למרות שזה דבילי להראות מחקרים על הנושא הזה, אתה ביקשת.
תראה את ההשפעה של קלנביוטרול ונוראפינפרין על העלייה בליפוליזה והורדת הליפוגנזה, ע"י הנמכת הרגישות לאינסולין.
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Domest Anim Endocrinol. 1989 Jan;6(1):59-69.
Influence of the beta 2-adrenergic agonist clenbuterol on insulin-stimulated lipogenesis in mouse adipocytes.
Orcutt AL, Cline TR, Mills SE.
Department of Animal Science, Purdue University, West Lafayette, IN 47907.
Growing mice fed the beta 2-adrenergic agonist clenbuterol (CB; 20ppm) had increased rate of growth and altered composition of gain (greater protein and less fat). Adipocytes prepared from the epididymal fat pads of treated and untreated mice were used to examine the influence of CB on lipid metabolism. Using cells from untreated mice, CB stimulated lipolysis to an equivalent maximum rate as epinephrine (EPI), but CB was far less potent (EC50 (microM); CB = 5, EPI = 0.2). Both CB and EPI inhibited insulin-stimulated lipogenesis over the physiological range of insulin concentrations. This inhibition was expressed as a dose-dependent decrease in tissue sensitivity to insulin and a decrease in maximal lipogenic capacity. Inhibition of maximal rate, but not of insulin sensitivity, could be stimulated by the addition of palmitate without EPI or CB. Adipocytes isolated from CB-treated mice did not differ from controls in sensitivity to insulin or in activity of fatty acid synthetase. Increased lipolysis and reduced lipogenesis as observed in vitro with CB are consistent with reduced fat accretion in CB-treated mice. However, the absence of detectable changes in adipocyte lipogenesis from CB-fed mice leaves open the question of the relevance of altered lipid metabolism to the observed changes in body composition.
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עריכה:
ההשפעה הליפולטית\מנמיכת הרגישות לאינסולין, על ידי הקפאין, היא בעצם על ידי השפעתו על האפינפרין. קפאין, כמו שציינתי, הוא חומר ממריץ SNS output. ע"י פעולה זו הוא מייעל ניוד\פירוק שומן, גורם להנמכת הרגישות לאינסולין ולהפחתת ניצול הפחמימות\חלבונים לאנרגיה.
אז האם נמנע גם מהאפינפרין\קטכולאמינים (הורמונים שורפי שומן) שמורידים את הרגישות לאינסולין, כחלק ממכניקת פעולתם?
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Diabetes Care. 2002 Feb;25(2):364-9.
Comment in:
Diabetes Care. 2002 Feb;25(2):399-400.
Caffeine can decrease insulin sensitivity in humans.
Keijzers GB, De Galan BE, Tack CJ, Smits P.
Department of Internal Medicine, University Medical Center Nijmegen, 6500 HB Nijmegen, the Netherlands.
OBJECTIVE: Caffeine is a central stimulant that increases the release of catecholamines. As a component of popular beverages, caffeine is widely used around the world. Its pharmacological effects are predominantly due to adenosine receptor antagonism and include release of catecholamines. We hypothesized that caffeine reduces insulin sensitivity, either due to catecholamines and/or as a result of blocking adenosine-mediated stimulation of peripheral glucose uptake. RESEARCH DESIGN AND METHODS: Hyperinsulinemic-euglycemic glucose clamps were used to assess insulin sensitivity. Caffeine or placebo was administered intravenously to 12 healthy volunteers in a randomized, double-blind, crossover design. Measurements included plasma levels of insulin, catecholamines, free fatty acids (FFAs), and hemodynamic parameters. Insulin sensitivity was calculated as whole-body glucose uptake corrected for the insulin concentration. In a second study, the adenosine reuptake inhibitor dipyridamole was tested using an identical protocol in 10 healthy subjects. RESULTS: Caffeine decreased insulin sensitivity by 15% (P < 0.05 vs. placebo). After caffeine administration, plasma FFAs increased (P < 0.05) and remained higher than during placebo. Plasma epinephrine increased fivefold (P < 0.0005), and smaller increases were recorded in plasma norepinephrine (P < 0.02) and blood pressure (P < 0.001). Dipyridamole did not alter insulin sensitivity and only increased plasma norepinephrine (P < 0.01). CONCLUSIONS: Caffeine can decrease insulin sensitivity in healthy humans, possibly as a result of elevated plasma epinephrine levels. Because dipyridamole did not affect glucose uptake, peripheral adenosine receptor antagonism does not appear to contribute to this effect.
גל.
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