View clinical trials related to Type1 Diabetes.
Filter by:Atmospheric pressure can influence how the body handles blood glucose. At high elevations, atmospheric pressure decreases. Research shows that both the elevation and the length of stay at that elevation can influence the body's glucose response. The investigators would like to find out if the change in pressure in the cabin environment during a flight affects the body's handling of glucose. Commercial planes usually fly at 40000 feet (12192 m) but the cabin pressure is re-pressurized to 8000 feet (2438 m) with cabin pressure fixed at 560 mmHg. The normal atmospheric pressure at sea level is 760 mmHg. Since the investigators cannot perform the studies in an aeroplane, a hypobaric chamber will be used to set to this low pressure which will reproduce the cabin environment during a commercial flight. The chamber is located at the research and development company, QinetiQ, MOD Boscombe. The objective of this study is to compare the effect of atmospheric pressure on glucose metabolism during simulated flight conditions during fasting and in response to a mixed liquid meal. This will involve attending three visits; visit 1 (screening), visit 2 and visit 4 and two phone visits. The duration of the study is 15 days or 1 month depending on the participant's availability. Visit 1, informed consent and screening, will take place at CEDAR, Royal Surrey County Hospital, Guildford, followed by two visits of the meal test in random order at CEDAR or QintetiQ, Visit 2, will be a meal test performed at 760 mmHg OR at 560mmHg. Visit 4, will be a further meal test at 560 mmHg OR 760 mmHg. The order of the meal test visits at different ambient pressures will be randomised. The two phone visits will take place the day after the meal test days to enquire about the patient's health after the test.
The overall objective of the study is to provide personalized nutritional advice based on the gut microbiota profile of children with type 1 diabetes (T1D) or obesity. Specifically, the primary objective of NUTRI-DIET is to validate a dietary model aimed at restoring bacterial species and/or anti-inflammatory metabolites in order to prevent extra-intestinal diseases characterized by dysbiosis, such as T1D and obesity. The primary endpoints of the study will be to monitor the glycemic control indices, i.e., blood glucose (mean of glycemic values, percentage of time-in-range value (TIR), which will be displayed by glycemic sensor) and glycated hemoglobin for diabetic children and Body mass index (BMI) z-score according to World Health Organization (WHO) recommendations (WHO BMI-for-age boys; WHO BMI-for-age girls) for obese children. The secondary objective of the study is to characterize the microbiota profile of the study patients and to test the algorithm under development built from the integration of diet and and gut microbiota composition data that were obtained during the previous observational study NUTRI-T1D.
Low Carbohydrate Diet (LCD) (< 130 g of carbohydrate per day) and ketogenic diet (< 50 g of carbohydrate per day) are popular among patients with type 1 diabetes (T1D). In most cases, LCD allow a better glycemic control and a important decrease of insulin requirements that cannot, however, be the sole result of low carbohydrate intake. However, due to the increase production of ketone bodies and the decrease of the insulin/glucagon rate, this diet is not without risk in T1D patients and some of them develop ketoacidosis. Type 1 diabetes is a autoimmune disease defined by the destruction of the pancreatic beta cells by the effector T cells, in condition of low regulatory T cells (Tregs). Indeed, some nutrients could regulate the plasticity and the function of Tregs, and be involved in the control of some autoimmune diseases in animals models thanks to a direct effect on immune cells of the digestive tract or an indirect effect by microbiota modulation. The study hypothesises that LCD may be able to restore residual insulin secretion in some patients by modulating immunity. The metabolic mechanisms leading to the effects described in patients with T1D patients under LCD have not been studied : in particular, there is no data on the evolution of the residual insulin secretion and no immunological parameter has been studied on these patients.