AI Article Synopsis
- - The study investigates the common assumption that brown adipose tissue (BAT) activity in humans can be accurately measured through glucose uptake observed via PET scanning using [F]FDG, which is the only method currently available for quantifying BAT activity.
- - Researchers conducted experiments on wildtype and genetically modified UCP1(-/-) mice to determine if glucose uptake was related to thermogenic activity, discovering that adrenergically induced glucose uptake can occur independently of UCP1 function.
- - The findings suggest that PET-FDG scanning does not exclusively indicate active BAT but rather any tissue that can uptake glucose through adrenergic pathways, highlighting the importance of UCP1 in sustaining BAT's anti-diabetic effects during prolonged β-adr
Article Abstract
Objective: Today, the presence and activity of brown adipose tissue (BAT) in adult humans is generally equated with the induced accumulation of [2-F]2-fluoro-2-deoxy-d-glucose ([F]FDG) in adipose tissues, as investigated by positron emission tomography (PET) scanning. In reality, PET-FDG is currently the only method available for quantification of BAT activity in adult humans. The underlying assumption is that the glucose uptake reflects the thermogenic activity of the tissue.
Methods: To examine this basic assumption, we here followed [F]FDG uptake by PET and by tissue [H]-2-deoxy-d-glucose uptake in wildtype and UCP1(-/-) mice, i.e. in mice that do or do not possess the unique thermogenic and calorie-consuming ability of BAT.
Results: Unexpectedly, we found that β-adrenergically induced (by CL-316,243) glucose uptake was UCP1-independent. Thus, whereas PET-FDG scans adequately reflect glucose uptake, this acute glucose uptake is not secondary to thermogenesis but is governed by an independent cellular signalling, here demonstrated to be mediated via the previously described KU-0063794-sensitive mTOR pathway.
Conclusions: Thus, PET-FDG scans do not exclusively reveal active BAT deposits but rather any tissue possessing an adrenergically-mediated glucose uptake pathway. In contrast, we found that the marked glucose uptake-ameliorating effect of prolonged β-adrenergic treatment was UCP1 dependent. Thus, therapeutically, UCP1 activity is required for any anti-diabetic effect of BAT activation.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5444022 | PMC |
| http://dx.doi.org/10.1016/j.molmet.2017.02.006 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Aerobic exercise timing affects mitochondrial dynamics and insulin resistance by regulating the circadian clock protein expression and NAD-SIRT1-PPARα-MFN2 pathway in the skeletal muscle of high-fat-diet-induced diabetes mice.
J Physiol Biochem
December 2024
Department of Exercise Physiology, Faculty of Sport Sciences, Shahid Rajaee Teacher Training University, Tehran, Iran.
The circadian clock regulates mitochondrial function and affects time-dependent metabolic responses to exercise. The present study aimed to determine the effects of aerobic exercise timing at the light-dark phase on the proteins expression of the circadian clock, mitochondrial dynamics, and, NAD-SIRT1-PPARα axis in skeletal muscle of high-fat diet-induced diabetic mice. In this experimental study, thirty male mice were randomly assigned into two groups based on time: the early light phase, ZT3, and the early dark phase, ZT15, and three groups at each time: (1) Healthy Control (HC), (2) Diabetic Control (DC), and (3) Diabetic + Exercise (DE).
View Article and Find Full Text PDFTreatment of occult radiculopathy in complex regional pain syndrome by anterior cervical discectomy and fusion following localization by [18F]fluorodeoxyglucose radioligand and PET/MRI: illustrative case.
J Neurosurg Case Lessons
December 2024
Neurosurgery Artificial Intelligence Lab, Stanford University School of Medicine, Stanford, California.
Background: The inability to localize pain generators often results in failed back surgery syndrome (FBSS). Structural imaging can identify multiple and/or noncausative abnormalities. Molecular imaging of glucose transporters offers the opportunity to localize metabolically active sites.
View Article and Find Full Text PDFTotal-body positron emission tomography: a tool for systemic, quantitative evaluation of the inflammatory burden of psoriatic arthritis.
Rheumatology (Oxford)
December 2024
Department of Radiology, University of California Davis, Sacramento, CA, USA.
Objectives: To test the hypothesis that recently-developed total body-positron emission tomography (TB-PET) imaging with integrated computed tomography (CT) will enable low-dose, quantitative, domain-specific evaluation of the total inflammatory burden of psoriatic arthritis (PsA), and associate with established outcome measures of the clinical domains of PsA.
Methods: Seventy-one adult participants (40 with PsA, 16 with rheumatoid arthritis (RA), and 15 with osteoarthritis (OA)) underwent 20-min TB-PET/CT scans using [18F]FDG, a glucose analogue radiotracer. [18F]FDG uptake was assessed qualitatively and quantitatively.
Immunometabolic reprogramming in macrophages infected with active and dormant : differential modulation of respiration, glycolysis, and fatty acid utilization.
Infect Immun
December 2024
Laboratory of Applied Immunology, Institute of Biology Sciences, University of Brasília, Brasília, Brazil.
Dormancy is an adaptation in which cells reduce their metabolism, transcription, and translation to stay alive under stressful conditions, preserving the capacity to reactivate once the environment reverts to favorable conditions. Dormancy and reactivation of () are closely linked to intracellular residency within macrophages. Our previous work showed that murine macrophages rely on the viable but not cultivable (VBNC-a dormancy phenotype) fungus from active , with striking differences in immunometabolic gene expression.
View Article and Find Full Text PDFOne hallmark of cancer is the upregulation and dependency on glucose metabolism to fuel macromolecule biosynthesis and rapid proliferation. Despite significant pre-clinical effort to exploit this pathway, additional mechanistic insights are necessary to prioritize the diversity of metabolic adaptations upon acute loss of glucose metabolism. Here, we investigated a potent small molecule inhibitor to Class I glucose transporters, KL-11743, using glycolytic leukemia cell lines and patient-based model systems.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!