Showing posts with label dioxin. Show all posts
Showing posts with label dioxin. Show all posts
Friday, October 29, 2010
Aryl Hydrocarbon Receptor Nuclear Translocator (ARNT) in Hepatocytes is Required for Aryl Hydrocarbon Receptor-Mediated Adaptive and Toxic Responses in Liver
CiteULike: Aryl Hydrocarbon Receptor Nuclear Translocator (ARNT) in Hepatocytes is Required for Aryl Hydrocarbon Receptor-Mediated Adaptive and Toxic Responses in Liver: "AHR-ARNT dimers within the hepatocyte direct the toxic and adaptive and developmental functions associated with the AHR and that developmental vascular events arise due to signaling in a distinct cell type expressing this dimeric pair"
Thursday, October 7, 2010
IDENTIFICATION OF THE ARYL HYDROCARBON RECEPTOR TA... [J Biol Chem. 2010] - PubMed result
IDENTIFICATION OF THE ARYL HYDROCARBON RECEPTOR TA... [J Biol Chem. 2010] - PubMed result: "The vitamin B3 constituent, nicotinamide (NAM), prevented TCDD suppression of glucose output, NAD(+), and gluconeogenic genes and stabilized PGC1α. The corrective effects of NAM could be attributed to increased NAD(+) levels and suppression of AHR target gene induction."
Saturday, September 4, 2010
Contaminants in Air Pollution Including Endotoxin and Dioxin May Increase Insulin Resistance~!
Complications associated with insulin resistance may play a significant role in environmental diseases including obesity, sleep apneas and potentially Gulf War Syndrome and chemical sensitivity just for examples. Other studies show that sustained endotoxin, a potential consideration in CFS and other environmental illnesses, is a common component of particulate matter and environmental pollutants may alter insuling signalling in muscle especially under sustained stress such as malnutrition. These conditions may potentiate one another if they occur at the same time.....
"TCDD stimulates expression and secretion of TNF-alpha in adipocytes through activation of AhR, ERK1/2, and JNK, and the secreted TNF-alpha causes the downregulation of IRbeta, IRS1, and GLUT4 through TNFR1, resulting in insulin resistance."
Read more: CiteULike: 2,3,7,8-tetrachlorodibenzo-p-dioxin impairs an insulin signaling pathway through the induction of tumor necrosis factor-alpha in adipocytes.:
For further understanding: IRS-1
McCowen, K. C., Ling, P. R., Ciccarone, A., Mao, Y., Chow, J. C., Bistrian, B. R., and Smith, R. J. (2001). Sustained endotoxemia leads to marked down-regulation of early steps in the insulin-signaling cascade. Critical care medicine, 29(4):839-846. http://www.citeulike.org/user/HEIRS/article/7782376
"TCDD stimulates expression and secretion of TNF-alpha in adipocytes through activation of AhR, ERK1/2, and JNK, and the secreted TNF-alpha causes the downregulation of IRbeta, IRS1, and GLUT4 through TNFR1, resulting in insulin resistance."
Read more: CiteULike: 2,3,7,8-tetrachlorodibenzo-p-dioxin impairs an insulin signaling pathway through the induction of tumor necrosis factor-alpha in adipocytes.:
For further understanding: IRS-1
McCowen, K. C., Ling, P. R., Ciccarone, A., Mao, Y., Chow, J. C., Bistrian, B. R., and Smith, R. J. (2001). Sustained endotoxemia leads to marked down-regulation of early steps in the insulin-signaling cascade. Critical care medicine, 29(4):839-846. http://www.citeulike.org/user/HEIRS/article/7782376
Sunday, July 25, 2010
Dioxin and Its Effects on Fat Metabolism and Insulin-Mediated Glucose Regulation~!
Hsu, H.-F. F., Tsou, T.-C. C., Chao, H.-R. R., Kuo, Y.-T. T., Tsai, F.-Y. Y., and Yeh, S.-C. C. (2010). Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on adipogenic differentiation and insulin-induced glucose uptake in 3t3-l1 cells. Journal of hazardous materials.
HEIRS Health Research Blog: Inflammation, Insulin Resistance and Decreased PPARs-- A Pathway to CFS?
This study shows in vitro evidence of TCDD's effects on fat cell metabolism, suggesting dioxin exposure in development of insulin resistance and type II diabetes. Interestingly, while PPAR-gamma was reduced an inhibitor of the AhR did not alter the change in glucose uptake.
HEIRS Health Research Blog: Inflammation, Insulin Resistance and Decreased PPARs-- A Pathway to CFS?
Saturday, July 24, 2010
Inflammation, Insulin Resistance and Decreased PPARs-- A Pathway to CFS?
I thought today I would review some points that I have made over the last several months about environmental illness specifically chronic fatigue syndrome. I do this today, because of recent research news that supports some of what I have been saying all along and that is that CFS is probably the result of stresses that alter cellular functioning and disrupt cellular metabolism. This is not a new thing but believe that many researchers have failed to notice that many of the symptoms may be caused by alterations in glucose metabolism and insulin activity and include some influences like what occur in
sickness syndrome even though CFS and sickness syndrome are not the same thing. Sickness syndrome is a variety of changes that occur in the body as a response to sickness and provides a mechanism to fight whatever is causing the sickness. Personally, I can recognize it more in animals because humans have been taught that we "must" overcome --- and that goes for being ill too that usually leads to more sickness.
Michael Maes has probably been the leader in the idea of sickness syndrome in relation to CFS. In his last report, he definitely makes the distinction and I have to agree with him. CFS is not sickness syndrome and is more due to inflammation and oxidative and nitrosative stress and pathogenic conditions and permeability can be to blame. Again, I agree and am critical of some that try to base everything about CFS on oxidative stress because it does not really explain how one "gets there"! In my view, it all comes down to and the problem with labels and this always has been my issue..... IN this case, how can we understand where one illness like CFS starts and another one ends such as sickness syndrome if noone really has defined the former CFS well in the first place? It is my belief that sickness syndrome may be a prelude to CFS or maybe the beginning point of it, and different factors can inhibit or lead to a "full-blown" case of CFS and recognizing the biological factors that play a part may in fact, help to prevent CFS in its most severe form. As far as oxidative and nitrosative stress in CFS, I think if you just leave it at..then it is doing a disservice not only to the condition but to those who suffer from it. The reason I say this is because of the nature of oxidative/nitrosative stress --- it is a natural result of cellular processes. Just saying that CFS is caused from too much of these stresses does nothing to answer what is causing the overwhelming oxidative stress in the first place in CFS. Maes has implied that endotoxin may be a pathway to CFS and bacterial infection has potential for causing oxidative stress and changing environments and altered methylation. But the possibility that other environmental factors such as hyperglycemia and high-fat diets which promote bacterial translocation and consequently activate certain immune responses leadin to CFS also, can not be dismissed. I have suggested that the failure of the antioxidant system to adequately meet the needs of oxidative stress or maybe even at all to any real level may play a very important role. In other blogs, we have noted that oxidative and nitrosative stress is needed to activate this system and nutritional and genetic factors may influence the speed and level of activation. So if we have overwhelming oxidative stress -- it makes sense that something like underactivation of the antioxidant system may be at fault or is just not working. So in essence, it should be a no-brainer to look at the Nrf2-Keap1 and other proteins it controls to get a better handle on what may be causing the failure of an adaptive immune response and elevations in inflammatory markers and oxidative stress that are obviously maladaptive.
Several new studies some evidence that a failure in the antioxidant system could contribute to CFS. It is not a direct road I admit, but considering I have been following these paths for 3 years now. They make sense to me, mainly because I look for the CFS from a more holistic and systems theory perspective. For someone that has been trained both in anthropology and biology, this perspective works better for me when I need to find out the answers to different questions that need to be investigated. In addition, one could ask what is a direct road or pathway in reference to disease anyway....to me, it is all relative and most always depends on personal interpretation. Several months ago, I blogged that environmental pollutants may contribute to diabetes and insulin resistance. Since then several other reports conclude this may be the case and many studies have provided evidence how inflammation can lead to insulin resistance and diabetes through the down-regulation of genes and up-regulation of inflammatory cytokines. Several inflammatory markers, not just one, can contribute and can be produced as a consequence of the stress response including TNF-a, Il-1, Il-6. Some of these activate other responses that lead to neuroinflammation and also alteration of neurotransmitters and have other effects on brain chemistry which could be characteristic of the cognitive dysfunction associated with CFS.
It has been suspected that pollutants lead to the alteration of a class of class of genes. I refer to them most often as PARRs and may include PPAR-gamma, PARR-delta and PARR-alpha. I have discussed both PPAR-gamma and PPAR-alpha at length in different discussions and most notably, PPAR-gamma is an important anti-inflammatory which helps prevent the development of insulin resistance in addition to other functions and may help repress autoimmunity. (Klotz) Recently, a study of the combination of pioglitizone and caffeic acid, demonstrated significant improvement in a mouse model of chronic fatigue. In this study, the results showed improvements in running wheel activity, locomotor activity and anxiety. Other improvements included reductions in oxidative damage including lipid peroxidation and nitrite concentration and increased glutatione and catalase levels in addition to altering mitochondrial function. When one digs a little deeper, interesting things appear related to the actions of these compounds. Caffeic acid is an antioxidant and anti-inflammatory that while having potential hazard qualities, also demonstrates the ability to " suppress MMP-9 enzyme activity and down-regulate NF-κB through inhibition of protein IKK and activation of Nrf2 (Lee) and other studies provide in vitro evidence it may effect DNA methylation.(Wipedia)" In contrast, pioglitizone is an anti-hyperglycemic medication and "stimulates the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) and to a lesser extent PPAR-α. Both of these compounds act through PARR-gamma directly or indirectly via Nrf which may explain why their benefits in the CFS model is synergistic compared to when they were used alone. (Kumar) Generally, PARRs modulates the transcription of the insulin-sensitive genes involved in the control of glucose and lipid metabolism in the muscle, adipose tissue, and the liver. (Wipedia)" What this says to me is that CFS very well could be considered a condition that is a consequence of significantly disrupted normal glucose uptake and cellular and energy metabolism and altered immune function in different tissues.
I have also postulated that the aryl hydrocarbon may play an important role in both CFS and MCS and there are several "conditions" that lead me to make this assumption and the hypothesis but unfortunately, how this interaction occurs is quite "muddy". First, it has been demonstrated that there is a close connection in the actions of the AhR and the Nrf2 in response to environmental pollutants and their "gene batteries". Second, I have suggested that abnormal signalling from the AhR may influence the functioning of several proteins including the Nrf2 even though the specific mechanismin of how this is achieved is not entirely understood. Third, dioxin which persists in the environment, albeit at lower levels in the last decade in many locales but still present in food, has been associated with diabetes and activates the AhR. Four, for some time it has been believed the AhR may inhibit PPAR-gamma and therefore leads us to environmental conditions, at least physiologically, of elevated inflammation and an increased risk for diabetes. (Remillard) Arguably, the role of the AhR on PPAR-gamma depends on the tissue. (Kitchner, Shin) However, dioxins are bioaccumulative and activation of the AhR and its effects on PPAR-gamma may spill over to surrounding tissues. Lastly, a new study has shown that Nrf2 drives PPAR-gamma in protecting against oxidant injury at least in the respiratory system. Taking all this into account, it is safe to at least suggest that CFS may be influenced by fluctuations in PPAR-gamma and the proteins that regulate it and factors that upregulate it may be beneficial or preventative against CFS. Because PPAR-gamma demonstrates inhibitory properties on autoimmune responses, its absence may play significantly in the "loss of tolerance" responses of chemical sensitivity and inflammatory bowel disease. Other studies show PPAR-gamma has as an important regulatory function with HO-1 and may be neuroprotective against Parkinson's (Lui, Schintu) and influences mitochondrial biogenesis through PGC-1a (Miglio). In other blogs, I discuss how certain nutritional compounds such as resveratrol and EGCG in different foods have shown some benefit and their modes of actions address some of the issues that are discussed in the paragraphs above. IN addition, because these proteins can be effected by methylation this explains the inheritabilty factor that exists with CFS that is not explained just by the presence of oxidative stress.
Notes:
Cho, H.-Y. Y., Gladwell, W., Wang, X., Chorley, B., Bell, D., Reddy, S. P., and Kleeberger, S. R. (2010). Nrf2-regulated ppargamma expression is critical to protection against acute lung injury in mice. American journal of respiratory and critical care medicine, 182(2):170-182. http://www.citeulike.org/user/HEIRS/article/6854883?show_msg=already_posted
Kumar, A., Vashist, A., and Kumar, P. (2010). Potential role of pioglitazone, caffeic acid and their combination against fatigue syndrome-induced behavioural, biochemical and mitochondrial alterations in mice. Inflammopharmacology. http://www.citeulike.org/user/HEIRS/article/7474822
Yang, J.-Y. Y., Della-Fera, M. A. A., Rayalam, S., Ambati, S., Hartzell, D. L., Park, H. J. J., and Baile, C. A. (2008). Enhanced inhibition of adipogenesis and induction of apoptosis in 3t3-l1 adipocytes with combinations of resveratrol and quercetin. Life sciences, 82(19-20):1032-1039. http://www.citeulike.org/user/HEIRS/article/7537205
Pioglitazone. Wipedia. Retrieved on July 24, 2010. http://en.wikipedia.org/wiki/Pioglitazone
Caffeic Acid. Wipedia. Retrieved on July 24, 2010. http://en.wikipedia.org/wiki/Caffeic_Acid
Zhou, M., Wu, R., Dong, W., Jacob, A., and Wang, P. (2008). Endotoxin downregulates peroxisome proliferator-activated receptor-gamma via the increase in tnf-alpha release. Am J Physiol Regul Integr Comp Physiol, 294(1):R84-92. http://www.citeulike.org/user/HEIRS/article/2439726
Remillard, R. B. and Bunce, N. J. (2002). Linking dioxins to diabetes: epidemiology and biologic plausibility. Environmental health perspectives, 110(9):853-858. http://www.ncbi.nlm.nih.gov/pubmed/12204817
Kintscher, U. and Law, R. E. (2005). Ppargamma-mediated insulin sensitization: the importance of fat versus muscle. Am J Physiol Endocrinol Metab, 288(2):E287-291. http://www.citeulike.org/user/HEIRS/article/3824606
Shin, S., Wakabayashi, N., Misra, V., Biswal, S., Lee, G. H., Agoston, E. S., Yamamoto, M., and Kensler, T. W. (2007). Nrf2 modulates aryl hydrocarbon receptor signaling: Influence on adipogenesis. Mol. Cell. Biol., 27(20):7188-7197. http://www.citeulike.org/user/HEIRS/article/3787182
Klotz, L., Burgdorf, S., Dani, I., Saijo, K., Flossdorf, J., Hucke, S., Alferink, J., Novak, N., Beyer, M., Mayer, G., Langhans, B., Klockgether, T., Waisman, A., Eberl, G., Schultze, J., Famulok, M., Kolanus, W., Glass, C., Kurts, C., and Knolle, P. A. (2009). The nuclear receptor ppargamma selectively inhibits th17 differentiation in a t cell-intrinsic fashion and suppresses cns autoimmunity. J. Exp. Med., 206(10):2079-2089. http://www.citeulike.org/user/HEIRS/article/5778777
Liu, S. H. H., Yang, C. N. N., Pan, H. C. C., Sung, Y. J. J., Liao, K. K. K., Chen, W. B. B., Lin, W. Z. Z., and Sheu, M. L. L. (2010). Il-13 downregulates ppar-gamma/heme oxygenase-1 via er stress-stimulated calpain activation: aggravation of activated microglia death. Cellular and molecular life sciences : CMLS. http://www.citeulike.org/user/HEIRS/article/6826740
Schintu, N., Frau, L., Ibba, M., Caboni, P., Garau, A., Carboni, E., and Carta, A. R. (2009). Ppar-gamma-mediated neuroprotection in a chronic mouse model of parkinson's disease. The European journal of neuroscience, 29(5):954-963. http://www.citeulike.org/user/HEIRS/article/4136907
Miglio, G., Rosa, A. C., Rattazzi, L., Collino, M., Lombardi, G., and Fantozzi, R. (2009). Ppargamma stimulation promotes mitochondrial biogenesis and prevents glucose deprivation-induced neuronal cell loss. Neurochemistry international, 55(7):496-504. http://www.citeulike.org/user/HEIRS/article/5345204
Lee, Y., Shin, D.-H. H., Kim, J.-H. H., Hong, S., Choi, D., Kim, Y.-J. J., Kwak, M.-K. K., and Jung, Y. (2010). Caffeic acid phenethyl ester-mediated nrf2 activation and ikappab kinase inhibition are involved in nfkappab inhibitory effect: Structural analysis for nfkappab inhibition. European journal of pharmacology, 643(1):21-28. http://www.citeulike.org/user/HEIRS/article/7394789
sickness syndrome even though CFS and sickness syndrome are not the same thing. Sickness syndrome is a variety of changes that occur in the body as a response to sickness and provides a mechanism to fight whatever is causing the sickness. Personally, I can recognize it more in animals because humans have been taught that we "must" overcome --- and that goes for being ill too that usually leads to more sickness.
Michael Maes has probably been the leader in the idea of sickness syndrome in relation to CFS. In his last report, he definitely makes the distinction and I have to agree with him. CFS is not sickness syndrome and is more due to inflammation and oxidative and nitrosative stress and pathogenic conditions and permeability can be to blame. Again, I agree and am critical of some that try to base everything about CFS on oxidative stress because it does not really explain how one "gets there"! In my view, it all comes down to and the problem with labels and this always has been my issue..... IN this case, how can we understand where one illness like CFS starts and another one ends such as sickness syndrome if noone really has defined the former CFS well in the first place? It is my belief that sickness syndrome may be a prelude to CFS or maybe the beginning point of it, and different factors can inhibit or lead to a "full-blown" case of CFS and recognizing the biological factors that play a part may in fact, help to prevent CFS in its most severe form. As far as oxidative and nitrosative stress in CFS, I think if you just leave it at..then it is doing a disservice not only to the condition but to those who suffer from it. The reason I say this is because of the nature of oxidative/nitrosative stress --- it is a natural result of cellular processes. Just saying that CFS is caused from too much of these stresses does nothing to answer what is causing the overwhelming oxidative stress in the first place in CFS. Maes has implied that endotoxin may be a pathway to CFS and bacterial infection has potential for causing oxidative stress and changing environments and altered methylation. But the possibility that other environmental factors such as hyperglycemia and high-fat diets which promote bacterial translocation and consequently activate certain immune responses leadin to CFS also, can not be dismissed. I have suggested that the failure of the antioxidant system to adequately meet the needs of oxidative stress or maybe even at all to any real level may play a very important role. In other blogs, we have noted that oxidative and nitrosative stress is needed to activate this system and nutritional and genetic factors may influence the speed and level of activation. So if we have overwhelming oxidative stress -- it makes sense that something like underactivation of the antioxidant system may be at fault or is just not working. So in essence, it should be a no-brainer to look at the Nrf2-Keap1 and other proteins it controls to get a better handle on what may be causing the failure of an adaptive immune response and elevations in inflammatory markers and oxidative stress that are obviously maladaptive.
Several new studies some evidence that a failure in the antioxidant system could contribute to CFS. It is not a direct road I admit, but considering I have been following these paths for 3 years now. They make sense to me, mainly because I look for the CFS from a more holistic and systems theory perspective. For someone that has been trained both in anthropology and biology, this perspective works better for me when I need to find out the answers to different questions that need to be investigated. In addition, one could ask what is a direct road or pathway in reference to disease anyway....to me, it is all relative and most always depends on personal interpretation. Several months ago, I blogged that environmental pollutants may contribute to diabetes and insulin resistance. Since then several other reports conclude this may be the case and many studies have provided evidence how inflammation can lead to insulin resistance and diabetes through the down-regulation of genes and up-regulation of inflammatory cytokines. Several inflammatory markers, not just one, can contribute and can be produced as a consequence of the stress response including TNF-a, Il-1, Il-6. Some of these activate other responses that lead to neuroinflammation and also alteration of neurotransmitters and have other effects on brain chemistry which could be characteristic of the cognitive dysfunction associated with CFS.
It has been suspected that pollutants lead to the alteration of a class of class of genes. I refer to them most often as PARRs and may include PPAR-gamma, PARR-delta and PARR-alpha. I have discussed both PPAR-gamma and PPAR-alpha at length in different discussions and most notably, PPAR-gamma is an important anti-inflammatory which helps prevent the development of insulin resistance in addition to other functions and may help repress autoimmunity. (Klotz) Recently, a study of the combination of pioglitizone and caffeic acid, demonstrated significant improvement in a mouse model of chronic fatigue. In this study, the results showed improvements in running wheel activity, locomotor activity and anxiety. Other improvements included reductions in oxidative damage including lipid peroxidation and nitrite concentration and increased glutatione and catalase levels in addition to altering mitochondrial function. When one digs a little deeper, interesting things appear related to the actions of these compounds. Caffeic acid is an antioxidant and anti-inflammatory that while having potential hazard qualities, also demonstrates the ability to " suppress MMP-9 enzyme activity and down-regulate NF-κB through inhibition of protein IKK and activation of Nrf2 (Lee) and other studies provide in vitro evidence it may effect DNA methylation.(Wipedia)" In contrast, pioglitizone is an anti-hyperglycemic medication and "stimulates the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) and to a lesser extent PPAR-α. Both of these compounds act through PARR-gamma directly or indirectly via Nrf which may explain why their benefits in the CFS model is synergistic compared to when they were used alone. (Kumar) Generally, PARRs modulates the transcription of the insulin-sensitive genes involved in the control of glucose and lipid metabolism in the muscle, adipose tissue, and the liver. (Wipedia)" What this says to me is that CFS very well could be considered a condition that is a consequence of significantly disrupted normal glucose uptake and cellular and energy metabolism and altered immune function in different tissues.
I have also postulated that the aryl hydrocarbon may play an important role in both CFS and MCS and there are several "conditions" that lead me to make this assumption and the hypothesis but unfortunately, how this interaction occurs is quite "muddy". First, it has been demonstrated that there is a close connection in the actions of the AhR and the Nrf2 in response to environmental pollutants and their "gene batteries". Second, I have suggested that abnormal signalling from the AhR may influence the functioning of several proteins including the Nrf2 even though the specific mechanismin of how this is achieved is not entirely understood. Third, dioxin which persists in the environment, albeit at lower levels in the last decade in many locales but still present in food, has been associated with diabetes and activates the AhR. Four, for some time it has been believed the AhR may inhibit PPAR-gamma and therefore leads us to environmental conditions, at least physiologically, of elevated inflammation and an increased risk for diabetes. (Remillard) Arguably, the role of the AhR on PPAR-gamma depends on the tissue. (Kitchner, Shin) However, dioxins are bioaccumulative and activation of the AhR and its effects on PPAR-gamma may spill over to surrounding tissues. Lastly, a new study has shown that Nrf2 drives PPAR-gamma in protecting against oxidant injury at least in the respiratory system. Taking all this into account, it is safe to at least suggest that CFS may be influenced by fluctuations in PPAR-gamma and the proteins that regulate it and factors that upregulate it may be beneficial or preventative against CFS. Because PPAR-gamma demonstrates inhibitory properties on autoimmune responses, its absence may play significantly in the "loss of tolerance" responses of chemical sensitivity and inflammatory bowel disease. Other studies show PPAR-gamma has as an important regulatory function with HO-1 and may be neuroprotective against Parkinson's (Lui, Schintu) and influences mitochondrial biogenesis through PGC-1a (Miglio). In other blogs, I discuss how certain nutritional compounds such as resveratrol and EGCG in different foods have shown some benefit and their modes of actions address some of the issues that are discussed in the paragraphs above. IN addition, because these proteins can be effected by methylation this explains the inheritabilty factor that exists with CFS that is not explained just by the presence of oxidative stress.
Notes:
- Endotoxin is considered potential pathway to CFS and inhibits PPAR-gamma through Tnf-a (Zhou)
- It as been suggested that XMRV may play a role in CFS - I would suggest that while XMRV may be a piggy-back condition, any pathogen or infection or pollutant that inhibits PPARs and increase inflammatory mediators contribute to CFS.
Cho, H.-Y. Y., Gladwell, W., Wang, X., Chorley, B., Bell, D., Reddy, S. P., and Kleeberger, S. R. (2010). Nrf2-regulated ppargamma expression is critical to protection against acute lung injury in mice. American journal of respiratory and critical care medicine, 182(2):170-182. http://www.citeulike.org/user/HEIRS/article/6854883?show_msg=already_posted
Kumar, A., Vashist, A., and Kumar, P. (2010). Potential role of pioglitazone, caffeic acid and their combination against fatigue syndrome-induced behavioural, biochemical and mitochondrial alterations in mice. Inflammopharmacology. http://www.citeulike.org/user/HEIRS/article/7474822
Yang, J.-Y. Y., Della-Fera, M. A. A., Rayalam, S., Ambati, S., Hartzell, D. L., Park, H. J. J., and Baile, C. A. (2008). Enhanced inhibition of adipogenesis and induction of apoptosis in 3t3-l1 adipocytes with combinations of resveratrol and quercetin. Life sciences, 82(19-20):1032-1039. http://www.citeulike.org/user/HEIRS/article/7537205
Pioglitazone. Wipedia. Retrieved on July 24, 2010. http://en.wikipedia.org/wiki/Pioglitazone
Caffeic Acid. Wipedia. Retrieved on July 24, 2010. http://en.wikipedia.org/wiki/Caffeic_Acid
Zhou, M., Wu, R., Dong, W., Jacob, A., and Wang, P. (2008). Endotoxin downregulates peroxisome proliferator-activated receptor-gamma via the increase in tnf-alpha release. Am J Physiol Regul Integr Comp Physiol, 294(1):R84-92. http://www.citeulike.org/user/HEIRS/article/2439726
Remillard, R. B. and Bunce, N. J. (2002). Linking dioxins to diabetes: epidemiology and biologic plausibility. Environmental health perspectives, 110(9):853-858. http://www.ncbi.nlm.nih.gov/pubmed/12204817
Kintscher, U. and Law, R. E. (2005). Ppargamma-mediated insulin sensitization: the importance of fat versus muscle. Am J Physiol Endocrinol Metab, 288(2):E287-291. http://www.citeulike.org/user/HEIRS/article/3824606
Shin, S., Wakabayashi, N., Misra, V., Biswal, S., Lee, G. H., Agoston, E. S., Yamamoto, M., and Kensler, T. W. (2007). Nrf2 modulates aryl hydrocarbon receptor signaling: Influence on adipogenesis. Mol. Cell. Biol., 27(20):7188-7197. http://www.citeulike.org/user/HEIRS/article/3787182
Klotz, L., Burgdorf, S., Dani, I., Saijo, K., Flossdorf, J., Hucke, S., Alferink, J., Novak, N., Beyer, M., Mayer, G., Langhans, B., Klockgether, T., Waisman, A., Eberl, G., Schultze, J., Famulok, M., Kolanus, W., Glass, C., Kurts, C., and Knolle, P. A. (2009). The nuclear receptor ppargamma selectively inhibits th17 differentiation in a t cell-intrinsic fashion and suppresses cns autoimmunity. J. Exp. Med., 206(10):2079-2089. http://www.citeulike.org/user/HEIRS/article/5778777
Liu, S. H. H., Yang, C. N. N., Pan, H. C. C., Sung, Y. J. J., Liao, K. K. K., Chen, W. B. B., Lin, W. Z. Z., and Sheu, M. L. L. (2010). Il-13 downregulates ppar-gamma/heme oxygenase-1 via er stress-stimulated calpain activation: aggravation of activated microglia death. Cellular and molecular life sciences : CMLS. http://www.citeulike.org/user/HEIRS/article/6826740
Schintu, N., Frau, L., Ibba, M., Caboni, P., Garau, A., Carboni, E., and Carta, A. R. (2009). Ppar-gamma-mediated neuroprotection in a chronic mouse model of parkinson's disease. The European journal of neuroscience, 29(5):954-963. http://www.citeulike.org/user/HEIRS/article/4136907
Miglio, G., Rosa, A. C., Rattazzi, L., Collino, M., Lombardi, G., and Fantozzi, R. (2009). Ppargamma stimulation promotes mitochondrial biogenesis and prevents glucose deprivation-induced neuronal cell loss. Neurochemistry international, 55(7):496-504. http://www.citeulike.org/user/HEIRS/article/5345204
Lee, Y., Shin, D.-H. H., Kim, J.-H. H., Hong, S., Choi, D., Kim, Y.-J. J., Kwak, M.-K. K., and Jung, Y. (2010). Caffeic acid phenethyl ester-mediated nrf2 activation and ikappab kinase inhibition are involved in nfkappab inhibitory effect: Structural analysis for nfkappab inhibition. European journal of pharmacology, 643(1):21-28. http://www.citeulike.org/user/HEIRS/article/7394789
Wednesday, June 16, 2010
Dioxin downregulation folate carrier transport through the AhR.
deregulation of this essential transport pathway represents a novel regulatory mechanism how dioxins display their toxic effects through the Ah receptorCiteULike: Dioxin mediates downregulation of the reduced folate carrier transport activity via the arylhydrocarbon receptor signalling pathway.: "Halwachs, S., Lakoma, C., Gebhardt, R., Schäfer, I., Seibel, P., and Honscha, W. (2010). Dioxin mediates downregulation of the reduced folate carrier transport activity via the arylhydrocarbon receptor signalling pathway. Toxicology and applied pharmacology, 246(1-2):100-106."
Saturday, April 24, 2010
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