background: Mild cognitive impairment (MCI) is a state between normal cognition and dementia. However, MCI diagnosis does not necessarily guarantee the progression to dementia. Since no previous study investigated brain positron emission tomography (PET) imaging of MCI-- to-normal reversion, we provided PET imaging of MCI-to-normal reversion using the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Methods: We applied comprehensive neuropsychological criteria (NP criteria), consisting of mem- ory, language, and attention/executive function domains, to include patients with a baseline diagno- sis of MCI (n=613). According to the criteria, the year 1 status of the patients was categorized into three groups (reversion: n=105, stable MCI: n=422, conversion: n=86). Demographic, neuropsycho- logical, genetic, CSF, and cognition biomarker variables were compared between the groups. Addi- tionally, after adjustment for confounding variables, the deposition pattern of amyloid-β and cere- bral glucose metabolism were compared between three groups via AV45- and FDG-PET modali- ties, respectively. Results: MCI reversion rate was 17.1% during one year of follow-up. The reversion group had the lowest frequency of APOE ε4+ subjects, the highest CSF level of amyloid-β, and the lowest CSF levels of t-tau and p-tau. Neuropsychological assessments were also suggestive of better cognitive performance in the reversion group. Patients with reversion to normal state had higher glucose metabolism in bilateral angular and left middle/inferior temporal gyri, when compared to those with stable MCI state. Meanwhile, lower amyloid-β deposition at baseline was observed in the fron- tal and parietal regions of the reverted subjects. On the other hand, the conversion group showed lower cerebral glucose metabolism in bilateral angular and bilateral middle/inferior temporal gyri compared to the stable MCI group, whereas the amyloid-β accumulation was similar between the groups. Conclusions: This longitudinal study provides novel insight regarding the application of PET imag- ing in predicting MCI transition over time.


2012 ◽  
Vol 303 (9) ◽  
pp. E1134-E1141 ◽  
Author(s):  
Jason M. Ng ◽  
Koichiro Azuma ◽  
Carol Kelley ◽  
Richard Pencek ◽  
Zofia Radikova ◽  
...  

Excess amounts of abdominal subcutaneous (SAT) and visceral (VAT) adipose tissue (AT) are associated with insulin resistance, even in normal-weight subjects. In contrast, gluteal-femoral AT (GFAT) is hypothesized to offer protection against insulin resistance. Dynamic PET imaging studies were undertaken to examine the contributions of both metabolic activity and size (volume) of these depots in systemic glucose metabolism. Nonobese, healthy volunteers ( n = 15) underwent dynamic PET imaging uptake of [18F]FDG at a steady-state (20 mU·m−2·min−1) insulin infusion. PET images of tissue [18F]FDG activity were coregistered with MRI to derive K values for insulin-stimulated rates of fractional glucose uptake within tissue. Adipose tissue volume was calculated from DEXA and MRI. VAT had significantly higher rates of fractional glucose uptake per volume than SAT ( P < 0.05) or GFAT ( P < 0.01). KGFAT correlated positively ( r = 0.67, P < 0.01) with systemic insulin sensitivity [glucose disappearance rate (Rd)] and negatively with insulin-suppressed FFA ( r = −0.71, P < 0.01). SAT ( r = −0.70, P < 0.01) and VAT mass ( r = −0.55, P < 0.05) correlated negatively with Rd, but GFAT mass did not. We conclude that rates of fractional glucose uptake within GFAT and VAT are significantly and positively associated with systemic insulin sensitivity in nonobese subjects. Furthermore, whereas SAT and VAT amounts are confirmed to relate to systemic insulin resistance, GFAT amount is not associated with insulin resistance. These dynamic PET imaging studies indicate that both quantity and quality of specific AT depots have distinct roles in systemic insulin resistance and may help explain the metabolically obese but normal-weight phenotype.


2018 ◽  
Vol 45 (4) ◽  
pp. 1423-1433 ◽  
Author(s):  
Mingyao Liu ◽  
Hongwei Cao ◽  
Yuting Hou ◽  
Guopeng Sun ◽  
Deshan Li ◽  
...  

Background/Aims: The liver is a vital organ in vertebrates and has a wide range of functions, including glucose absorption, glycogen storage and glucose production. Fibroblast growth factor (FGF)-21 is a metabolic regulator that is primarily produced by the liver. In this paper, we studied the effect of FGF-21 on glucose metabolism in the liver. Methods: The glucose uptake of cells was detected by 2-Deoxy-d-[3H] glucose; the synergy between insulin and FGF-21 was evaluated. The mRNA expression of GLUT1-4, G6Pase and PEPCK was detected by real-time PCR. Glycogen synthesis was examined by the anthrone method. Blood samples to monitor glucose in db/db diabetic mice were obtained by tail snip. Glucose metabolism in the liver and adipose tissues was observed by fluorescence microscopy. Results: In this study, FGF-21 stimulated glucose uptake by liver cells in both a dose and time-dependent manner, and at the same time, FGF-21 specifically stimulated GLUT1 expression in the liver cells. Furthermore, FGF-21 demonstrated a synergistic effect with insulin on glucose absorption, which is in accordance with enhanced GLUT-1 and -4 expression. Treatment with FGF-21 increased glycogen storage in liver cells. Consistent with in vitro results, FGF-21 lowered the plasma glucose level and stimulated GLUT1 expression and glycogen synthesis in db/db diabetic mice. Simultaneously, FGF-21 inhibited the gene expression of G6Pase and PEPCK. Conclusion: Our results suggest that FGF-21 clears up plasma glucose by stimulating glucose absorption in the liver of diabetic animals and decreases glucose release from the liver by inhibiting gluconeogenesis. Overall, these data indicate that the liver is an important target organ of FGF-21 to regulate glucose metabolism.


2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Jingfeng Wang ◽  
Zhiming Li ◽  
Yanyan Wang ◽  
Jingjing Zhang ◽  
Weipeng Zhao ◽  
...  

Cardiac diastolic dysfunction has emerged as a growing type of heart failure. The present study aims to explore whether Qiliqiangxin (QL) can benefit cardiac diastolic function in spontaneously hypertensive rat (SHR) through enhancement of cardiac glucose metabolism. Fifteen 12-month-old male SHRs were randomly divided into QL-treated, olmesartan-treated, and saline-treated groups. Age-matched WKY rats served as normal controls. Echocardiography and histological analysis were performed. Myocardial glucose uptake was determined by 18F-FDG using small-animal PET imaging. Expressions of several crucial proteins and key enzymes related to glucose metabolism were also evaluated. As a result, QL improved cardiac diastolic function in SHRs, as evidenced by increased E′/A′and decreased E/E′ (P<0.01). Meanwhile, QL alleviated myocardial hypertrophy, collagen deposits, and apoptosis (P<0.01). An even higher myocardial glucose uptake was illustrated in QL-treated SHR group (P<0.01). Moreover, an increased CS activity and ATP production was observed in QL-treated SHRs (P<0.05). QL enhanced cardiac glucose utilization and oxidative phosphorylation in SHRs by upregulating AMPK/PGC-1α axis, promoting GLUT-4 expression, and regulating key enzymes related to glucose aerobic oxidation such as HK2, PDK4, and CS (P<0.01). Our data suggests that QL improves cardiac diastolic function in SHRs, which may be associated with enhancement of myocardial glucose metabolism.


2013 ◽  
Vol 106 ◽  
pp. S107
Author(s):  
A. Roszak ◽  
B. Urbanski ◽  
E. Burchardt ◽  
J. Kazmierska ◽  
Z. Warenczak-Florczak ◽  
...  

2016 ◽  
Vol 621 ◽  
pp. 126-132 ◽  
Author(s):  
Ramona E. von Leden ◽  
Reed G. Selwyn ◽  
Shalini Jaiswal ◽  
Colin M. Wilson ◽  
Guzal Khayrullina ◽  
...  

2018 ◽  
Vol 01 (01) ◽  
pp. 27-31 ◽  
Author(s):  
Haibo Tan ◽  
Xiuming Li ◽  
Kai Wei ◽  
Yihui Guan

Aim: To assess the changes of brain glucose metabolism and abnormal intracerebral loop in early Parkinson’s disease (PD) patients with visual spatial dysfunction by [Formula: see text]F-fluorodeoxyglucose ([Formula: see text]F-FDG) positron emission tomography (PET) imaging. Materials and Methods: This study includes three groups: early PD patients with visual spatial dysfunction ([Formula: see text]), early PD patients without visual spatial dysfunction ([Formula: see text]) and healthy controls ([Formula: see text]). Resting-state [Formula: see text]F-FDG PET was performed to obtain the imaging of brain glucose metabolism. Statistical Parametric Mapping (SPM) was used for data analyses to compare the brain glucose metabolic changes among different groups. Results: Compared with the healthy controls, early PD patients (with/without visual spatial dysfunction) showed hypermetabolism in putamen, globus pallidus, thalamus, pons, cerebellum and primary motor cortex, and hypometabolism in part of the occipital and temporal lobes. Compared with early PD patients without visual spatial dysfunction, those with visual spatial dysfunction further showed hypometabolism in visual regions including bilateral lateral prefrontal cortices and posterior parietal lobules, besides occipital and temporal lobes. Conclusion: The occurrence of abnormal glucose metabolism in the brain visual processing areas was closely associated with visual spatial dysfunction in PD patients.


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