Abstract
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.
Highlights
Caffeine (1,3,7-trimethylxanthine) is a plant alkaloid found in food and beverages consumed daily worldwide
IBMX has been more thoroughly studied in animal adipose-derived cells than in native human adipocytes and since our aim was to examine in humans the potential PrAOdependent actions of methylxanthines, we took advantage of the observations accumulated in rodents and human with this agent before exploring caffeine’s effects on glucose handling in both animal and human fat cells
Considering that, as for IBMX, caffeine lipolytic effects are well documented in adipocytes [33,34,35] and since we recently reported that caffeine hampers the antilipolytic effect of insulin in mouse adipocytes [36], we focused our attention on how caffeine was able to impair insulin stimulation of glucose uptake and incorporation into lipids
Summary
Caffeine (1,3,7-trimethylxanthine) is a plant alkaloid found in food and beverages consumed daily worldwide. The mean daily intake of caffeine, was estimated to be 4 mg/kg of body weight in adults [1], and was more recently reassessed to average 165 mg (850 μmoles) per individual in the U.S population [2]. Many consumers of coffee, chocolate, and caffeinated beverages or adulterated food supplements [3] exceed this intake, approaching the no observable adverse effect level (NOAEL) for cardiovascular effects, established at 260 mg caffeine [4]. Anorexic, and somnolytic central actions, caffeine directly affects peripheral tissues, among them, the adipose depots. This study aims at exploring putative novel properties of caffeine that involve the role it plays in fat accumulation and body weight regulation. Caffeine has been considered as an anti-obesity drug [6], and has been found to interact directly with adipocytes or cultured preadipose cells in in vitro experiments at micromolar to supramillimolar levels
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