View clinical trials related to Hypoglycemia.
Filter by:This is a clinical study to examine rates hypoglycemia (self-report, EHR review, and review of values from a FDA approved continuous glucose monitoring system (CGMS)). Subjects will wear either blinded or unblinded CGMS. This is a 1:1 assignment with one group (50%) wearing 1 unblinded/1 blinded CGMS and the other group 50% wearing 2 blinded CGMS. The assignment will be computer based in a random fashion. Participants will continue with their usual diabetes management and glycemic monitoring profile as per usual. Those assigned to an unblinded CGMS can use the CGMS to manage their glucose levels at their own discretion. Individuals recruited will be those Type 2 diabetes who are deemed to be at high risk for hypoglycemia or low risk for hypoglycemia from a point score system established in an affiliated study.
This study tests the hypothesis that, compared to prior normal blood sugar, prior low blood sugar impairs cardiovascular autonomic function. The proposed studies will also test the hypothesis that the effects of prior low blood sugar on cardiovascular autonomic function are blocked by administration of a mineralocorticoid receptor antagonist.
We will study the effect of hypoglycemia (low blood sugar) on baroreflex sensitivity in participants with well controlled type 2 diabetes.
The investigator propose to test the safety and efficacy of a regimen that combines Omega-3 Fatty Acids and Vitamin D in a design that considers timing and duration of administration in relation to their effects and predicted synergies.
The purpose of this research study is to learn more about how sugar levels in the liver affect the ability of people both with and without type 1 diabetes. People with type 1 diabetes do not make their own insulin, and are therefore required to give themselves injections of insulin in order to keep their blood sugar under control. However, very often people with type 1 diabetes give themselves too much insulin and this causes their blood sugar to become very low, which can have a negative impact on their health. When the blood sugar becomes low, healthy people secrete hormones such as glucagon and epinephrine (i.e., adrenaline), which restore the blood sugar levels to normal by increasing liver glucose production into the blood. However, in people with type 1 diabetes, the ability to release glucagon and epinephrine is impaired and this reduces the amount of sugar the liver is able to release. People with type 1 diabetes also have unusually low stores of sugar in their livers. It has been shown in animal studies that when the amount of sugar stored in the liver is increased, it increases the release of glucagon and epinephrine during insulin-induced hypoglycemia. In turn, this increase in hormone release boosts liver sugar production. However, it is not known if increased liver sugar content can influence these responses in people with and without type 1 diabetes. In addition, when people with type 1 diabetes do experience an episode of low blood sugar, it impairs their responses to low blood sugar the next day. It is also unknown whether this reduction in low blood sugar responses is caused by low liver sugar levels. The investigators want to learn more about how liver sugar levels affect the ability to respond to low blood sugar.
Can a type 1 diabetic adult avoid low glucoses and regain hypoglycemia awareness using a hybrid closed loop insulin delivery system? Involvement is 22 months (13 visits) and includes a 4-week Screening Phase and an 18-month Intervention Phase. Participants will undergo 3 Hyperinsulinemic Clamps done at: Baseline (before starting the device and after completing the screening), 6 months (after using the device 6 months), and after using the device for 18 months. This metabolic testing will allow us to measure improvement in hypoglycemia awareness.
To determine the effect of sympathetic neural and hormonal (epinephrine) input on islet cell hormonal responses to insulin-induced hypoglycemia in type 1 diabetic recipients of intrahepatic islet transplantation. We hypothesize that α-adrenergic (neural) blockage will abolish insulin-mediated suppression of C-peptide, attenuating α-cell glucagon secretion during hypoglycemia, and that β-adrenergic (hormonal) blockage will have no effect. Glucose counterregulatory responses will be measured during hyperinsulinemic euglycemic-hypoglycemic clamps on three occasions with randomized, double-blind administration of the α-adrenergic blocker phentolamine, the β-adrenergic blocker propranolol, or placebo. The demonstration of neural rather than hormonal regulation of the transplanted islet cell response to hypoglycemia is critical for understanding the mechanism for protection from hypoglycemia afforded by intrahepatically transplanted.
This study is designed to evaluate the safety, efficacy, and pharmacokinetic profile of single ascending doses of exendin 9-39 administered by subcutaneous route in subjects with post-bariatric hypoglycemia.
Development of a training concept for health care professionals (nursing and medical staff), according to the current guidelines on treatment of in-patients with Diabetes. Primary endpoint is the change in hypoglycaemia rates comparing data before and after the training. Hereby we can derive the effects of staff training on the quality of health care in this patient population.
Current islet transplantation into the portal vein of the liver has shown the unique ability of islets to stabilize blood glucose levels and prevent severe hypoglycemia in a selected group of subjects with Type 1 diabetes. The main limitations of islet transplantation are the need for systemic immunosuppression to maintain function and the loss of islet function over time. Additionally, many studies have demonstrated that the current site of transplantation in the liver is not an ideal site due to several factors. These factors include (1) significant liver inflammation following islet infusion; (2) potential for life-threatening procedure-related complications such as bleeding and thrombosis; (3) high levels of immunosuppressive drugs and GI toxins in the liver contributing to islet toxicity; (4) the inability to retrieve islets after infusion; and (5) development of graft dysfunction in a number of recipients of intrahepatic allogeneic and autologous islets. The implantation of islets into the omentum will allow adequate engraftment of islets onto the omentum and will lead to comparable or superior functional and clinical outcomes than in the traditional intrahepatic site.