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Velikyan, I. & Eriksson, O. (2020). Advances in GLP-1 receptor targeting radiolabeled agent development and prospective of theranostics. Theranostics, 10(1), 437-461
Öppna denna publikation i ny flik eller fönster >>Advances in GLP-1 receptor targeting radiolabeled agent development and prospective of theranostics
2020 (Engelska)Ingår i: Theranostics, ISSN 1838-7640, E-ISSN 1838-7640, Vol. 10, nr 1, s. 437-461Artikel, forskningsöversikt (Refereegranskat) Published
Abstract [en]

In the light of theranostics/radiotheranostics and prospective of personalized medicine in diabetes and oncology, this review presents prior and current advances in the development of radiolabeled imaging and radiotherapeutic exendin-based agents targeting glucagon-like peptide-1 receptor. The review covers chemistry, preclinical, and clinical evaluation. Such critical aspects as structure-activity-relationship, stability, physiological potency, kidney uptake, and dosimetry are discussed.

Nyckelord
Exendin-4, insulinoma, GLP-1, diabetes, PET, SPECT
Nationell ämneskategori
Cancer och onkologi Radiologi och bildbehandling
Identifikatorer
urn:nbn:se:uu:diva-398791 (URN)10.7150/thno.38366 (DOI)000497314800030 ()
Tillgänglig från: 2019-12-11 Skapad: 2019-12-11 Senast uppdaterad: 2019-12-11Bibliografiskt granskad
Eriksson, O., Velikyan, I., Haack, T., Bossart, M., Evers, A., Laitinen, I., . . . Wagner, M. (2019). Assessment of glucagon receptor occupancy by Positron Emission Tomography in non-human primates. Scientific Reports, 9, Article ID 14960.
Öppna denna publikation i ny flik eller fönster >>Assessment of glucagon receptor occupancy by Positron Emission Tomography in non-human primates
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2019 (Engelska)Ingår i: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 9, artikel-id 14960Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

The glucagon receptor (GCGR) is an emerging target in anti-diabetic therapy. Reliable biomarkers for in vivo activity on the GCGR, in the setting of dual glucagon-like peptide 1/glucagon (GLP-1/GCG) receptor agonism, are currently unavailable. Here, we investigated [Ga-68]Ga-DO3A-S01-GCG as a biomarker for GCGR occupancy in liver, the tissue with highest GCGR expression, in non-human primates (NHP) by PET. [Ga-68]Ga-DO3A-S01-GCG was evaluated by dynamic PET in NHPs by a dose escalation study design, where up to 67 mu g/kg DO3A-S01-GCG peptide mass was co-injected. The test-retest reproducibility of [Ga-68]Ga-DO3A-S01-GCG binding in liver was evaluated. Furthermore, we investigated the effect of pre-treatment with acylated glucagon agonist 1-GCG on [Ga-68]GaDO3A-S01-GCG binding in liver. [Ga-68]Ga-DO3A-S01-GCG bound to liver in vivo in a dose-dependent manner. Negligible peptide mass effect was observed for DO3A-S01-GCG doses <0.2 mu g/kg. In vivo K-d for [Ga-68]Ga-DO3A-S01-GCG corresponded to 0.7 mu g/kg, which indicates high potency. The test-retest reproducibility for [Ga-68]Ga-DO3A-S01-GCG binding in liver was 5.7 +/- 7.9%. Pre-treatment with 1-GCG, an acylated glucagon agonist, resulted in a GCGR occupancy of 61.5 +/- 9.1% in liver. Predicted human radiation dosimetry would allow for repeated annual [Ga-68]Ga-DO3A-S01-GCG PET examinations. In summary, PET radioligand [Ga-68]Ga-DO3A-S01-GCG is a quantitative biomarker of in vivo GCGR occupancy.

Ort, förlag, år, upplaga, sidor
Nature Publishing Group, 2019
Nationell ämneskategori
Radiologi och bildbehandling
Identifikatorer
urn:nbn:se:uu:diva-399094 (URN)10.1038/s41598-019-51530-0 (DOI)000490988200019 ()31628379 (PubMedID)
Tillgänglig från: 2019-12-16 Skapad: 2019-12-16 Senast uppdaterad: 2019-12-16Bibliografiskt granskad
Velikyan, I., Haack, T., Bossart, M., Evers, A., Laitinen, I., Larsen, P., . . . Eriksson, O. (2019). First-in-class positron emission tomography tracer for the glucagon receptor. EJNMMI Research, 9, Article ID 17.
Öppna denna publikation i ny flik eller fönster >>First-in-class positron emission tomography tracer for the glucagon receptor
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2019 (Engelska)Ingår i: EJNMMI Research, ISSN 2191-219X, E-ISSN 2191-219X, Vol. 9, artikel-id 17Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

The glucagon receptor (GCGR) is emerging as an important target in anti-diabetic therapy, especially as part of the pharmacology of dual glucagon-like peptide-1/glucagon (GLP-1/GCG) receptor agonists. However, currently, there are no suitable biomarkers that reliably demonstrate GCG receptor target engagement.

Methods: Two potent GCG receptor peptide agonists, S01-GCG and S02-GCG, were labeled with positron emission tomography (PET) radionuclide gallium-68. The GCG receptor binding affinity and specificity of the resulting radiopharmaceuticals [68Ga]Ga-DO3A-S01-GCG and [68Ga]Ga-DO3A-S02-GCG were evaluated in HEK-293 cells overexpressing the human GCG receptor and on frozen hepatic sections from human, non-human primate, and rat. In in vivo biodistribution, binding specificity and dosimetry were assessed in rat.

Results: [68Ga]Ga-DO3A-S01-GCG in particular demonstrated GCG receptor-mediated binding in cells and liver tissue with affinity in the nanomolar range required for imaging. [68Ga]Ga-DO3A-S01-GCG binding was not blocked by co-incubation of a GLP-1 agonist. In vivo binding in rat liver was GCG receptor specific with low non-specific binding throughout the body. Moreover, the extrapolated human effective doses, predicted from rat biodistribution data, allow for repeated PET imaging potentially also in combination with GLP-1R radiopharmaceuticals.

Conclusion: [68Ga]Ga-DO3A-S01-GCG thus constitutes a first-in-class PET tracer targeting the GCG receptor, with suitable properties for clinical development. This tool has potential to provide direct quantitative evidence of GCG receptor occupancy in humans.

Nyckelord
Glucagon, GCG, GLP-1 receptor, Dual agonist, Type 2 diabetes
Nationell ämneskategori
Radiologi och bildbehandling
Identifikatorer
urn:nbn:se:uu:diva-378994 (URN)10.1186/s13550-019-0482-0 (DOI)000459043900002 ()30771019 (PubMedID)
Tillgänglig från: 2019-03-19 Skapad: 2019-03-19 Senast uppdaterad: 2019-03-19Bibliografiskt granskad
Eriksson, O. (2019). GPR44 as a Target for Imaging Pancreatic Beta-Cell Mass. Current Diabetes Reports, 19(8), Article ID 49.
Öppna denna publikation i ny flik eller fönster >>GPR44 as a Target for Imaging Pancreatic Beta-Cell Mass
2019 (Engelska)Ingår i: Current Diabetes Reports, ISSN 1534-4827, E-ISSN 1539-0829, Vol. 19, nr 8, artikel-id 49Artikel, forskningsöversikt (Refereegranskat) Published
Abstract [en]

Purpose of Review Quantitative markers for beta-cell mass (BCM) in human pancreas are currently lacking. Medical imaging using positron emission tomography (PET) markers for beta-cell restricted targets may provide an accurate and non-invasive measurement of BCM, to assist diagnosis and treatment of metabolic disease. GPR44 was recently discovered as a putative marker for beta cells and this review summarizes the developments so far. Recent Findings Several small molecule binders targeting GPR44 have been radiolabeled for PET imaging and evaluated in vitro and in small and large animal models. C-11-AZ12204657 and C-11-MK-7246 displayed a dose-dependent and GPR44-mediated binding to beta cells both in vitro and in vivo, with negligible uptake in exocrine pancreas. Summary GPR44 represents an attractive target for visualization of BCM. Further progress in radioligand development including clinical testing is expected to clarify the role of GPR44 as a surrogate marker for BCM in humans.

Ort, förlag, år, upplaga, sidor
Springer, 2019
Nyckelord
Beta-cell imaging, Islet imaging, Beta-cell mass, GPR44, PET, Diabetes
Nationell ämneskategori
Endokrinologi och diabetes
Identifikatorer
urn:nbn:se:uu:diva-390420 (URN)10.1007/s11892-019-1164-z (DOI)000473164900004 ()31250117 (PubMedID)
Tillgänglig från: 2019-08-12 Skapad: 2019-08-12 Senast uppdaterad: 2019-08-12Bibliografiskt granskad
Elksnis, A., Martinell, M., Eriksson, O. & Espes, D. (2019). Heterogeneity of Metabolic Defects in Type 2 Diabetes and Its Relation to Reactive Oxygen Species and Alterations in Beta-Cell Mass. Frontiers in Physiology, 10, Article ID 107.
Öppna denna publikation i ny flik eller fönster >>Heterogeneity of Metabolic Defects in Type 2 Diabetes and Its Relation to Reactive Oxygen Species and Alterations in Beta-Cell Mass
2019 (Engelska)Ingår i: Frontiers in Physiology, ISSN 1664-042X, E-ISSN 1664-042X, Vol. 10, artikel-id 107Artikel, forskningsöversikt (Refereegranskat) Published
Abstract [en]

Type 2 diabetes (T2D) is a complex and heterogeneous disease which affects millions of people worldwide. The classification of diabetes is at an interesting turning point and there have been several recent reports on sub-classification of T2D based on phenotypical and metabolic characteristics. An important, and perhaps so far underestimated, factor in the pathophysiology of T2D is the role of oxidative stress and reactive oxygen species (ROS). There are multiple pathways for excessive ROS formation in T2D and in addition, beta-cells have an inherent deficit in the capacity to cope with oxidative stress. ROS formation could be causal, but also contribute to a large number of the metabolic defects in T2D, including beta-cell dysfunction and loss. Currently, our knowledge on beta-cell mass is limited to autopsy studies and based on comparisons with healthy controls. The combined evidence suggests that beta-cell mass is unaltered at onset of T2D but that it declines progressively. In order to better understand the pathophysiology of T2D, to identify and evaluate novel treatments, there is a need for in vivo techniques able to quantify beta-cell mass. Positron emission tomography holds great potential for this purpose and can in addition map metabolic defects, including ROS activity, in specific tissue compartments. In this review, we highlight the different phenotypical features of T2D and how metabolic defects impact oxidative stress and ROS formation. In addition, we review the literature on alterations of beta-cell mass in T2D and discuss potential techniques to assess beta-cell mass and metabolic defects in vivo.

Ort, förlag, år, upplaga, sidor
Frontiers Media S.A., 2019
Nyckelord
type 2 diabetes, diabetes classification, oxygen stress, reactive oxygen species, beta-cell, beta-cell mass, imaging, positron emission tomography
Nationell ämneskategori
Biokemi och molekylärbiologi
Identifikatorer
urn:nbn:se:uu:diva-378233 (URN)10.3389/fphys.2019.00107 (DOI)000458732800001 ()
Forskningsfinansiär
BarndiabetesfondenSvenska Sällskapet för Medicinsk Forskning (SSMF)Science for Life Laboratory - a national resource center for high-throughput molecular bioscienceStiftelsen familjen Ernfors fondDiabetesförbundetGöran Gustafssons Stiftelse för främjande av vetenskaplig forskning vid Uppsala universitet och Kungl tekniska högskolan (UU/KTH)
Tillgänglig från: 2019-03-15 Skapad: 2019-03-15 Senast uppdaterad: 2019-03-15Bibliografiskt granskad
Eriksson, O., Selvaraju, R., Berglund, M. & Espes, D. (2019). Metabolically Active Brown Adipose Tissue Is Found in Adult Subjects with Type 1 Diabetes.. International Journal of Molecular Sciences, 20(23), Article ID E5827.
Öppna denna publikation i ny flik eller fönster >>Metabolically Active Brown Adipose Tissue Is Found in Adult Subjects with Type 1 Diabetes.
2019 (Engelska)Ingår i: International Journal of Molecular Sciences, ISSN 1422-0067, E-ISSN 1422-0067, Vol. 20, nr 23, artikel-id E5827Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Type 1 diabetes (T1D) is characterized by the loss of insulin-producing cells and hence insulin secretion and metabolic control. In addition to insulin, there are a number of hormones and cytokines that influence metabolism, and many of these can be secreted from brown adipose tissue (BAT). However, the presence and activity of BAT in T1D have not been studied, despite the fact that preclinical studies have shown that transplantation of BAT in mouse models of T1D can restore metabolic control. The metabolic activity of BAT, white adipose tissue (WAT), and skeletal muscle was investigated in patients with T1D (n = 11) by 2-deoxy-2-(18F)fluoro-D-glucose PET/CT after cold stimulation. Functional BAT was detected in 4 out of 11 individuals with T1D with a prevalence of 36%. The glucose utilization rate in the supraclavicular BAT regions ranged from 0.75-38.7 µmol × min-1 × 100 g-1. The glucose utilization per gram tissue was higher in BAT when compared with both WAT (p = 0.049) and skeletal muscle (p = 0.039). However, no correlation between BAT activity and metabolic control or insulin requirements was found. In conclusion, for the first time, cold-induced BAT was detected in patients with T1D with a wide range in metabolic activity. Contrary to findings in animal models, the metabolic activity of BAT had negligible impact on insulin requirements or metabolic control in T1D under normal physiological conditions.

Nyckelord
brown adipose tissue, metabolic control, positron emission tomography, type 1 diabetes
Nationell ämneskategori
Endokrinologi och diabetes
Identifikatorer
urn:nbn:se:uu:diva-399124 (URN)10.3390/ijms20235827 (DOI)000504428300009 ()31757005 (PubMedID)
Forskningsfinansiär
Magnus Bergvalls StiftelseFredrik och Ingrid Thurings StiftelseScience for Life Laboratory - a national resource center for high-throughput molecular bioscienceEXODIAB - Excellence of Diabetes Research in Sweden
Tillgänglig från: 2019-12-12 Skapad: 2019-12-12 Senast uppdaterad: 2020-01-22Bibliografiskt granskad
Espes, D., Manell, E., Rydén, A., Carlbom, L., Weis, J., Jensen-Waern, M., . . . Eriksson, O. (2019). Pancreatic perfusion and its response to glucose as measured by simultaneous PET/MRI. Acta Diabetologica, 56(10), 1113-1120
Öppna denna publikation i ny flik eller fönster >>Pancreatic perfusion and its response to glucose as measured by simultaneous PET/MRI
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2019 (Engelska)Ingår i: Acta Diabetologica, ISSN 0940-5429, E-ISSN 1432-5233, Vol. 56, nr 10, s. 1113-1120Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

AIMS: Perfusion of the pancreas and the islets of Langerhans is sensitive to physiological stimuli and is dysregulated in metabolic disease. Pancreatic perfusion can be assessed by both positron emission tomography (PET) and magnetic resonance imaging (MRI), but the methods have not been directly compared or benchmarked against the gold-standard microsphere technique.

METHODS: Pigs (n = 4) were examined by [15O]H2O PET and intravoxel incoherent motion (IVIM) MRI technique simultaneously using a hybrid PET/MRI scanner. The pancreatic perfusion was measured both at basal conditions and after intravenous (IV) administration of up to 0.5 g/kg glucose.

RESULTS: Pancreatic perfusion increased by 35%, 157%, and 29% after IV 0.5 g/kg glucose compared to during basal conditions, as assessed by [15O]H2O PET, IVIM MRI, and microspheres, respectively. There was a correlation between pancreatic perfusion as assessed by [15O]H2O PET and IVIM MRI (r = 0.81, R2 = 0.65, p < 0.01). The absolute quantification of pancreatic perfusion (ml/min/g) by [15O]H2O PET was within a 15% error of margin of the microsphere technique.

CONCLUSION: Pancreatic perfusion by [15O]H2O PET was in agreement with the microsphere technique assessment. The IVIM MRI method has the potential to replace [15O]H2O PET if the pancreatic perfusion is sufficiently large, but not when absolute quantitation is required.

Ort, förlag, år, upplaga, sidor
Springer, 2019
Nyckelord
Diabetes, Hybrid scanner, PET/MRI scanner, Pancreas perfusion
Nationell ämneskategori
Endokrinologi och diabetes Radiologi och bildbehandling
Identifikatorer
urn:nbn:se:uu:diva-383433 (URN)10.1007/s00592-019-01353-2 (DOI)000486160600003 ()31028528 (PubMedID)
Forskningsfinansiär
Stiftelsen familjen Ernfors fondGöran Gustafssons Stiftelse för främjande av vetenskaplig forskning vid Uppsala universitet och Kungl tekniska högskolan (UU/KTH)DiabetesförbundetBarndiabetesfondenEXODIAB - Excellence of Diabetes Research in SwedenScience for Life Laboratory - a national resource center for high-throughput molecular bioscience
Tillgänglig från: 2019-05-14 Skapad: 2019-05-14 Senast uppdaterad: 2019-10-31Bibliografiskt granskad
Eriksson, J., Roy, T., Sawadjoon, S., Bachmann, K., Sköld, C., Larhed, M., . . . Odell, L. R. (2019). Synthesis and preclinical evaluation of the CRTH2 antagonist [11C]MK-7246 as a novel PET tracer and potential surrogate marker for pancreatic beta-cell mass. Nuclear Medicine and Biology, 71, 1-10
Öppna denna publikation i ny flik eller fönster >>Synthesis and preclinical evaluation of the CRTH2 antagonist [11C]MK-7246 as a novel PET tracer and potential surrogate marker for pancreatic beta-cell mass
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2019 (Engelska)Ingår i: Nuclear Medicine and Biology, ISSN 0969-8051, E-ISSN 1872-9614, Vol. 71, s. 1-10Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Introduction: MK-7246 is a potent and selective antagonist for chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2). Within the pancreas CRTH2 is selectively expressed in pancreatic β-cells where it is believed to play a role in insulin release. Reduction in β-cell mass and insufficient insulin secretion in response to elevated blood glucose levels is a hallmark for type 1 and type 2 diabetes. Reported here is the synthesis of [11C]MK-7246 and initial preclinical evaluation towards CRTH2 imaging. The aim is to develop a method to quantify β-cell mass with PET and facilitate non-invasive studies of disease progression in individuals with type 2 diabetes.

Methods: The precursor N-desmethyl-O-methyl MK-7246 was synthesized in seven steps and subjected to methylation with [11C]methyl iodide followed by hydrolysis to obtain [11C]MK-7246 labelled in the N-methyl position. Preclinical evaluation included in vitro radiography and immune-staining performed in human pancreatic biopsies. Biodistribution studies were performed in rat by PET-MRI and in pig by PET-CT imaging. The specific tracer uptake was examined in pig by scanning before and after administration of MK-7246 (1 mg/kg). Predicted dosimetry of [11C]MK-7246 in human males was estimated based on the biodistribution in rat.

Results: [11C]MK-7246 was obtained with activities sufficient for the current investigations (270±120 MBq) and a radiochemical purity of 93±2%. The tracer displayed focal binding in areas with insulin positive islet of Langerhans in human pancreas sections. Baseline uptake in pig was significantly reduced in CRTH2-rich areas after administration of MK-7246; pancreas (66% reduction) and spleen (88% reduction). [11C]MK-7246 exhibited a safe human predicted dosimetry profile as extrapolated from the rat biodistribution data.

Conclusions: Initial preclinical in vitro and in vivo evaluation of [11C]MK-7246 show binding and biodistribution properties suitable for PET imaging of CRTH2. Further studies are warranted to assess its potential in β-cell mass imaging and CRTH2 drug development.

Nationell ämneskategori
Organisk kemi Läkemedelskemi
Identifikatorer
urn:nbn:se:uu:diva-381559 (URN)10.1016/j.nucmedbio.2019.04.002 (DOI)000475837000001 ()
Forskningsfinansiär
Vetenskapsrådet, 2018-05133Knut och Alice Wallenbergs StiftelseBarndiabetesfondenGöran Gustafssons stiftelse för naturvetenskaplig och medicinsk forskning (KVA)
Tillgänglig från: 2019-04-11 Skapad: 2019-04-11 Senast uppdaterad: 2019-09-13Bibliografiskt granskad
Kang, N.-Y., Soetedjo, A. A., Amirruddin, N. S., Chang, Y.-T., Eriksson, O. & Teo, A. K. (2019). Tools for Bioimaging Pancreatic beta Cells in Diabetes. Trends in Molecular Medicine, 25(8), 708-722
Öppna denna publikation i ny flik eller fönster >>Tools for Bioimaging Pancreatic beta Cells in Diabetes
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2019 (Engelska)Ingår i: Trends in Molecular Medicine, ISSN 1471-4914, E-ISSN 1471-499X, Vol. 25, nr 8, s. 708-722Artikel, forskningsöversikt (Refereegranskat) Published
Abstract [en]

When diabetes is diagnosed, the majority of insulin-secreting pancreatic beta cells are already dysfunctional or destroyed. This beta cell dysfunction/destruction usually takes place over many years, making timely detection and clinical intervention difficult. For this reason, there is immense interest in developing tools to bioimage beta cell mass and/or function noninvasively to facilitate early diagnosis of diabetes as well as to assist the development of novel antidiabetic therapies. Recent years have brought significant progress in beta cell imaging that is now inching towards clinical applicability. We explore here the need to bioimage human beta cells noninvasively in various types of diabetes, and we discuss current and emerging tools for bioimaging beta cells. Further developments in this field are expected to facilitate beta cell imaging in diabetes.

Ort, förlag, år, upplaga, sidor
Elsevier, 2019
Nationell ämneskategori
Endokrinologi och diabetes
Identifikatorer
urn:nbn:se:uu:diva-391427 (URN)10.1016/j.molmed.2019.05.004 (DOI)000477707700007 ()31178230 (PubMedID)
Forskningsfinansiär
Science for Life Laboratory - a national resource center for high-throughput molecular bioscience
Tillgänglig från: 2019-10-03 Skapad: 2019-10-03 Senast uppdaterad: 2019-10-03Bibliografiskt granskad
Lahesmaa, M., Eriksson, O., Gnad, T., Oikonen, V., Bucci, M., Hirvonen, J., . . . Nuutila, P. (2018). Cannabinoid Type 1 Receptors Are Upregulated During Acute Activation of Brown Adipose Tissue. Diabetes, 67(7), 1226-1236
Öppna denna publikation i ny flik eller fönster >>Cannabinoid Type 1 Receptors Are Upregulated During Acute Activation of Brown Adipose Tissue
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2018 (Engelska)Ingår i: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 67, nr 7, s. 1226-1236Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Activating brown adipose tissue (BAT) could provide a potential approach for the treatment of obesity and metabolic disease in humans. Obesity is associated with upregulation of the endocannabinoid system, and blocking the cannabinoid type 1 receptor (CB1R) has been shown to cause weight loss and to decrease cardiometabolic risk factors. These effects may be mediated partly via increased BAT metabolism, since there is evidence that CB1R antagonism activates BAT in rodents. To investigate the significance of CB1R in BAT function, we quantified the density of CB1R in human and rodent BAT using the positron emission tomography radioligand [F-18]FMPEP-d(2) and measured BAT activation in parallel with the glucose analog [F-18]fluorodeoxyglucose. Activation by cold exposure markedly increased CB1R density and glucose uptake in the BAT of lean men. Similarly, 3-receptor agonism increased CB1R density in the BAT of rats. In contrast, overweight men with reduced BAT activity exhibited decreased CB1R in BAT, reflecting impaired endocannabinoid regulation. Image-guided biopsies confirmed CB1R mRNA expression in human BAT. Furthermore, CB1R blockade increased glucose uptake and lipolysis of brown adipocytes. Our results highlight that CB1Rs are significant for human BAT activity, and the CB1Rs provide a novel therapeutic target for BAT activation in humans.

Ort, förlag, år, upplaga, sidor
AMER DIABETES ASSOC, 2018
Nationell ämneskategori
Endokrinologi och diabetes
Identifikatorer
urn:nbn:se:uu:diva-358271 (URN)10.2337/db17-1366 (DOI)000435927000003 ()29650773 (PubMedID)
Forskningsfinansiär
EU, FP7, Sjunde ramprogrammet, 278373Deutsche Forschungsgemeinschaft (DFG), GN 108/1-1Deutsche Forschungsgemeinschaft (DFG), RTG 1873
Tillgänglig från: 2018-08-29 Skapad: 2018-08-29 Senast uppdaterad: 2018-08-29Bibliografiskt granskad
Organisationer
Identifikatorer
ORCID-id: ORCID iD iconorcid.org/0000-0002-2515-8790

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