Kumar said:Insulin called human insulin.
TT, sorry, it is differanciate. Still you could have understood it as BSM could.![]()
You mean "differentiate"? Rolfe answered you.
-TT
Kumar said:Insulin called human insulin.
TT, sorry, it is differanciate. Still you could have understood it as BSM could.![]()
What's wrong with you own Google?Kumar said:Can you give me any link/referance which mentions clinical trials in which BG levels are checked by reducing/discontinuing of diabetes oral medicines or injected insulin for some time in diabetic/IR patients?
Kumar said:Can you give me any link/referance which mentions clinical trials in which BG levels are checked by reducing/discontinuing of diabetes oral medicines or injected insulin for some time in diabetic/IR patients?
Kumar said:Can you give me any link/referance which mentions clinical trials in which BG levels are checked by reducing/discontinuing of diabetes oral medicines or injected insulin for some time in diabetic/IR patients?
That is ok, but I think there can be a limit of getting fat from extra sugar & carbs with extra insulin. Previously, I discussed somewhere that if IR for getting extra fat can also be there, but no one coul tell it properly. Can you tell if IR for getting fat (may be protiensalso) is there or not?ThirdTwin said:What do you mean by "checked"? Please further clarify.
In the meantime, I told you before - a long time ago - that you can make fat diabetics on insulin skinnier by adjusting their insulin dose downward and getting them to avoid excess dietary sugars and carbohydrates. If you get too much insulin without tight diabetic control, you will get fat.
-TT
Kumar said:That is ok, but I think there can be a limit of getting fat from extra sugar & carbs with extra insulin. Previously, I discussed somewhere that if IR for getting extra fat can also be there, but no one coul tell it properly. Can you tell if IR for getting fat (may be protiensalso) is there or not?
Kumar said:But here, I just want to be sure that if excess insulin in blood is not a cause of getting IR condition? It looks to me that clinical trials by reducung/discontinuing diabetic medicines in diabetic/IR patients are not yet done in view of anticipation/thinking of adversities. But I think it may mean something.
More commonly, people will develop insulin resistance (Type 2 Diabetes) rather than a true deficiency of insulin. In this case, the levels of insulin in the blood are similar or even a little higher than in normal, non-diabetic individuals. However, many cells of Type 2 diabetics respond sluggishly to the insulin they make and therefore their cells cannot absorb the sugar molecules well. This leads to blood sugar levels which run higher than normal. Occasionally Type 2 diabetics will need insulin shots but most of the time other methods of treatment will work.
http://www.endocrineweb.com/diabetes/2insulin.html
Kumar said:I don't understand, why question as asked in my last post always remains unawnsered. I have asked this question from so many reputed authorities in diabetes, but no one gives reply to me.???
Badly Shaved Monkey said:It's been answered several times, but since the problem of understanding seesm so profound let's try one more time.
The raised blood insulin in Type 2 diabetes is like shouting at a deaf person. As the person gets deafer you need to shout louder to get them to hear. The raised voice did not cause the deafness, the subsequently greater shouting does not make the deafness get worse it's just what has to be done to get the deaf person to hear what you are saying.
How are insulin resistance, pre-diabetes, and type 2 diabetes linked?
If you have insulin resistance, your muscle, fat, and liver cells do not use insulin properly. The pancreas tries to keep up with the demand for insulin by producing more. Eventually, the pancreas cannot keep up with the body's need for insulin, and excess glucose builds up in the bloodstream. Many people with insulin resistance have high levels of blood glucose and high levels of insulin circulating in their blood at the same time."
http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/
If you have insulin resistance, your body's cells do not respond well to insulin.
Insulin resistance is a stepping-stone to type 2 diabetes.
Lack of exercise and excess weight contribute to insulin resistance.
Engaging in moderate physical activity and maintaining proper weight can help prevent insulin resistance.
Two classes of drugs can improve response to insulin and are used by prescription for type 2 diabetes--biguanides and thiazolidinediones. Other medicines used for diabetes act by other mechanisms. Alpha-glucosidase inhibitors restrict or delay the absorption of carbohydrates after eating, resulting in a slower rise of blood glucose levels. Sulfonylureas and meglitinides increase insulin production.
The DPP showed that the diabetes drug metformin, a biguanide, reduced the risk of diabetes in those with pre-diabetes but was much less successful than losing weight and increasing activity. In another study, treatment with troglitazone, a thiazolidinedione later withdrawn from the market following reports of liver toxicity, delayed or prevented type 2 diabetes in Hispanic women with a history of gestational diabetes. Acarbose, an alpha-glucosidase inhibitor, has been effective in delaying development of type 2 diabetes. Additional studies using other diabetes medicines and some types of blood pressure medicines to prevent diabetes are under way. No drug has been approved by the Food and Drug Administration (FDA) specifically for insulin resistance or pre-diabetes.
In the past decade, improved knowledge about the pathology of type 2 diabetes has dramatically changed the options available to manage high blood glucose levels associated with type 2 diabetes. There are 3 major pathological processes involved in type 2 diabetes:
deficient secretion of insulin from the pancreas;
resistance to the physiologic effects of insulin; and
unrestrained production and release of glucose from the liver.
Medications used to treat type 2 diabetes alter these pathophysiological processes.
Some medications stimulate the pancreas to produce more insulin. All oral agents that stimulate increased insulin production can cause hypoglycemia.
Other drugs decrease insulin resistance at the tissue level or interfere with glucose production and release from the liver. A separate class of oral anti-diabetes agents slows the intestinal absorption of carbohydrates.
Oral anti-diabetes drugs are most commonly used for patients who are obese, are more than 40 years old, and have stable type 2 diabetes of less than 5 years duration. Oral anti-diabetes drugs are used as an adjunct to dietary and exercise management strategies to manage type 2 diabetes.
Oral anti-diabetes agents are not appropriate for patients with the following conditions:
Type 1 diabetes
Allergy to sulfonylurea compounds
Pregnancy or lactation – the effect of oral anti-diabetes agents on the fetus and newborn is unknown. Women who are attempting to become pregnant or who are unsure of when they might become pregnant should avoid using oral anti-diabetes agents.
Major surgery, serious infection, trauma, and conditions such as acute myocardial infarction – these are situations of high stress in which oral anti-diabetes agents are often ineffective in controlling high blood glucose levels.
Impaired hepatic or renal function – oral anti-diabetes agents are metabolized in the liver and most are excreted by the kidney. Serious episodes of hypoglycemia or worsening renal function can occur in patients with poor kidney or liver function.
Kumar writes:
Thanks for reply. Sorry but it didn't answer my question.
"Many people with insulin resistance have high levels of blood glucose and high levels of insulin circulating in their blood at the same time."
Elevated concentrations of glucose within the B cell ultimately leads to membrane depolarization and an influx of extracellular calcium. The resulting increase in intracellular calcium is thought to be one of the primary triggers for exocytosis of insulin-containing secretory granules. The mechanisms by which elevated glucose levels within the B cell cause depolarization is not clearly established, but seems to result from metabolism of glucose and other fuel molecules within the cell, perhaps sensed as an alteration of ATP:ADP ratio and transduced into alterations in membrane conductance.
Increased levels of glucose within B cells also appears to activate calcium-independent pathways that participate in insulin secretion.