View clinical trials related to Diabetes Mellitus, Type 2.
Filter by:The present study seeks to tailor the original Program ACTIVE (Adults Coming Together to Increase Vital Exercise) to meet the cultural norms and needs of adult Black men with comorbid Type 2 diabetes and depression by using focus groups comprised of Black men with Type 2 diabetes. The use of peer perspectives allows for an improved strategy to reach, retain, and improve outcomes in this population. Following the tailoring of program materials, the intervention (Program ACTIVE) will be facilitated with Black men with comorbid Type 2 diabetes and depression using evidence-based cognitive behavioral therapy and community-based exercise interventions.
This phase III trial compares the effect of adding tocilizumab to standard of care versus standard of care alone in treating cytokine release syndrome (CRS) in patients with SARS-CoV-2 infection. CRS is a potentially serious disorder caused by the release of an excessive amount of substance that is made by cells of the immune system (cytokines) as a response to viral infection. Tocilizumab is used to decrease the body's immune response. Adding tocilizumab to standard of care may work better in treating CRS in patients with SARS-CoV-2 infection compared to standard of care alone.
Diabetes is a chronic disease that affects a large part of the United States population. The majority of patients with diabetes will experience gastrointestinal symptoms. One of the most troublesome gastrointestinal symptoms that diabetes can cause is diarrhea, otherwise known as "Diabetic Diarrhea." This occurs because diabetes does damage to nerves that control the gut and prevent it from functioning normally. Currently, there are only several medications used to treat the symptoms of Diabetic Diarrhea, but many of these medications have serious side effects or do not work well. We are investigating the drug eluxadoline for the treatment of Diabetic Diarrhea. Eluxadoline is a gut-specific medication that is FDA approved to treat diarrhea related to irritable bowel syndrome (IBS-D). Our hypothesis is eluxadoline will safely and successfully reduce diarrhea symptoms (number of stools and less liquid stools) and improve the quality of life in patients with Diabetic Diarrhea when compared with placebo. Each patient with Diabetic Diarrhea who participates will take both eluxadoline and a placebo drug at separate times over a period of several months as part of a crossover study design. While on each medication, eluxadoline or placebo, the participants will keep a diary of symptoms and will be followed by the medical team through a combination of office visits and questionnaires. There will be five planned office visits and intermittent phone calls (questionnaires, surveys) over the 140-day study period. Participants will not be permitted to use any other anti-diarrhea medication during the study period and will continue on medication for management of their diabetes.
Work Package 1: Observational cohort pilot safety study Work Package 2: Randomised, double-blind, placebo controlled pilot study Work Package 3: Observer-blind pilot RCT
This study compares the effect and safety of 2 dose schedules for semaglutide (study medicine) in people with type 2 diabetes previously treated with a diabetes medicine similar to semaglutide. The study will also evaluate the use of a new pen-injector for semaglutide used to inject medicine under the skin, at a new dose of 2 mg. People taking part in the study will take this medicine together with their current diabetes tablets other than semaglutide. Participants will either get a start dose of 0.25 mg semaglutide or 0.50 mg semaglutide, and the dose will be gradually increased to 2.0 mg semaglutide - which treatment is decided by chance. Participants will inject semaglutide under the skin once a week, any time of the day. When the dose reaches 2.0 mg semaglutide, participants will inject the medicine with a new type of pen-injector. The study will last for about 24 weeks. Participants will have 9 visits and 1 phone call with the study doctor. At 9 visits participants will have blood taken and at 2 visits they will have eye examination done. Women cannot take part if pregnant, breast-feeding or planning to become pregnant during the study period. Women who are able to get pregnant will be checked 10 times for pregnancy via urine tests.
The key purpose of this study is to determine and understand the safety and effectiveness of blue light phototherapy in the treatment and healing of infected diabetic wounds, as well as determining if this treatment is capable of reducing the bacterial population number within infected wounds. The investigators' lab recently discovered that a specific survival protein called catalase can be destroyed through blue light exposure. Given that a majority of bacteria species contains catalase, it is hypothesized that the destruction of this protein can improve the effectiveness of antimicrobial wound dressings commonly used to treat infected diabetic wounds, therefore further reducing the amount of bacteria within the wound and increasing the rate of healing. By reducing the overall bacterial population within these diabetic infected wounds, the ability for these diabetic wounds to heal will be enhanced, allowing for greater reductions in wound size over the course of the treatment. In this study, 40 subjects will be enrolled and randomly assigning subjects to either a control group or a phototherapy receiving experimental group. While control subjects will receive standard weekly debridement treatment procedures for infected diabetic ulcers, experimental subjects will receive standard weekly debridement treatment alongside 2 sessions of phototherapy every week over the course of 12 weeks. Bacterial swab samples will be taken alongside the excised debrided infect tissue for the purpose of bacterial population analysis. For each patient, the changes in total bacterial population, wound size, and subject satisfaction will be recorded and analyzed to determine the effectiveness of pulsed light phototherapy.
The diverse community of gut microbes commonly referred to as the 'gut microbiome', is increasingly suggested to play significant roles in health and disease, and to affect even distant non-GI organs by metabolite signaling. Type 2 diabetes mellitus (T2DM) patients feature a distinct gut microbiome signature4, while modulating the gut microbiome by either antibiotics or fecal microbial transplantation (FMT) is suggested to impact insulin sensitivity. Originally designed to treat obesity, bariatric surgeries often induce a robust and rapid weight-independent improvement in glucose homeostasis within days. Early diabetes remission following bariatric surgery is hypothesized to be mediated by rapid alterations in the gut microbiome and bile acids composition, however, the exact mechanism is yet to be uncovered. Elucidating this mechanism is important as it may form the basis of a new therapeutic modality in diabetes. The investigators intend to deeply characterize early post-bariatric changes in the gut microbiome of diabetic patients, as well as their gut mucosal transcriptome and metabolome, by using state-of-the-art experimental and computational pipelines. Additionally, The investigators will utilize a unique mouse model of bariatric surgery under germ-free conditions, developed at the Elinav lab, that allows us to dissect the role of microbes in post-operative metabolic improvements.
Primary Objective: • To compare the immunogenicity of Gan & Lee Insulin Lispro Injection and EU-authorized Humalog following treatment in adult subjects with T1DM Secondary Objectives: - To evaluate the safety of Gan & Lee Insulin Lispro Injection in comparison with that of EU authorized Humalog following treatment in adult subjects with T1DM - To evaluate the efficacy of Gan & Lee Insulin Lispro Injection in comparison with that of EU authorized Humalog following treatment in adult subjects with T1DM
Worldwide, diabetic kidney disease (DKD) is the most common cause of chronic and end stage kidney disease. Large-sized prospective randomized clinical trials indicate that intensified glucose and blood pressure control, the latter especially by using agents that interfere with the renin-angiotensin-aldosterone system (RAS), halts the onset and (particularly) the progression of DKD, in both type 1 Diabetes Mellitus (T1DM) and type 2 Diabetes Mellitus (T2DM) patients. However, despite the wide use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), a considerable amount of patients develop DKD (20-40%), indicating an unmet need for renoprotective therapies as DKD largely causes the increased mortality risk from cardiovascular disease (CVD) in people with diabetes. Sodium-glucose linked transporters (SGLT-2) inhibitors are a relatively novel glucose-lowering drug for the treatment of T2DM as they lower plasma glucose levels by blocking renal glucose reabsorption. In addition, these agents exert pleiotropic actions beyond glucose control. As such, SGLT-2 inhibitors decrease proximal sodium reabsorption, reduce blood pressure, body weight and uric acid. In large trials and likely through these pleiotropic effects, SGLT2 inhibitors reduce cardiovascular mortality, hospitalization for heart failure and reduce end stage kidney disease. At this point in time, the renoprotective mechanisms involved with SGLT-2 inhibition still remain speculative, though a consistent finding is that SGLT-2 inhibitors reduce estimated eGFR after first dosing, which is reversible after treatment cessation. This "dip" indicates a renal hemodynamic phenomenon reminiscent of the RAS blockers and is thought to reflect a reduction in intraglomerular pressure. The mechanisms of this observation have only been partially investigated by us and others. From studies in peolpe with T1DM it is hypothesized that SGLT-2 inhibition increases sodium chloride delivery to the macula densa, which in turn augments the afferent arteriolar resistances, known as tubuloglomerular feedback (TGF), consequently reducing glomerular (hyper)filtration and hydrostatic pressure. Recently a trial has been conducted in humans with T2DM to investigate if this also holds true in these patients. Suprisingly, this study showed that the renohemodynamic actions of SGLT-2 inhibition in T2DM are not due to afferent vasoconstriction but rather efferent vasodilation [van Bommel/van Raalte Kidney International 2019 in press]. The investigators realized that the SGLT-2 associated dip in eGFR remains insufficient understood. The increase in sodium excretion following SGLT-2 inhibition peaks at day 2-3 after which it normalizes. It is unknown whether this drop in eGFR is related to this peak in sodium excretion, as the drop remains after normalization of sodium excretion. Therefore it might be possible that glucosuria, by inducing osmotic diuresis, is the main driver of the reduction in intraglomerular pressure more than sodium, since SGLT-2 inhibitors cause persisting glucosuria. Furthermore, it is known that SGLT-2 induced glucosuria and possibly sodium excretion is dependent of renal function and HbA1c and consequently is diminished in people with CKD or without T2DM. However, the renoprotective effects in T2DM are also observed in patients with impaired kidney function and seem statistically independent of glucose levels. Until now it has not been investigated whether or not the SGLT-2 induced eGFR alterations occur in people with CKD with or without T2DM. It is clinically relevant to understand the renal hemodynamics of SGLT-2 inhibitors in these populations since then it is possible to interpret the results from the ongoing trials in people with CKD without T2DM, such as EMPA-KIDNEY and DAPA-CKD. Recently, potential mediators of renal arterole tone, such as adenosine, have been measured to gain more insight into mechanisms of SGLT-2 inhibitor-induced changes in renal hemodynamics. Adenosine is known to augment preglomerular arteriolar resistance. Adenosine was significantly increased after SGLT-2 inhibition, as was also observed in patients with type 1 diabetes. However, it can also induce postglomerular vasodilation via A2aR activation in the presence of RAS blockade. One study in T1DM rats has shown that increased adenosine generation by the macula densa in response to SGLT-2 inhibition suppresses hyperfiltration, as the improvements in preglomerular arteriolar resistance were abolished after adenosine antagonist administration. To date, this has not been investigated in T2DM humans. Therefore, this trial will assess TGF responses with and without adenosine blockade by caffeine.
Major cardiovascular events are greatest in liver transplant recipients with sustained post-transplantation diabetes1. However, the optimal A1c target after transplantation has not been studied. The objective is to understand the optimal A1c target post liver and combined liver and kidney transplant. Strict A1c control will improve mortality and cardiovascular risk post liver and combined liver and kidney transplant and improve complications post liver and combined liver and kidney transplant.