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....

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]

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.