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05-04-2012, 05:42 PM | #11 | ||
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Senior Member
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This is incredible, Rick, thank you so much for sharing. I wonder, though, what do we do about this? How can we not take sinemet? Maybe the fermented papaya and fava bean therapies are better than levodopa for more reasons than I thought....
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05-04-2012, 07:37 PM | #12 | |||
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In Remembrance
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I may have already posted this in the doc I sent, but if not, once one wades through the following to their conclusion, it seems that working and stretching the long muscles may counter the effect, at least partially. -Rick
1: Am J Physiol Endocrinol Metab. 2005 Aug;289(2):E241-50. Epub 2005 Mar 1. Contraction activates glucose uptake and glycogen synthase normally in muscles from dexamethasone-treated rats. Ruzzin J, Jensen J. Dept. of Physiology, National Institute of Occupational Health, PO Box 8149 Dep., N-0033, Oslo, Norway. Glucocorticoids cause insulin resistance in skeletal muscle. The aims of the present study were to investigate the effects of contraction on glucose uptake, insulin signaling, and regulation of glycogen synthesis in skeletal muscles from rats treated with the glucocorticoid analog dexamethasone (1 mg x kg(-1) x day(-1) ip for 12 days). Insulin resistance in dexamethasone-treated rats was confirmed by reduced insulin-stimulated glucose uptake (approximately 35%), glycogen synthesis (approximately 70%), glycogen synthase activation (approximately 80%), and PKB Ser(473) phosphorylation (approximately 40%). Chronic dexamethasone treatment did not impair glucose uptake during contraction in soleus or epitrochlearis muscles. In epitrochlearis (but not in soleus), the presence of insulin during contraction enhanced glucose uptake to similar levels in control and dexamethasone-treated rats. Contraction also increased glycogen synthase fractional activity and dephosphorylated glycogen synthase at Ser(645), Ser(649), Ser(653), and Ser(657) normally in muscles from dexamethasone-treated rats. After contraction, insulin-stimulated glycogen synthesis was completely restored in epitrochlearis and improved in soleus from dexamethasone-treated rats. Contraction did not increase insulin-stimulated PKB Ser(473) or glycogen synthase kinase-3 (GSK-3) phosphorylation. Instead, contraction increased GSK-3beta Ser(9) phosphorylation in epitrochlearis (but not in soleus) in muscles from control and dexamethasone-treated rats. In conclusion, contraction stimulates glucose uptake normally in dexamethasone-induced insulin resistant muscles. After contraction, insulin's ability to stimulate glycogen synthesis was completely restored in epitrochlearis and improved in soleus from dexamethasone-treated rats. PMID: 15741240 [PubMed - indexed for MEDLINE]
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
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"Thanks for this!" says: | Conductor71 (05-05-2012) |
05-05-2012, 10:26 AM | #13 | |||
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Senior Member
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Thanks so much Rick for giving me all the research ammo I could have; that annotated review article is a treasure- have never seen anything else like it.
Well off to get that glucose monitor today...still trying to get a recommendation on an endo. |
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