T1D (T1D) is dramatically increasing in children and adolescents and there is a growing need for viable treatment options. Many factors are associated with glycemic control, including fat, carbohydrate, and protein, as well as more specific aspects of these macronutrients. Carbohydrates have been shown time and time again to be significantly associated with postprandial glucose. To pinpoint which aspect of carbohydrates has a significant effect on postprandial glucose, it’s important that we explore the relationship between them.
20 adolescent males and females between the ages of 11 and 18 were given 6 days of meals constructed by researchers to mimic the DASH diet guidelines. Previous research has shown DASH diet guidelines to have a significant impact on postprandial glucose. Participants consumed the foods at their usual …show more content…
Chronic inflammation causes the islet beta cells to undergo apoptosis and further the immune response (Kitagawa). This process inhibits the islet beta cells’ function of sensing glucose in circulation and releasing insulin to increase the body’s glucose uptake capability. Some of the differentiated T cells remain as memory cells, continuing the destruction process (Acharjee). The destruction of these cells results in decreased glucose control, which can contribute to both hypoglycemia and ketoacidosis, even if insulin is utilized correctly. T1Ddevelops over the course of many years. The first stage, or preclinical phase, of T1D is defined as the point at which beta cell destruction takes place. The disease is not fully developed until insulin production is unable to maintain normal glucose metabolism and inhibit fatty acid metabolism (Gan). This disease is not widely understood and is associated with an increased risk of mortality that expands further with poor glucose
20 adolescent males and females between the ages of 11 and 18 were given 6 days of meals constructed by researchers to mimic the DASH diet guidelines. Previous research has shown DASH diet guidelines to have a significant impact on postprandial glucose. Participants consumed the foods at their usual …show more content…
Chronic inflammation causes the islet beta cells to undergo apoptosis and further the immune response (Kitagawa). This process inhibits the islet beta cells’ function of sensing glucose in circulation and releasing insulin to increase the body’s glucose uptake capability. Some of the differentiated T cells remain as memory cells, continuing the destruction process (Acharjee). The destruction of these cells results in decreased glucose control, which can contribute to both hypoglycemia and ketoacidosis, even if insulin is utilized correctly. T1Ddevelops over the course of many years. The first stage, or preclinical phase, of T1D is defined as the point at which beta cell destruction takes place. The disease is not fully developed until insulin production is unable to maintain normal glucose metabolism and inhibit fatty acid metabolism (Gan). This disease is not widely understood and is associated with an increased risk of mortality that expands further with poor glucose