scholarly journals High doses of catecholamines activate glucose transport in human adipocytes independently from adrenoceptor stimulation or vanadium addition

2022 ◽  
Vol 13 (1) ◽  
pp. 37-53
Author(s):  
Christian Carpéné ◽  
Nathalie Boulet ◽  
Jean-Louis Grolleau ◽  
Nathalie Morin
Diabetes ◽  
1989 ◽  
Vol 38 (10) ◽  
pp. 1217-1225 ◽  
Author(s):  
M. K. Sinha ◽  
C. Buchanan ◽  
N. Leggett ◽  
L. Martin ◽  
P. G. Khazanie ◽  
...  

1995 ◽  
Vol 144 (2) ◽  
pp. 147-151 ◽  
Author(s):  
Lesley Heseltine ◽  
Judith M. Webster ◽  
Roy Taylor

Molecules ◽  
2021 ◽  
Vol 26 (13) ◽  
pp. 3831
Author(s):  
Wiem Haj Ahmed ◽  
Nathalie Boulet ◽  
Anaïs Briot ◽  
Barry J. Ryan ◽  
Gemma K. Kinsella ◽  
...  

Caffeine is a plant alkaloid present in food and beverages consumed worldwide. It has high lipid solubility with recognized actions in the central nervous system and in peripheral tissues, notably the adipose depots. However, the literature is scant regarding caffeine’s influence on adipocyte functions other than lipolysis, such as glucose incorporation into lipids (lipogenesis) and amine oxidation. The objective of this study was to explore the direct effects of caffeine and of isobutylmethylxanthine (IBMX) on these adipocyte functions. Glucose transport into fat cells freshly isolated from mice, rats, or humans was monitored by determining [3H]-2-deoxyglucose (2-DG) uptake, while the incorporation of radiolabeled glucose into cell lipids was used as an index of lipogenic activity. Oxidation of benzylamine by primary amine oxidase (PrAO) was inhibited by increasing doses of caffeine in human adipose tissue preparations with an inhibition constant (Ki) in the millimolar range. Caffeine inhibited basal and insulin-stimulated glucose transport as well as lipogenesis in rodent adipose cells. The antilipogenic action of caffeine was also observed in adipocytes from mice genetically invalidated for PrAO activity, indicating that PrAO activity was not required for lipogenesis inhibition. These caffeine inhibitory properties were extended to human adipocytes: relative to basal 2-DG uptake, set at 1.0 ± 0.2 for 6 individuals, 0.1 mM caffeine tended to reduce uptake to 0.83 ± 0.08. Insulin increased uptake by 3.86 ± 1.11 fold when tested alone at 100 nM, and by 3.21 ± 0.80 when combined with caffeine. Our results reinforce the recommendation of caffeine’s potential in the treatment or prevention of obesity complications.


Diabetologia ◽  
2002 ◽  
Vol 45 (8) ◽  
pp. 1128-1135 ◽  
Author(s):  
Björnholm M. ◽  
Al-Khalili L. ◽  
Dicker A. ◽  
Näslund E. ◽  
Rössner S. ◽  
...  

1992 ◽  
Vol 22 (4) ◽  
pp. 292-299 ◽  
Author(s):  
J. W. KOLACZYNSKI ◽  
M.-R. TASKINEN ◽  
H. HILDEN ◽  
T. KIVILUOTO ◽  
K. CANTELL ◽  
...  

1997 ◽  
Vol 21 (4) ◽  
pp. 261-266 ◽  
Author(s):  
M Maslowska ◽  
AD Sniderman ◽  
R Germinario ◽  
K Cianflone

1998 ◽  
Vol 274 (2) ◽  
pp. E257-E264 ◽  
Author(s):  
Jae K. Wi ◽  
Jason K. Kim ◽  
Jang H. Youn

The relationships between postabsorptive glucose concentration and hepatic glucose output (HGO) and glucose clearance were studied in rats one day after treatment with various doses of streptozotocin (STZ; 0, 15, 30, 40, 50, or 75 mg/kg; n = 6 per dose; study 1). Glucose fluxes were estimated using a prolonged (6-h) infusion of [3-3H]glucose to ensure complete tracer equilibration at hyperglycemia. Postabsorptive glucose was significantly increased at the high doses of STZ (50 and 75 mg/kg; P < 0.01) and was strongly correlated with glucose clearance across all doses ( r = −0.85, P < 0.001) but less strongly with HGO ( r = 0.46, P < 0.01). In the group treated with 50 mg/kg STZ, postabsorptive glucose was increased twofold compared with the control (i.e., zero dose) group, with no change in HGO and a 45% decrease in glucose clearance, indicating that the hyperglycemia was due to a decrease in glucose clearance. To understand the cellular mechanisms of decreased glucose clearance in STZ diabetic rats, skeletal muscle glucose clearance and intracellular glucose and glucose 6-phosphate (G-6- P) concentrations were determined in normal and STZ (50 mg/kg) diabetic rats at their postabsorptive glucose levels as well as at matched hyperglycemia (12 mM; study 2). Glucose clearance was significantly decreased in soleus ( P< 0.05) muscles of the diabetic rats, and this was associated with significantly decreased intracellular glucose and G-6- P levels at matched hyperglycemia ( P < 0.05), suggestive of decreased glucose transport. In conclusion, postabsorptive hyperglycemia in STZ diabetic rats was largely due to decreased glucose clearance, although increased HGO may also have been a contributing factor at the highest STZ dose. The decrease in postabsorptive glucose clearance in STZ diabetic rats appeared to be associated with an impairment of glucose transport in soleus (type I) muscles.


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