Skip to comments.Indian scientists claim to have found 'cure' for diabetes
Posted on 01/07/2004 1:04:15 AM PST by TheConservator
Indian scientists claimed to have developed a "cure" to diabetes from a plant found in West Bengal's Purulia hills.
"The drug - 'ICB201' - has been derived from a plant after it was noticed that people in Purulia hills used it in case of diabetic problems," Dr S Bhattacharya of Indian Institute of Chemical Biology, Kolkata, whose team developed the drug, said at the Science Congress on Tuesday evening.
Bhattacharya, while delivering the BC Guha Memorial Award Lecture on "Confronting Diabetic Type II: A global Epidemic", claimed "probably the answer to 'Type-II' diabetes has been found".
Asserting that earlier there was "practically no drug to treat the Type II diabetes", he said 'ICB201' acts by lowering the fatty acid levels in blood. Higher levels of fatty acids in blood diminish activity of insulin which causes diabetes".
The Phase I toxicity studies on mice have been carried out and the data would be submitted to concerned authorities. Phase II studies would start in about two-three months and the drug is likely to hit the market in next two to three years, Bhattacharya said.
Pointing out that patents were being filed for the "invention", he said work on the medicine started four years back. However, he refused to reveal the name of the plant.
Bhattacharya said "it is now being realised that more than glucose, it is the levels of fatty acids which play more important role in diabetes. The disease was being found even in thin people. In fact it was shown in animals that if fat is removed, diabetes manifests and if fat is replaced, diabetes disappears."
It happens because fat cells take fatty acids from circulation thus lowering their levels, he said.
"Over 95 per cent of all diabetic patients suffer from type II diabetes. Both Type I and Type II diabetes are characterised by an increase in blood sugar.
"While in Type I, there is deficiency of insulin, Type II is independent of insulin. However, in both the types, levels of glucose rise in the blood," he said.
In Type II diabetes, the insulin, though present, is unable to act, thereby leading to enhanced glucose levels, he said, adding "currently both the disease types are treated by giving insulin to the patients which actually can do harm."
Seems to me we're already finding a "cure" to diabetes, at least as a preventative step. By getting the tons of stinkin' sugars, processed junk and additives out of our diets. Couldn't changing the diets to those with diabetes help reverse it?
Exp Clin Endocrinol Diabetes. 2001;109(4):S516-26..
Triglycerides, fatty acids and insulin resistance--hyperinsulinemia.
Kraegen EW, Cooney GJ, Ye J, Thompson AL. Garvan Institute of Medical Research, St Vincent's Hospital. Sydney NSW, Australia.
There is now much interest in the mechanisms by which altered lipid metabolism might contribute to insulin resistance as is found in Syndrome X or in Type II diabetes. This review considers recent evidence obtained in animal models and its relevance to humans, and also likely mechanisms and strategies for the onset and amelioration of insulin resistance. A key tissue for development of insulin resistance is skeletal muscle. Animal models of Syndrome X (eg high fat fed rat) exhibit excess accumulation of muscle triglyceride coincident with development of insulin resistance. This seems to also occur in humans and several studies demonstrate increased muscle triglyceride content in insulin resistant states. Recently magnetic resonance spectroscopy has been used to demonstrate that at least some of the lipid accumulation is inside the muscle cell (myocyte). Factors leading to this accumulation are not clear, but it could derive from elevated circulating free fatty acids, basal or postprandial triglycerides, or reduced muscle fatty acid oxidation.
Supporting a link with adipose tissue metabolism, there appears to be a close association of muscle and whole body insulin resistance with the degree of abdominal obesity. While causal relationships are still to be clearly established, there are now quite plausible mechanistic links between muscle lipid accumulation and insulin resistance, which go beyond the classic Randle glucose-fatty acid cycle. In animal models, dietary changes or prior exercise which reduce muscle lipid accumulation also improve insulin sensitivity. It is likely that cytosolic accumulation of the active form of lipid in muscle, the long chain fatty acyl CoAs, is involved, leading to altered insulin signalling [sic] or enzyme activities (eg glycogen synthase) either directly or via chronic activation of mediators such as protein kinase C. Unless there is significant weight loss, short or medium term dietary manipulation does not alter insulin sensitivity as much in humans as in rodent models, and there is considerable interest in pharmacological intervention. Studies using PPARgamma receptor agonists, the thiazolidinediones, have supported the principle that reduced muscle lipid accumulation is associated with increased insulin sensitivity. Other potent systemic lipid-lowering agents such as PPARalpha receptor agonists (eg fibrates) or antilipolytic agents (eg nicotinic acid analogues) might improve insulin sensitivity but further work is needed, particularly to clarify implications for muscle metabolism. In conclusion, evidence is growing that excess muscle and liver lipid accumulation causes or exacerbates insulin resistance in Syndrome X and in Type II diabetes; development of strategies to prevent this seem very worthwhile.
I will say that many "low fat" foods (soup especially) bump up the sodium content for flavor. I have found some low sodium/low fat soups (and could probably make such a thing myself in the kitchen).
I'd much rather fight diabetes with diet and exercise than to take the pills this article is talking about.
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