scholarly journals Overexpression of Adiponectin Receptor 1 Inhibits Brown and Beige Adipose Tissue Activity in Mice

2021 ◽  
Vol 22 (2) ◽  
pp. 906
Author(s):  
Yu-Jen Chen ◽  
Chiao-Wei Lin ◽  
Yu-Ju Peng ◽  
Chao-Wei Huang ◽  
Yi-Shan Chien ◽  
...  
Keyword(s):  
Body Temperature ◽  
Transgenic Mice ◽  
Glucose Uptake ◽  
Ct Scanning ◽  
Adipose Tissues ◽  
Mitochondrial Markers ◽  
Adiponectin Receptor 1 ◽  
Pet Ct ◽  
Cold Induction

Adult humans and mice possess significant classical brown adipose tissues (BAT) and, upon cold-induction, acquire brown-like adipocytes in certain depots of white adipose tissues (WAT), known as beige adipose tissues or WAT browning/beiging. Activating thermogenic classical BAT or WAT beiging to generate heat limits diet-induced obesity or type-2 diabetes in mice. Adiponectin is a beneficial adipokine resisting diabetes, and causing “healthy obese” by increasing WAT expansion to limit lipotoxicity in other metabolic tissues during high-fat feeding. However, the role of its receptors, especially adiponectin receptor 1 (AdipoR1), on cold-induced thermogenesis in vivo in BAT and in WAT beiging is still elusive. Here, we established a cold-induction procedure in transgenic mice over-expressing AdipoR1 and applied a live 3-D [18F] fluorodeoxyglucose-PET/CT (18F-FDG PET/CT) scanning to measure BAT activity by determining glucose uptake in cold-acclimated transgenic mice. Results showed that cold-acclimated mice over-expressing AdipoR1 had diminished cold-induced glucose uptake, enlarged adipocyte size in BAT and in browned WAT, and reduced surface BAT/body temperature in vivo. Furthermore, decreased gene expression, related to thermogenic Ucp1, BAT-specific markers, BAT-enriched mitochondrial markers, lipolysis and fatty acid oxidation, and increased expression of whitening genes in BAT or in browned subcutaneous inguinal WAT of AdipoR1 mice are congruent with results of PET/CT scanning and surface body temperature in vivo. Moreover, differentiated brown-like beige adipocytes isolated from pre-adipocytes in subcutaneous WAT of transgenic AdipoR1 mice also had similar effects of lowered expression of thermogenic Ucp1, BAT selective markers, and BAT mitochondrial markers. Therefore, this study combines in vitro and in vivo results with live 3-D scanning and reveals one of the many facets of the adiponectin receptors in regulating energy homeostasis, especially in the involvement of cold-induced thermogenesis.

Overexpression of hexokinase II increases insulinand exercise-stimulated muscle glucose uptake in vivo

1999 ◽  
Vol 276 (1) ◽  
pp. E70-E77 ◽  
Author(s):  
Amy E. Halseth ◽  
Deanna P. Bracy ◽  
David H. Wasserman
Keyword(s):  
Skeletal Muscle ◽  
Carotid Artery ◽  
Transgenic Mice ◽  
Glucose Uptake ◽  
Treadmill Exercise ◽  
Jugular Vein ◽  
Important Determinant ◽  
Hexokinase Ii

The hypothesis of this investigation was that glucose uptake would be increased in skeletal muscle of transgenic mice (TG) overexpressing hexokinase II (HK II) compared with their nontransgenic littermates (NTG) during euglycemic hyperinsulinemia and treadmill exercise. For insulin experiments, catheters were surgically implanted in the jugular vein and carotid artery for infusions and sampling, respectively. Conscious mice underwent experiments ∼5 days later in which 4 mU ⋅ kg−1 ⋅ min−1insulin and variable glucose ( n = 7 TG and n = 7 NTG) or saline ( n = 5 TG and n = 4 NTG) was infused for 140 min. Over the last 40 min of the experiments, 2-deoxy-[3H]glucose ([2-3H]DG) was infused, after which muscles were removed. For the exercise experiments, jugular vein catheters were surgically implanted. Five days later, mice received a bolus of [2-3H]DG and then remained sedentary ( n = 6 TG and n = 8 NTG) or ran on a motorized treadmill ( n = 12 TG and n = 8 NTG) for 30 min. TG and NTG had similar muscle [2-3H]DG 6-phosphate ([2-3H]DGP) accumulation in the basal state ( P > 0.05). In the hyperinsulinemic experiments, TG required ∼25% more glucose to maintain euglycemia ( P < 0.05), and muscle [2-3H]DGP accumulation normalized to infusate [2-3H]DG was similarly increased ( P < 0.05). In the exercise experiments, muscle [2-3H]DGP accumulation was significantly greater in TG than NTG ( P < 0.05). In conclusion, we did not detect an effect of HK II overexpression on muscle [2-3H]DGP accumulation under basal conditions. Hyperinsulinemia and exercise shift the control of muscle glucose uptake so that phosphorylation is a more important determinant of the rate of this process.

scholarly journals Bone marrow adipose tissue is a unique adipose subtype with distinct roles in systemic glucose homeostasis

2019 ◽  
Author(s):  
Karla J. Suchacki ◽  
Adriana A.S. Tavares ◽  
Domenico Mattiucci ◽  
Erica L. Scheller ◽  
Giorgos Papanastasiou ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Adipose Tissue ◽  
Glucose Uptake ◽  
Glucose Homeostasis ◽  
List Type ◽  
Bone Marrow Adipose Tissue ◽  
Marrow Adipose Tissue ◽  
Pet Ct ◽  
Basal Glucose Uptake

SUMMARYBone marrow adipose tissue (BMAT) represents >10% of total adipose mass, yet unlike white or brown adipose tissues (WAT or BAT), its role in systemic metabolism remains unclear. Using transcriptomics, we reveal that BMAT is molecularly distinct to WAT but is not enriched for brown or beige adipocyte markers. Instead, pathway analysis indicated altered glucose metabolism and decreased insulin responsiveness in BMAT. We therefore tested these functions in mice and humans using positron emission tomography–computed tomography (PET/CT) with 18F-fluorodeoxyglucose, including establishing a new method for BMAT identification from clinical CT scans. This revealed that BMAT resists insulin- and cold-stimulated glucose uptake and is thus functionally distinct to WAT and BAT. However, BMAT displayed greater basal glucose uptake than axial bones or subcutaneous WAT, underscoring its potential to influence systemic glucose homeostasis. These PET/CT studies are the first to characterise BMAT function in vivo and identify BMAT as a distinct, major subtype of adipose tissue.HIGHLIGHTSBone marrow adipose tissue (BMAT) is molecularly distinct to other adipose subtypes.BMAT is less insulin responsive than WAT and, unlike BAT, is not cold-responsive.Human BMAT has greater basal glucose uptake than axial bone or subcutaneous WAT.We establish a PET/CT method for BMAT localisation and functional analysis in vivo.

Effects of chronic Akt activation on glucose uptake in the heart

2006 ◽  
Vol 290 (5) ◽  
pp. E789-E797 ◽  
Author(s):  
Takashi Matsui ◽  
Tomohisa Nagoshi ◽  
Eun-Gyoung Hong ◽  
Ivan Luptak ◽  
Kirsten Hartil ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Glucose Uptake ◽  
Ex Vivo ◽  
Fold Increase ◽  
Histochemical Staining ◽  
Perfused Heart ◽  
Akt Activation ◽  
Glycogen Deposition ◽  
Basal Glucose Uptake

Acute activation of the serine-threonine kinase Akt is cardioprotective and increases glucose uptake, at least in part, through enhanced expression of GLUT4 on the sarcolemma. The effects of chronic Akt activation on glucose uptake in the heart remain unclear. To address this issue, we examined the effects of chronic Akt activation on glucose uptake, glycogen storage, and relevant glucose transporters in the hearts of transgenic mice. We found that chronic cardiac activation of Akt led to a substantial increase in the rate of basal glucose uptake ( P < 0.05) but blunted the response to insulin (1.9 vs. 18.1-fold increase compared with baseline) using NMR in ex vivo perfused heart. Basal glucose uptake was also increased in Akt transgenic mice in vivo ( P < 0.005). These changes were associated with an increase on glycogen deposition, examined with histochemical staining, biochemical (>6-fold, P < 0.001) and in vivo radioactive (5-fold, P < 0.01) assays. Studies in chimeric hearts of female X-linked transgenic Akt mice suggested that increased glycogen deposition occurred as a cell autonomous effect of transgene expression. Interestingly, although sarcolemmal GLUT1 was not significantly altered, chronic Akt activation actually decreased plasma membrane GLUT4. Moreover, intracellular pools of GLUT1 were modestly reduced, whereas intracellular GLUT4 was substantially reduced. It seems likely that neither GLUT1 nor GLUT4 explains the increase in basal glucose uptake but that these reductions contribute to the loss of insulin responsiveness that we observed. These data demonstrate that chronic Akt activation increases basal glucose uptake and glycogen deposition while inhibiting the response to insulin.

Insulin stimulation of glucose uptake in skeletal muscles and adipose tissues in vivo is NO dependent

1998 ◽  
Vol 274 (4) ◽  
pp. E692-E699 ◽  
Author(s):  
Denis Roy ◽  
Mylène Perreault ◽  
André Marette
Keyword(s):  
Glucose Uptake ◽  
Skeletal Muscles ◽  
Whole Body ◽  
Glucose Disposal ◽  
Adipose Tissues ◽  
Peripheral Tissues ◽  
Nos Inhibitor ◽  
Oxide Synthase

The purpose of this study was to investigate whether in vivo nitric oxide synthase (NOS) inhibition influences insulin-mediated glucose disposal in rat peripheral tissues. The NOS inhibitor N G-nitro-l-arginine methyl ester (l-NAME) or saline was infused constantly during a hyperinsulinemic-euglycemic clamp in normal rats. Glucose utilization rates of insulin-sensitive tissues (individual muscles, heart, and adipose tissues) were simultaneously determined using tracer infusion of 2-deoxy-d-[3H]glucose (2-[3H]DG). NOS blockade with l-NAME resulted in significant ( P < 0.05) reduction in both whole body glucose disposal (−16%, P < 0.01) and plasma 2-[3H]DG disappearance rate (−30%, P < 0.05) during hyperinsulinemic-euglycemic clamp.l-NAME significantly decreased insulin-stimulated glucose uptake in heart (−62%, P = 0.01), soleus (−42%, P = 0.05), red (−53%, P < 0.001) and white (−62%, P < 0.001) gastrocnemius, tibialis (−57%, P < 0.01), and quadriceps (−33%, P < 0.05) muscles. The NOS inhibitor also decreased insulin action in brown interscapular (−47%, P < 0.01), retroperitoneal (−52%, P = 0.07), and gonadal (−66%, P = 0.06) adipose tissues. In contrast to in vivo NOS blockade,l-NAME failed to affect basal or insulin-stimulated 2-[3H]DG transport in isolated soleus or extensor digitorum longus muscles in vitro. These results support the hypothesis that the action of insulin to augment glucose uptake by skeletal muscles and other peripheral insulin-sensitive tissues in vivo is NO dependent.

In-vivo-Detektion des Betastrahlers Yttrium-90 im PET/CT nach Selektiver Interner Radiotherapie (SIRT) der Leber

2011 ◽  
Vol 183 (S 01) ◽  
Author(s):  
MK Werner ◽  
J Kupferschläger ◽  
K Brechtel ◽  
T Beyer ◽  
R Bares ◽  
...  
Keyword(s):  
Pet Ct ◽  
Yttrium 90

Visual and quantitative approach to bone marrow foci of increased glucose uptake on PET/CT in a case of aplastic anaemia

2010 ◽  
Vol 49 (02) ◽  
pp. N10-N12 ◽  
Author(s):  
F. Cicone ◽  
M. Stalder ◽  
D. Geiger ◽  
A. Cairoli ◽  
A. Bischof Delaloye ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Glucose Uptake ◽  
Aplastic Anaemia ◽  
Quantitative Approach ◽  
Pet Ct

Von Hippel-Lindau syndrome: in vivo portrait with 68Ga-DOTANOC PET-CT

2017 ◽  
Author(s):  
Moreira Ana Paula ◽  
Gracinda Costa ◽  
de Lima Joao Pedroso
Keyword(s):  
Von Hippel Lindau ◽  
Pet Ct ◽  
Von Hippel Lindau Syndrome

Regulation of glucose uptake and metabolism by working muscle. An in vivo analysis

Diabetes ◽  
1993 ◽  
Vol 42 (7) ◽  
pp. 956-965 ◽  
Author(s):  
B. A. Zinker ◽  
D. B. Lacy ◽  
D. Bracy ◽  
J. Jacobs ◽  
D. H. Wasserman
Keyword(s):  
Glucose Uptake ◽  
In Vivo Analysis ◽  
Uptake And Metabolism
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