hehehe,geht mal wieder um nahrungszusammensetzung;-)
zitat kurt:aber wie ich schon sagte, die UCP's scheinen den hauptunterschied in der rmr auszumachen, vermutlich sogar mehr noch als der muskelstoffwechsel an sich. wobei das auch genetisch festgelegt ist und durch "manipulation" (wie z.b. die ernährung) nur marginal beeinflusst werden kann.
da surf ich ein bissi rum und schon springen mich wieder die ucp´s an:
Am J Physiol Endocrinol Metab 2001 Dec;281(6):E1197-E1204
Polyunsaturated fatty acids stimulate hepatic UCP-2 expression via a PPARalpha-mediated pathway.
Armstrong MB, Towle HC
Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, Minnesota 55455.
[Record supplied by publisher]
The discovery of homologs of the brown fat uncoupling protein(s) (UCP) UCP-2 and UCP-3 revived the hypothesis of uncoupling protein involvement in the regulation of energy metabolism. Thus we hypothesized that UCP-2 would be regulated in the hepatocyte by fatty acids, which are known to control other energy-related metabolic processes. Treatment with 250 &mgr;M palmitic acid was without effect on UCP-2 expression, whereas 250 &mgr;M oleic acid exhibited a modest eightfold increase. Eicosapentaenoic acid (EPA), a polyunsaturated fatty acid, exerted a 50-fold upregulation of UCP-2 that was concentration dependent. This effect was seen within 12 h and was maximal by 36 h. Aspirin blocked the induction of UCP-2 by EPA, indicating involvement of the prostaglandin pathway. Hepatocytes treated with arachidonic acid, the immediate precursor to the prostaglandins, also exhibited an aspirin-inhibitable increase in UCP-2 levels, further supporting the involvement of prostaglandins in regulating hepatic UCP-2. The peroxisome proliferator-activated receptor-alpha (PPARalpha) agonist Wy-14643 stimulated UCP-2 mRNA levels as effectively as EPA. These data indicate that UCP-2 is upregulated by polyunsaturated fatty acids, potentially through a prostaglandin/PPARalpha-mediated pathway.
Br J Nutr 2000 Mar;83 Suppl 1:S59-66
Polyunsaturated fatty acid regulation of gene transcription: a mechanism to improve energy balance and insulin resistance.
Clarke SD
Graduate Program of Nutritional Sciences, University of Texas at Austin 78712, USA. stevedclarke@mail.utexas.edu
This review addresses the hypothesis that polyunsaturated fatty acids (PUFA), particularly those of the n-3 family, play essential roles in the maintenance of energy balance and glucose metabolism. The data discussed indicate that dietary PUFA function as fuel partitioners in that they direct glucose toward glycogen storage, and direct fatty acids away from triglyceride synthesis and assimilation and toward fatty acid oxidation. In addition, the n-3 family of PUFA appear to have the unique ability to enhance thermogenesis and thereby reduce the efficiency of body fat deposition. PUFA exert their effects on lipid metabolism and thermogenesis by upregulating the transcription of the mitochondrial uncoupling protein-3, and inducing genes encoding proteins involved in fatty acid oxidation (e.g. carnitine palmitoyltransferase and acyl-CoA oxidase) while simultaneously down-regulating the transcription of genes encoding proteins involved in lipid synthesis (e.g. fatty acid synthase). The potential transcriptional mechanism and the transcription factors affected by PUFA are discussed. Moreover, the data are interpreted in the context of the role that PUFA may play as dietary factors in the development of obesity and insulin resistance. Collectively the results of these studies suggest that the metabolic functions governed by PUFA should be considered as part of the criteria utilized in defining the dietary needs for n-6 and n-3 PUFA, and in establishing the optimum dietary ratio for n-6:n-3 fatty acids.
da hab ich nun eine frage:wenn es so wäre, das die n3´s die ucp-aktivität beeinflussen und gleichzeitig die ucp´s einen signifikanten einfluss auf die rmr haben, dann könnte man doch daraus schliessen,das die zusammensetzung der nahrung nicht vollkommen gleichgültig ist(bzw das ich kein kompletter trottel bin,der unnötigerweise 2x 15-20g leinöl in seine saftln schüttet;-)))
wie du siehst,bin vorsichtig,lol,wäre,könnte...
aber du musst zugeben(oder auch nicht...),das es in letzter zeit studien gibt,die in die richtung weisen...
grüsse,klaus
ps:und wer 30-40g leinöl am tag verdrückt,hat ein resultat verdient!!!soviel mut gehört belohnt;-))))
zitat kurt:aber wie ich schon sagte, die UCP's scheinen den hauptunterschied in der rmr auszumachen, vermutlich sogar mehr noch als der muskelstoffwechsel an sich. wobei das auch genetisch festgelegt ist und durch "manipulation" (wie z.b. die ernährung) nur marginal beeinflusst werden kann.
da surf ich ein bissi rum und schon springen mich wieder die ucp´s an:
Am J Physiol Endocrinol Metab 2001 Dec;281(6):E1197-E1204
Polyunsaturated fatty acids stimulate hepatic UCP-2 expression via a PPARalpha-mediated pathway.
Armstrong MB, Towle HC
Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, Minnesota 55455.
[Record supplied by publisher]
The discovery of homologs of the brown fat uncoupling protein(s) (UCP) UCP-2 and UCP-3 revived the hypothesis of uncoupling protein involvement in the regulation of energy metabolism. Thus we hypothesized that UCP-2 would be regulated in the hepatocyte by fatty acids, which are known to control other energy-related metabolic processes. Treatment with 250 &mgr;M palmitic acid was without effect on UCP-2 expression, whereas 250 &mgr;M oleic acid exhibited a modest eightfold increase. Eicosapentaenoic acid (EPA), a polyunsaturated fatty acid, exerted a 50-fold upregulation of UCP-2 that was concentration dependent. This effect was seen within 12 h and was maximal by 36 h. Aspirin blocked the induction of UCP-2 by EPA, indicating involvement of the prostaglandin pathway. Hepatocytes treated with arachidonic acid, the immediate precursor to the prostaglandins, also exhibited an aspirin-inhibitable increase in UCP-2 levels, further supporting the involvement of prostaglandins in regulating hepatic UCP-2. The peroxisome proliferator-activated receptor-alpha (PPARalpha) agonist Wy-14643 stimulated UCP-2 mRNA levels as effectively as EPA. These data indicate that UCP-2 is upregulated by polyunsaturated fatty acids, potentially through a prostaglandin/PPARalpha-mediated pathway.
Br J Nutr 2000 Mar;83 Suppl 1:S59-66
Polyunsaturated fatty acid regulation of gene transcription: a mechanism to improve energy balance and insulin resistance.
Clarke SD
Graduate Program of Nutritional Sciences, University of Texas at Austin 78712, USA. stevedclarke@mail.utexas.edu
This review addresses the hypothesis that polyunsaturated fatty acids (PUFA), particularly those of the n-3 family, play essential roles in the maintenance of energy balance and glucose metabolism. The data discussed indicate that dietary PUFA function as fuel partitioners in that they direct glucose toward glycogen storage, and direct fatty acids away from triglyceride synthesis and assimilation and toward fatty acid oxidation. In addition, the n-3 family of PUFA appear to have the unique ability to enhance thermogenesis and thereby reduce the efficiency of body fat deposition. PUFA exert their effects on lipid metabolism and thermogenesis by upregulating the transcription of the mitochondrial uncoupling protein-3, and inducing genes encoding proteins involved in fatty acid oxidation (e.g. carnitine palmitoyltransferase and acyl-CoA oxidase) while simultaneously down-regulating the transcription of genes encoding proteins involved in lipid synthesis (e.g. fatty acid synthase). The potential transcriptional mechanism and the transcription factors affected by PUFA are discussed. Moreover, the data are interpreted in the context of the role that PUFA may play as dietary factors in the development of obesity and insulin resistance. Collectively the results of these studies suggest that the metabolic functions governed by PUFA should be considered as part of the criteria utilized in defining the dietary needs for n-6 and n-3 PUFA, and in establishing the optimum dietary ratio for n-6:n-3 fatty acids.
da hab ich nun eine frage:wenn es so wäre, das die n3´s die ucp-aktivität beeinflussen und gleichzeitig die ucp´s einen signifikanten einfluss auf die rmr haben, dann könnte man doch daraus schliessen,das die zusammensetzung der nahrung nicht vollkommen gleichgültig ist(bzw das ich kein kompletter trottel bin,der unnötigerweise 2x 15-20g leinöl in seine saftln schüttet;-)))
wie du siehst,bin vorsichtig,lol,wäre,könnte...
aber du musst zugeben(oder auch nicht...),das es in letzter zeit studien gibt,die in die richtung weisen...
grüsse,klaus
ps:und wer 30-40g leinöl am tag verdrückt,hat ein resultat verdient!!!soviel mut gehört belohnt;-))))
))