scholarly journals The Impact of Obesity on Tumor Glucose Uptake in Breast and Lung Cancer

2020 ◽  
Vol 4 (2) ◽  
Author(s):  
Brooks P Leitner ◽  
Rachel J Perry
Keyword(s):  
Lung Cancer ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Protective Effects ◽  
Clinical Prognosis ◽  
Computed Tomography Images ◽  
Positron Emission ◽  
Altered Glucose ◽  
Poor Outcomes ◽  
The Impact

Abstract Obesity confers an increased incidence and poorer clinical prognosis in more than 10 cancer types. Paradoxically, obesity may provide protection from poor outcomes in lung cancer. Mechanisms for the obesity-cancer links are not fully elucidated, with altered glucose metabolism being a promising candidate. Using 18F-fluorodeoxyglucose positron-emission-tomography/computed tomography images from The Cancer Imaging Archive, we explored the relationship between body mass index (BMI) and glucose metabolism in several cancers. In 188 patients (BMI mean [SD] = 27.7 [5.1], range = 17.4–49.3 kg/m2), higher BMI was associated with greater tumor glucose uptake in breast cancer (r = 0.36; P = .02) and with lower tumor glucose uptake in non-small cell lung cancer (r = -0.26; P = .048) using two-sided Pearson correlations. No relationship was observed in soft tissue sarcoma or squamous cell carcinoma. Harnessing the National Cancer Institute’s open-access database, we demonstrate altered tumor glucose metabolism as a potential mechanism for the detrimental and protective effects of obesity on breast and lung cancer, respectively.

Etiology of Solitary Extrapulmonary Positron Emission Tomography and Computed Tomography Findings in Patients With Lung Cancer

2005 ◽  
Vol 23 (28) ◽  
pp. 6846-6853 ◽  
Author(s):  
Didier Lardinois ◽  
Walter Weder ◽  
Marina Roudas ◽  
Gustav K. von Schulthess ◽  
Michaela Tutic ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Lung Cancer ◽  
Positron Emission Tomography ◽  
Ct Imaging ◽  
Emission Tomography ◽  
Whole Body ◽  
Benign Tumors ◽  
Positron Emission ◽  
Pet Ct ◽  
The Impact

Purpose The aim of this prospective study was to assess the incidence and the nature of solitary extrapulmonary [18F] fluorodeoxyglucose (FDG) accumulations in patients with non–small-cell lung cancer (NSCLC) staged with integrated positron emission tomography and computed tomography (PET/CT) and to evaluate the impact on management. Patients and Methods A total of 350 patients with NSCLC underwent whole-body PET/CT imaging. All solitary extrapulmonary FDG accumulations were evaluated by histopathology, further imaging, or clinical follow-up. Results PET/CT imaging revealed extrapulmonary lesions in 110 patients. In 72 patients (21%), solitary lesions were present. A diagnosis was obtained in 69 of these patients, including 37 (54%) with solitary metastases and 32 (46%) with lesions unrelated to the lung primary. Histopathologic examinations of these 32 lesions revealed a second clinically unsuspected malignancy or a recurrence of a previous diagnosed carcinoma in six patients (19%) and a benign tumor or inflammatory lesion in 26 patients (81%). The six malignancies consisted of carcinoma of the breast in two patients, and carcinoma of the orbit, esophagus, prostate, and non-Hodgkin's lymphoma in one patient each. Benign tumors and inflammatory lesions included eight colon adenomas, four Warthin's tumors, one granuloma of the lower jaw, one adenoma of the thyroid gland, one compensatory muscle activity due to vocal chord palsy, two occurrences of arthritis, three occurrences of reflux esophagitis, two occurrences of pancreatitis, two occurrences of diverticulitis, one hemorrhoidal inflammation, and one rib fracture. Conclusion Solitary extrapulmonary FDG accumulations in patients with newly diagnosed lung cancer should be analyzed critically for correct staging and optimal therapy, given that up to half of the lesions may represent unrelated malignancies or benign disease.

scholarly journals Impact of Global Mean Normalization on Regional Glucose Metabolism in the Human Brain

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Kristian N. Mortensen ◽  
Albert Gjedde ◽  
Garth J. Thompson ◽  
Peter Herman ◽  
Maxime J. Parent ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Human Brain ◽  
Disease Biomarkers ◽  
Eyes Closed ◽  
Positron Emission ◽  
Congenitally Blind ◽  
Eyes Open ◽  
Health And Disease ◽  
The Impact ◽  
Global Mean

Because the human brain consumes a disproportionate fraction of the resting body’s energy, positron emission tomography (PET) measurements of absolute glucose metabolism (CMRglc) can serve as disease biomarkers. Global mean normalization (GMN) of PET data reveals disease-based differences from healthy individuals as fractional changes across regions relative to a global mean. To assess the impact of GMN applied to metabolic data, we compared CMRglc with and without GMN in healthy awake volunteers with eyes closed (i.e., control) against specific physiological/clinical states, including healthy/awake with eyes open, healthy/awake but congenitally blind, healthy/sedated with anesthetics, and patients with disorders of consciousness. Without GMN, global CMRglc alterations compared to control were detected in all conditions except in congenitally blind where regional CMRglc variations were detected in the visual cortex. However, GMN introduced regional and bidirectional CMRglc changes at smaller fractions of the quantitative delocalized changes. While global information was lost with GMN, the quantitative approach (i.e., a validated method for quantitative baseline metabolic activity without GMN) not only preserved global CMRglc alterations induced by opening eyes, sedation, and varying consciousness but also detected regional CMRglc variations in the congenitally blind. These results caution the use of GMN upon PET-measured CMRglc data in health and disease.

scholarly journals Dobutamine-tagged MRI for inotropic reserve assessment in severe CAD: relationship with PET findings

2004 ◽  
Vol 286 (5) ◽  
pp. H1946-H1953 ◽  
Author(s):  
Alejandro N. Mazzadi ◽  
Marc F. Janier ◽  
Benjamin Brossier ◽  
Xavier André-Fouët ◽  
Eugene McFadden ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Low Dose ◽  
Hibernating Myocardium ◽  
Tagged Mri ◽  
Positron Emission ◽  
Artery Disease ◽  
Tagged Magnetic Resonance Imaging ◽  
The Impact ◽  
The Relationship ◽  
Contractile Performance

The impact of blood flow reductions on the intramyocardial inotropic reserve has not yet been established in coronary artery disease (CAD). We therefore evaluated in severe CAD the relationship between positron emission tomography (PET) patterns of perfusion and glucose uptake and the corresponding tagged magnetic resonance imaging (tagged MRI) values of midmyocardial strains under low-dose dobutamine. Eighteen patients underwent tagged MRI (at rest, with dobutamine) and H 152O/18Ffluorodeoxyglucose PET. Regional midmyocardial circumferential shortening ( Ecc) and PET patterns (normal, match viable, mismatch viable, and infarcted) were assessed in three tagged MRI/PET short-axis slices. Regional Ecc at rest correlated with both perfusion ( r = 0.49) and glucose uptake ( r = 0.58). The presence of the inotropic reserve was similar in normal, match viable, and infarcted (∼40% of regions vs. 52% in mismatch viable, P < 0.05), but the extent of the increase after dobutamine was lower in infarcted regions ( P = 0.06). Within each PET pattern, regions were grouped according to their Ecc values at rest into three categories (high, intermediate, and low contractile performance). In mismatch viable (hibernation), the inotropic reserve was similar among the three categories, but in the other PET patterns the presence and extent of the inotropic reserve was higher in those regions with lowest Ecc (without significant differences in perfusion). In severe CAD, the presence of the inotropic reserve assessed by midmyocardial changes under dobutamine does not relate to resting perfusion. At a similar level of perfusion, the presence of the inotropic reserve is inversely related to contractile performance at rest, but our results suggest that it may not be true for hibernating myocardium.

scholarly journals Maternal hypothyroidism in mice influences glucose metabolism in adult offspring

2019 ◽  
Author(s):  
Yasmine Kemkem ◽  
Daniela Nasteska ◽  
Anne De Bray ◽  
Paula Bargi-Souza ◽  
Rodrigo A. Peliciari-Garcia ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Thyroid Hormones ◽  
Beta Cell ◽  
Endocrine Pancreas ◽  
Adult Offspring ◽  
Altered Glucose ◽  
The Impact

ABSTRACTDuring pregnancy, maternal metabolic diseases and hormonal imbalance may alter fetal beta cell development and/or proliferation, thus leading to an increased risk for developing type 2 diabetes in adulthood. Although thyroid hormones play an important role in fetal endocrine pancreas development, the impact of maternal hypothyroidism on glucose homeostasis in adult offsprings remains poorly understood. Here, we show that when fed normal chow, adult mice born to hypothyroid mothers were more glucose-tolerant due to beta cell hyperproliferation and increased insulin sensitivity. However, following high fat feeding, these offsprings became profoundly hyperinsulinemic, insulin-resistant and glucose-intolerant compared to controls from euthyroid mothers. Suggesting presence of epigenetic changes, altered glucose metabolism was maintained in a second generation of animals. As such, gestational hypothyroidism induces long-term and persistent alterations in endocrine pancreas function, which may have important implications for type 2 diabetes prevention in affected individuals.SIGNIFICANCEDiabetes and hypothyroidism are two major public health issues, affecting ∼ 9 and 2 % of the population worldwide, respectively. As master metabolic gatekeepers, the thyroid hormones play an essential role in metabolism and fetal development. However, gestation increases demand on the thyroid axis in the mother, leading to hypothyroidism in 0.5 % of pregnancies. Maternal hypothyroidism is associated with deficits in fetal growth that may lead to long-term alterations in metabolism in the offspring. We therefore sought to investigate the effects of gestational hypothyroidism on glucose metabolism in adult offspring and their descendants, and how this may predispose to diabetes development.

Interaction of carbohydrate and fat fuels in human skeletal muscle: impact of obesity and NIDDM

1996 ◽  
Vol 270 (3) ◽  
pp. E463-E470 ◽  
Author(s):  
L. J. Mandarino ◽  
A. Consoli ◽  
A. Jain ◽  
D. E. Kelley
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Basal Insulin ◽  
Glycogen Synthase ◽  
Pyruvate Dehydrogenase Complex ◽  
Dependent Diabetes Mellitus ◽  
Vastus Lateralis Muscle ◽  
The Impact ◽  
Insulin Replacement

The current study was undertaken to examine the impact that obesity and non-insulin-dependent diabetes mellitus (NIDDM) have on the ability of glucose to stimulate its own uptake and oxidation in muscle. Euglycemic and hyperglycemic clamp experiments were performed with somatostatin infusions so that insulin could be replaced to basal levels or to physiological hyperinsulinemia. Arteriovenous leg balance methods were used to measure the pathways of leg muscle glucose uptake, oxidation, and storage. Percutaneous biopsies of the vastus lateralis muscle were taken to determine the pyruvate dehydrogenase complex or glycogen synthase activities. During basal insulin replacement, obese compared with lean nondiabetic subjects had higher values for glucose uptake, respiratory quotient, and glucose oxidation (all P<0.05) and a higher proportion of leg energy expenditure derived from glucose. Obese NIDD patients had a greater reliance on fat calories than lean diabetics during basal insulin replacement (P< 0.05). Hyperinsulinemia increased leg glucose metabolism (P<0.001) in all groups, but obese NIDD patients were significantly more insulin resistant. Hyperglycemia in NIDDM compensated for insulin resistance to the extent that rates of glucose metabolism were the same as those for nondiabetics studied at euglycemia. When nondiabetics were studied at hyperglycemia matched to the diabetics, the insulin resistance was still readily apparent.

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