That does not make it the same. Many people have warm milk to help them sleep, and others have warm milk in their coffee, but a coffee is very different to a glass of warm milk.lyndacarol wrote:Growth factor is a component of insulin.
With diabetics injecting insulin every day, why are there studies on the effects of specific IGF-1? I think its because they are very different, and I have yet to read any scientific study saying they are in effect the same. I explicitly read effects for IGF-1, that are not suggested for "plain old" insulin. and I have also read how IGF-1 is different to the other IGF's (ie IGF-2, IGF-3 etc)lyndacarol wrote:They are in essence the same thing.
But IGF-1 will bind to components that insulin will not.lyndacarol wrote:If there are cells or substances that IGF (Insulin Growth Factor) will bind to, the growth factor in insulin will do the same.
but all the studies treat IGF-1 very differently to insulin, and I have yet to read the exact same effects for insulin, that are seen with IGF-1. A pure and concentrated component of something is not the same as what it is derived from.lyndacarol wrote:I do not believe the growth factor should act any differently if it is pure and concentrated from how it acts when in insulin.
To view or read the entire segment see:http://www.cbsnews.com/stories/2009/01/25/60minutes/main4752082.shtmlConvinced that they were on the right path, they fast-tracked the drug into human trials on people with untreated diabetes. The results were impressive: it significantly lowered glucose and insulin levels, without the patients changing their diet or taking any other drugs.
"Our hypothesis was that the metabolic syndrome is really a problem with how we store energy from food," Shulman explained. "The idea is that insulin resistance in muscle changes the pattern of energy storage."
After providing the study's subjects with two meals high in carbohydrates, Shulman and his colleagues turned to magnetic resonance spectroscopy to measure the production of liver and muscle triglyceride, the storage form of fat, and of glycogen, the storage form of carbohydrates. "What we found is that (insulin) sensitive individuals took the energy from carbohydrate in the meals and stored it away as glycogen in both liver and muscle," said Shulman.
In the insulin resistant subjects, the energy obtained from their carbohydrates rich meals was rerouted to liver triglyceride production, elevating triglycerides in the blood by as much as 60 percent and lowering HDL cholesterol (the good cholesterol) by 20 percent. "In contrast to the young, lean, insulin-sensitive subjects, who stored most of their ingested energy as liver and muscle glycogen, the young, lean, insulin-resistant subjects had a marked defect in muscle glycogen synthesis and diverted much more of their ingested carbohydrate into liver fat production," Shulman and his colleagues reported.
"What we see," he noted, "is alterations in patterns of energy storage. An additional key point is that the insulin resistance, in these young, lean, insulin resistant individuals, was if MS independent of abdominal obesity and circulating plasma adipocytokines, suggesting that these abnormalities develop later in the development of the metabolic syndrome."
The new findings promise to help untangle the early molecular events of a syndrome at the root of one of the world's most significant health issues. "Knowing how insulin resistance alters energy storage before it leads to more serious problems can help those susceptible prevent the onset of the metabolic syndrome," Shulman said.
Another key observation was that skeletal muscle insulin resistance precedes the development of insulin resistance in liver cells, and that fat production in the liver is increased. "These findings also have important implications for understanding the pathogenesis of nonalcoholic fatty liver disease, one of the most prevalent liver diseases in both adults and children Shulman said.
An American study has shown that glucosamine (often prescribed for joint problems) may cause insulin resistance.
lyndacarol wrote:Since I have suspected that glucosamine, a sugar-based supplement, and all artificial sweeteners stimulated the pancreas to produce insulin, I found the article's sentence especially interesting:
http://www.news-medical.net/health/Caus ... tance.aspxAn American study has shown that glucosamine (often prescribed for joint problems) may cause insulin resistance.
Has anyone seen this "American study?"
Mayo Clinic wrote:Question
Glucosamine: Does it affect blood sugar?
Is it safe to take glucosamine supplements if I have diabetes?
from Maria Collazo-Clavell, M.D.
Even though glucosamine is technically a type of sugar, it doesn't appear to affect blood glucose levels or insulin sensitivity. Some preliminary research had suggested that glucosamine might worsen insulin resistance, which can contribute to increases in blood sugar in people with type 2 diabetes. But subsequent studies refuted these findings.
Glucosamine is one of the most popular dietary supplements sold in the United States, although study results have been mixed regarding its ability to reduce osteoarthritis pain. While glucosamine doesn't appear to affect glucose levels or insulin sensitivity, the supplement can interact with other medications you might be taking — such as warfarin (Coumadin), a blood thinner.
lyndacarol wrote:NHE – a few more thoughts:
It is my understanding that "hyperinsulinemia (excess insulin)" is synonymous with "insulin resistance." The news-medical article stated "An American study has shown that glucosamine (often prescribed for joint problems) may cause insulin resistance."
Perhaps glucosamine does not raise blood glucose, just as the Mayo Clinic article does state (thank you so much, NHE, for that information), but affects only the pancreas and its insulin secretion.
Several years ago I read a Discover magazine article on artificial sweeteners; it was mentioned that artificial sweeteners increased insulin production in a mouse study. I suspect the same happens with humans. (Elsewhere, I have read that even a sweet sensation in the mouth causes the pancreas to secrete insulin.)
Although blood glucose is most commonly the trigger for insulin secretion, there may be MANY other reasons for the pancreas to pump out the hormone – the "sweetness" of artificial sweeteners, even infection of the pancreas by a virus or bacteria (even the inflammation of pancreatitis). I think the damaging culprit is insulin, not necessarily glucose.
Just sharing a few of my thoughts.
[b]Glucosamine-like supplement suppresses multiple sclerosis attacks
UCI study shows promise of metabolic therapy for autoimmune diseases
— Irvine, Calif., September 30, 2011 —
A glucosamine-like dietary supplement suppresses the damaging autoimmune response seen in multiple sclerosis, according to a UC Irvine study.
UCI’s Dr. Michael Demetriou, Ani Grigorian and others found that oral N-acetylglucosamine (GlcNAc), which is similar to but more effective than the widely available glucosamine, inhibited the growth and function of abnormal T-cells that in MS incorrectly direct the immune system to attack and break down central nervous system tissue that insulates nerves.
Study results appear online in The Journal of Biological Chemistry.
Earlier this year, Demetriou and colleagues discovered that environmental and inherited risk factors associated with MS — previously poorly understood and not known to be connected — converge to affect how specific sugars are added to proteins regulating the disease.
“This sugar-based supplement corrects a genetic defect that induces cells to attack the body in MS,” said Demetriou, associate professor of neurology and microbiology & molecular genetics, “making metabolic therapy a rational approach that differs significantly from currently available treatments.”
Virtually all proteins on the surface of cells, including immune cells such as T-cells, are modified by complex sugar molecules of variable sizes and composition. Recent studies have linked changes in these sugars to T-cell hyperactivity and autoimmune disease.
In mouse models of MS-like autoimmune disease, Demetriou and his team found that GlcNAc given orally to those with leg weakness suppressed T-cell hyperactivity and autoimmune response by increasing sugar modifications to the T-cell proteins, thereby reversing the progression to paralysis.
The study comes on the heels of others showing the potential of GlcNAc in humans. One reported that eight of 12 children with treatment-resistant autoimmune inflammatory bowel disease improved significantly after two years of GlcNAc therapy. No serious adverse side effects were noted.
“Together, these findings identify metabolic therapy using dietary supplements such as GlcNAc as a possible treatment for autoimmune diseases,” said Demetriou, associate director of UCI’s Multiple Sclerosis Research Center. “Excitement about this strategy stems from the novel mechanism for affecting T-cell function and autoimmunity — the targeting of a molecular defect promoting disease — and its availability and simplicity.”
He cautioned that more human studies are required to assess the full potential of the approach. GlcNAc supplements are available over the counter and differ from commercially popular glucosamine. People who purchase GlcNAc should consult with their doctors before use.[/b]
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