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Trending Topics. What Parents Need to Know. How to Treat Reactive Hypoglycemia Low blood sugar after a meal can leave you woozy and shaken but there are natural ways to treat it and get feeling right. There are different types of hypoglycemia. One type occurs in people who have diabetes, and doctors classify this as diabetic hypoglycemia.
It happens when the insulin injections or antidiabetic medication that a person takes removes too much sugar from the bloodstream. Reactive hypoglycemia is a rare form of the condition, which doctors classify as nondiabetic hypoglycemia. This often occurs approximately 2—4 hours after a meal.
Symptoms subside quickly after eating or drinking carbohydrates. Researchers have not yet fully identified the specific causes of reactive hypoglycemia. However, the condition stems from having too much insulin in the bloodstream at the wrong time. People with reactive hypoglycemia may experience some or all of the following symptoms 2—4 hours after a meal:. Most people who have reactive hypoglycemia do not require treatment.
Rather, doctors recommend dietary changes to manage the symptoms. That said, if a person needs immediate treatment, doctors advise eating or drinking something that contains 15 grams of carbohydrates.
Half a cup of juice contains this amount, but the juice should be the regular variety rather than a low calorie version that contains fewer carbohydrates. One study reports that certain people with reactive hypoglycemia may also benefit from taking antidiabetic drugs, such as metformin. Diabetes diet: Create your healthy-eating plan Diabetes foods: Can I substitute honey for sugar? Diabetes and liver Diabetes management: Does aspirin therapy prevent heart problems?
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Legal Conditions and Terms Any use of this site constitutes your agreement to the Terms and Conditions and Privacy Policy linked below. Advertising Mayo Clinic is a nonprofit organization and proceeds from Web advertising help support our mission. Thus, patients with hypoglycemia at 4 or 5 h who have a family history of diabetes and obesity may be more susceptible to diabetes than patients with hypoglycemia at 3 h.
Therefore, people with RH along with weight gain and with diabetes history in the family will benefit from a lifestyle modification as well as the appropriate antidiabetic approach in the prevention of diabetes.
RH clinically seen in three different forms as follows: idiopathic RH at min , alimentary within min and late RH at — min. Lack of first-phase insulin release, an excellent predictor of both types of diabetes, is thought to be the earliest sign of the adverse effects of hyperglycemia on beta-cells and insulin-sensitive tissues.
Thus, patients with hypoglycemia at 4 or 5 h who have those with a higher number of people with diabetes in the first-degree relative and who have obesity may be more susceptible to diabetes than patients with hypoglycemia at 3 h. Reactive hypoglycemia is seen in prediabetic states and diabetic patient diabetic RH , gastrointestinal dysfunction alimentary RH , and patients with hormone deficiency states hormonal RH.
However, large patient group characterized as having idiopathic RH. The reason for alimentary, hormonal, and diabetic RH is clear, whereas the idiopathic RH is complex. Characteristic alterations in insulin secretion accompany each of these conditions. Elevated insulin levels usually account for the hypoglycemia.
Some patients rarely show increased insulin sensitivity. In alimentary RH, rapid gastric emptying and increased plasma GLP-1 levels precede RH after oral glucose loading in gastrectomy patients,[ 4 ] most patients with idiopathic RH have a delayed insulin secretion that occurs inappropriately in conjunction with falling levels of plasma glucose. Elevated insulin levels also cause down-regulation of the insulin postreceptor signals on the muscle and fat cells, thus decreases insulin sensitivity.
Neither the OGTT nor the mixed meal test is really a suitable this diagnosis because they show false-positive and false-negative results, respectively. Occurring late postprandially hypoglycemia with a family history of diabetes, even if they are lean, should be considered at potential risk of diabetes in the future in patients with late RH. Insulin secretion is secreted in phases called the first and second phases.
The first phase of insulin is the rapid release of ready insulin in the first 10 minutes. Second phase insulin which is the slowly released insulin in 24 hours. Loss of first-phase insulin secretion and decreased second-phase insulin secretion are characteristic features of type 2 diabetes. In the early period of type 2 diabetes and in IGT, the first-phase insulin secretion declines with the loss.
Hypoglycemia, which occurs mostly after hours of food intake, is called postprandial reactive hypoglycemia. Prediabetes is an intermediate hyperglycaemia state with a high risk for type 2 diabetes. Until , only impaired glucose tolerance IGT was described as a transition from normal glucose tolerance to type 2 diabetes.
Prediabetes is a sign that the risk of developing diabetes is high in the future and poses a high risk not only for diabetes but also for cardiovascular diseases. Cardiovascular mortality is also significantly increased in prediabetic patients compared to patients with normal blood glucose.
Previous prospective randomized trials have shown that lifestyle modifications and pharmacological agents significantly reduce the risk of developing Type 2 DM and cardiovascular risk factors in prediabetic patients. These results indicate more exact insulin resistance in RH at 4 h or 5 h than in RH at 3 h. However, the origin of insulin resistance is different. Studies on hyperglycemia showed that the first and second phase of insulin secretion was significantly reduced in IGT.
A recent study showed that the first phase insulin secretion was significantly reduced in both IFG and IGT, while the second phase insulin secretion was only reduced in IGT.
It has been demonstrated that the effect of incretin is impaired with no decrease in GLP-1 or GIP levels as glucose sensitivity decreases in studies of obese dysglycemic teens.
Lupoli et al. Suggests that GLP-1 may be involved in the pathogenesis of idiopathic reactive hypoglycemia without prediabetes. Indeed, GLP-1 secretion was increased in the first 30 minutes. Insulin secretion was increased in the following 90 minutes after glucose load in IRH individuals. At the same time that there was suppression of glucagon secretion at min and a decrease in blood glucose levels at min. Incretin hormones potentiate the stimulus to insulin secretion in the postprandial period have been implicated as additional factors in the pathogenesis of type 2 diabetes.
Recently, studies demonstrated that potential role of these peptides in the abnormal handling of glucose by splanchnic tissues and perhaps, in decline in beta-cell insulin secretion. Early reactive hypoglycemia occurs in the first hours of OGTT. It may be due to accelerated gastric emptying, or exaggerated incretin effect. It is also possible that accelerated gastric emptying leads to increase of incretin. Insulin secretion increases in response to oral glucose stimulation. This occurs through increased glucagon-like peptide-1 GLP-1 and glucose-dependent insulinotropic polypeptide GIP and ultimately leads to hyperglycaemia with excessive insulin exocytosis and early upregulation of GLUT 4 channels.
In addition to increased insulin secretion, GLP-1 by suppressing the glucagon causes an insufficient response to hypoglycemia and accelerated gastric emptying, leading to early hypoglycemia.
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