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 mealtime, and documented foods consumed, time consumed and corresponding insulin dosage. A continuous glucose monitor was installed prior to consumption of test foods, and researchers combined this information with usual mealtime, documented foods consumed, time consumed, and corresponding insulin dosage. A linear regression analysis was run to determine if there was a relationship between postprandial glucose and the amount of fiber consumed. A separate analysis was run for each time point specified (30, 60, 90, 120, 150, 180 minutes postprandial) to determine the relationship between energy, fat, fiber, carbohydrate, time, date, time postprandial and patient ID as well as fiber area under the curve. It was determined that no significant relationship exists other than fiber area under the curve and postprandial glucose (ps usual intake. Literature Review What is T1D? T1D is defined as an autoimmune disease in which the body’s own immune system attacks islet beta cells, pancreatic cells that produce insulin (Acharjee, Bluestone). …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 control. Causes of T1D The direct cause of T1D onset is uncertain, however genetic factors, environmental factors, and viral infections are suspected to contribute. Greater than 85% of diagnosed T1D cases occur in the absence of an affected first-degree relative, however genetics is still considered a potent factor in the development of T1D (Acharjee, Gan). Studies have indicated that the Coxsackie virus B4 could have a part in the development of T1D, however little is known of the mechanism for which this occurs. Environmental factors also have an impact on the development of T1D. Studies have been conducted in different parts of the world with people of similar race and have found differences in the prevalence of diabetes. This suggests that environmental
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 mealtime, and documented foods consumed, time consumed and corresponding insulin dosage. A continuous glucose monitor was installed prior to consumption of test foods, and researchers combined this information with usual mealtime, documented foods consumed, time consumed, and corresponding insulin dosage. A linear regression analysis was run to determine if there was a relationship between postprandial glucose and the amount of fiber consumed. A separate analysis was run for each time point specified (30, 60, 90, 120, 150, 180 minutes postprandial) to determine the relationship between energy, fat, fiber, carbohydrate, time, date, time postprandial and patient ID as well as fiber area under the curve. It was determined that no significant relationship exists other than fiber area under the curve and postprandial glucose (ps usual intake. Literature Review What is T1D? T1D is defined as an autoimmune disease in which the body’s own immune system attacks islet beta cells, pancreatic cells that produce insulin (Acharjee, Bluestone). …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 control. Causes of T1D The direct cause of T1D onset is uncertain, however genetic factors, environmental factors, and viral infections are suspected to contribute. Greater than 85% of diagnosed T1D cases occur in the absence of an affected first-degree relative, however genetics is still considered a potent factor in the development of T1D (Acharjee, Gan). Studies have indicated that the Coxsackie virus B4 could have a part in the development of T1D, however little is known of the mechanism for which this occurs. Environmental factors also have an impact on the development of T1D. Studies have been conducted in different parts of the world with people of similar race and have found differences in the prevalence of diabetes. This suggests that environmental