Diabetes prevention is as basic as eating more healthfully, becoming more physically active and losing a few extra pounds. It's never too late to start. Making a few simple changes in your lifestyle now may help you avoid the serious health complications of diabetes in the future, such as nerve, kidney and heart damage. Consider these diabetes prevention tips from the American Diabetes Association.
Research shows that aerobic exercise and resistance training can help control diabetes. The greatest benefit comes from a fitness program that includes both. It's not clear why, but whole grains may reduce your risk of diabetes and help maintain blood sugar levels. Try to make at least half your grains whole grains. Many foods made from whole grains come ready to eat, including various breads, pasta products and cereals.
Look for the word "whole" on the package and among the first few items in the ingredient list. If you're overweight, diabetes prevention may hinge on weight loss. Every pound you lose can improve your health, and you may be surprised by how much. Participants in one large study who lost a modest amount of weight — around 7 percent of initial body weight — and exercised regularly reduced the risk of developing diabetes by almost 60 percent.
Low-carb diets, the glycemic index diet or other fad diets may help you lose weight at first.
But their effectiveness at preventing diabetes and their long-term effects aren't known. And by excluding or strictly limiting a particular food group, you may be giving up essential nutrients and often craving such foods. Instead, make variety and portion control part of your healthy-eating plan.
Share your concerns about diabetes prevention with your doctor. He or she will appreciate your efforts to prevent diabetes and may offer additional suggestions based on your medical history or other factors. Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission.
A single copy of these materials may be reprinted for noncommercial personal use only. Therefore, the dose would have to be reduced in patients with clinically significant liver disease.
Its action is based on the fact that although the response to glucose is lost in the first phase of insulin secretion, the response to certain amino acids like phenylalanine is conserved. Its pharmacokinetics are very similar to those of repaglinide, but with a still more rapid onset and disappearance of action, which causes an earlier and intense peak insulin secretion that disappears sooner. Therefore, the preprandial delay is shorter, as are possible late hypoglycemic crises. The best dose-response effectiveness is obtained with mg.
The history of the biguanides dates back to the Middle Ages, when the legume Galega officinalis , whose active principle is guanidine or galegin, was used for the treatment of diabetes mellitus.
Sintalin was introduced in Germany in but its toxic effects made it unusable. Between and , the biguanides were introduced on the market fenformin, buformin, and metformin and became very popular. Since metformin has again been made available on the U. At present it is one of the drugs most used in the treatment of type 2 diabetes. The biguanides, unlike the SUs, do not stimulate insulin secretion by the pancreatic beta cells. Therefore, strictly speaking they cannot be considered hypoglycemic agents because they only reduce glycemia in diabetic patients.
Their main mechanism of action is to reduce hepatic glucose production by decreasing both glyconeogenesis and glycogenolysis. Thus, it has been demonstrated that metformin favors the action of insulin in muscle tissue at different levels: by increasing the number of receptors and the affinity of insulin for its receptors, facilitating glucose transport through an increase in the expression, or activity, of GLUT-4, and stimulating non-oxidative glucose metabolism, which translates into an increase in glycogen deposits.
It is clear that metformin improves sensitivity to insulin and is a drug of first choice when insulin resistance is the predominant mechanism in the etiopathogenesis of diabetes.. Aside from reducing glycemia levels, the biguanides exercise other effects that are especially beneficial for diabetic patients. The biguanides are absorbed quickly in the small intestine and only fenformin binds to plasma proteins and suffers partial hepatic metabolization. Buformin and metformin do not bind to plasma proteins and are eliminated unchanged by the kidney. Peak plasma metformin concentration is reached h after it is taken.
It can be given two or three times a day. Undesirable effects and contraindications. These effects include anorexia, nausea, vomiting, abdominal discomfort, and a metallic taste, but undoubtedly the most frequent of them is diarrhea. A disorder in vitamin B 12 absorption has been reported in patients treated during prolonged periods. However, it has scant clinical repercussions. It is also prudent to discontinue the drug temporarily when radiological contrast is injected, due to the risk of acute kidney failure.
Although no studies have demonstrated teratogenic capacity or the ability to cross the placenta, its use is not recommended during pregnancy or breastfeeding. Drug selection and indications. As has been mentioned, the only biguanide recommended for clinical use is metformin. It is the drug of choice in overweight type 2 diabetics, since insulin resistance generally predominates over deficient insulin secretion in such cases. This minimizes side effects, especially diarrhea and other digestive problems, which are the main cause of withdrawal from treatment.
The therapeutic effectiveness of metformin is unquestioned and is comparable to that of the SUs. In addition, it is not associated with weight gain. In the UKDPS study, metformin was the only medication associated with a reduction in mortality in diabetic patients.
Aside from reducing microangiopathic complications, it also significantly reduced the risk of AMI and cerebrovascular accidents. Although this association has been demonstrated to be very effective, 42,53,55,56 due to the progressive nature of diabetes, the secretory capacity of the beta cell will deteriorate with time and many patients will require insulin.
In these cases, as long as a certain insulin secretion capacity persists, it is preferable to use combined therapy with oral drugs and to add insulin as a nocturnal dose administered before bedtime. Another option is to discontinue treatment with secretagogues and to use treatment with metformin and insulin.
This group of drugs of recent appearance have an action based on increasing sensitivity to insulin. In the first drug in this group, ciglitazone, was discovered, but it was not marketed due to its elevated toxicity. Since the mids, derivatives with a better safety profile have been developed: troglitazone, pioglitazone, and rosiglitazone. Mechanism of action, indications, and clinical effectiveness. This causes an increase in insulin-mediated peripheral uptake of glucose by muscle and adipose tissue.
This reduces lipolysis and results in a decrease in circulating free fatty acids, consequently improving insulin resistance. Since they act as insulin-sensitizing agents or, w, reducers of insulin resistance, their clinical effectiveness is clearly related with the presence of an insulin reserve. They do not reduce glucose levels in healthy subjects or in diabetics with clear insulinopenia unless they are administered in association with insulin. Its maximum concentration is reached within an hour of intake, plasma half-life is 3.
Its hypoglycemic action is dose-dependent and, in theory, it can be used in monotherapy or combined with secretagogues, metformin, or insulin. Nevertheless, the European Agency for the Evaluation of Medicinal Products so far has only approved its clinical use in combination with metformin in obese patients, or with SUs in cases in which metformin is contraindicated or not tolerated. The TZDs stimulate glucose uptake by insulin-sensitive tissues, whereas the main mechanism of action of metformin lies in the inhibition of hepatic glucose production and that of the SUs is based on an increase in endogenous insulin levels.
Therefore, it is logical that the combination of TZD with either metformin or SU has been shown to be very effective. Aside from significantly reducing baseline glycemia, postprandial glycemia, insulinemia, and HbA 1c , they change the lipid profile. Side effects and contraindications. The most serious toxic effect of the TZDs has been hepatoxicity. In sporadic cases, severe hepatocellular lesions that caused the death of the patients was documented, so it was withdrawn from the market.
Mild decreases in hematocrit and hemoglobin levels have been reported that do not seem to be related to disturbances in erythropoiesis and could be attributed to an increase in plasma volume. In addition, structural and functional cardiac disorders have also been communicated, but these effects have not been observed with rosiglitazone. At present, studies in humans have not included women who were pregnant or breastfeeding, or patients under the age of 18 years; therefore, TZDs cannot be used in such patients.