, the answer is yes.bedtime magnesium separately from a D3 by a few hours?
In non-plaque areas, the most notable immunostaining for Fetuin-A was seen in the Purkinje cells of the cerebellum in MS brains, a finding not seen in normal brains.
When researchers have measured seasonal variations in insulin levels in humans, they have invariably reported that insulin is highest in late fall and early winter -- twice as high, according to one 1984 study -- and lowest in late spring and early summer.
Numerous studies in Asia have demonstrated that compounds in turmeric can lead to a decrease in blood glucose, while increasing levels of blood insulin.
link1: Endocrinology. 2008 Jul;149(7):3549-58. Epub 2008 Apr 10. Links
Dietary curcumin significantly improves obesity-associated inflammation and diabetes in mouse models of diabesity.Weisberg SP, Leibel R, Tortoriello DV.
Russ Berrie Medical Science Pavilion, Diabetes and Endocrinology Research Center, Columbia University Medical Center, 1150 St. Nicholas Avenue, New York, NY 10032, USA.
Obesity is a major risk factor for the development of type 2 diabetes, and both conditions are now recognized to possess significant inflammatory components underlying their pathophysiologies. We tested the hypothesis that the plant polyphenolic compound curcumin, which is known to exert potent antiinflammatory and antioxidant effects, would ameliorate diabetes and inflammation in murine models of insulin-resistant obesity. We found that dietary curcumin admixture ameliorated diabetes in high-fat diet-induced obese and leptin-deficient ob/ob male C57BL/6J mice as determined by glucose and insulin tolerance testing and hemoglobin A1c percentages. Curcumin treatment also significantly reduced macrophage infiltration of white adipose tissue, increased adipose tissue adiponectin production, and decreased hepatic nuclear factor-kappaB activity, hepatomegaly, and markers of hepatic inflammation. We therefore conclude that orally ingested curcumin reverses many of the inflammatory and metabolic derangements associated with obesity and improves glycemic control in mouse models of type 2 diabetes. This or related compounds warrant further investigation as novel adjunctive therapies for type 2 diabetes in man.
PMID: 18403477 [PubMed - indexed for MEDLINE]
link1: Mol Nutr Food Res. 2008 Sep;52(9):995-1004. Links
Effect of curcumin supplementation on blood glucose, plasma insulin, and glucose homeostasis related enzyme activities in diabetic db/db mice.Seo KI, Choi MS, Jung UJ, Kim HJ, Yeo J, Jeon SM, Lee MK.
Department of Food and Nutrition, Sunchon National University, Jeonnam, Republic of Korea.
We investigated the effect of curcumin on insulin resistance and glucose homeostasis in male C57BL/KsJ-db/db mice and their age-matched lean non-diabetic db/+ mice. Both db/+ and db/db mice were fed with or without curcumin (0.02%, wt/wt) for 6 wks. Curcumin significantly lowered blood glucose and HbA 1c levels, and it suppressed body weight loss in db/db mice. Curcumin improved homeostasis model assessment of insulin resistance and glucose tolerance, and elevated the plasma insulin level in db/db mice. Hepatic glucokinase activity was significantly higher in the curcumin-supplemented db/db group than in the db/db group, whereas glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities were significantly lower. In db/db mice, curcumin significantly lowered the hepatic activities of fatty acid synthase, beta-oxidation, 3-hydroxy-3-methylglutaryl coenzyme reductase, and acyl-CoA: cholesterol acyltransferase. Curcumin significantly lowered plasma free fatty acid, cholesterol, and triglyceride concentrations and increased the hepatic glycogen and skeletal muscle lipoprotein lipase in db/db mice. Curcumin normalized erythrocyte and hepatic antioxidant enzyme activities (superoxide dismutase, catalase, gluthathione peroxidase) in db/db mice that resulted in a significant reduction in lipid peroxidation. However, curcumin showed no effect on the blood glucose, plasma insulin, and glucose regulating enzyme activities in db/+ mice. These results suggest that curcumin seemed to be a potential glucose-lowering agent and antioxidant in type 2 diabetic db/db mice, but had no affect in non-diabetic db/+ mice.
PMID: 18398869 [PubMed - in process]
link1: Kidney Int. 2008 Oct 29. [Epub ahead of print]
Inhibition of C-jun N-terminal kinase improves insulin sensitivity but worsens albuminuria in experimental diabetes.Ijaz A, Tejada T, Catanuto P, Xia X, Elliot SJ, Lenz O, Jauregui A, Saenz MO, Molano RD, Pileggi A, Ricordi C, Fornoni A.
 1Division of Nephrology and Hypertension, University of Miami Miller School of Medicine, Miami, Florida, USA  2Diabetes Research Institute, University of Miami Miller School of Medicine, Miami, Florida, USA.
C-jun N-terminal kinase (JNK) regulates both the development of insulin resistance and inflammation. Podocytes of the widely used db/db mouse model of diabetic nephropathy lose their ability to respond to insulin as albuminuria develops, in comparison to control db/+ mice. Here we tested whether JNK inhibition or its gene deletion would prevent albuminuria in experimental diabetes. Phosphorylated/total JNK was significantly increased in vivo in glomeruli of db/db compared to db/+ mice. Treatment of podocytes isolated from these two strains of mice with tumor necrosis factor-alpha caused greater phosphorylation of JNK in those obtained from diabetic animals. When db/db mice were treated with a cell-permeable TAT-JNK inhibitor peptide, their insulin sensitivity and glycemia significantly improved compared to controls. We induced diabetes in JNK1 knockout mice with streptozotocin and found that they had significantly better insulin sensitivity compared to diabetic wild-type or JNK2 knockout mice. Albuminuria was, however, worse in all mice treated with the JNK inhibitor and in diabetic JNK2 knockout mice compared to controls. Nephrin expression was also reduced in JNK inhibitor-treated mice compared to controls. A similar degree of mesangial expansion was found in all diabetic mice. Our study shows that targeting JNK to improve systemic insulin sensitivity does not necessarily prevent diabetic nephropathy.Kidney International advance online publication, 29 October 2008; doi:10.1038/ki.2008.559.
PMID: 18971923 [PubMed - as supplied by publisher]
Isn't that a stretch? I remember looking for the link previously, and didn't find any text that made the same connection / leap between the two. I think the Wiki says IGF-1 can bind to some similar things insulin can (nice and general when you don't know what your talking about ), but not that insulin acts in anyway like IGF?lyndacarol wrote:... insulin growth factor (and, therefore, insulin) increases myelination...
The capability of adeno-associated virus (AAV) to be retrogradely transported efficiently from muscle to motor neurons of the spinal cord was used to overcome the difficulty routinely encountered when attempting chronic delivery of molecules into the CNS.
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