Active clinical trials for "Insulin Resistance"

This study will investigate the molecular mechanisms of atypical-antipsychotic induced insulin resistance. This will be accomplished by administering olanzapine or placebo to healthy subjects for 7 days and analyzing genetic and protein changes in peripheral tissues known to play an important role in insulin resistance pathophysiology.

Objective 1: Characterize indices of systemic inflammation and gut microbiota composition and function after chronic (12 weeks) intake of pulses compared to control diet in human OW/OB-IR participants. Objective 2: Characterize dietary- and microbial-derived metabolite pools after regular intake of pulses (12 weeks) in human participants with OW/OB-IR compared to control diet. Objective 3: Characterize cognitive functioning after chronic (12 weeks) intake of pulses compared to control diet in human OW/OB-IR participants.

The purpose of this study is to study the effects of sleep restriction on the production of two hormones, cortisol and testosterone. The investigators aim to show that changing these hormones leads to insulin resistance, which is an important cause of type 2 diabetes mellitus. The investigators may also study the effect of sleep restriction on your food intake and cravings, mood, inflammation, metabolism (including bone), and other hormones. Inflammation is your body's response to stress and injury. Bone metabolism is a process of how your body regenerates (renews) new bone cells and removes old bone cells. Hormones are natural substances (materials) that are produced in the body and that influences (effects) the way the body grows or develops.

Purpose/Objectives: To investigate the effect of hyperglucagonemia on insulin action, particularly on adipose tissue. Research Design/Plan: Normal glucose tolerant subjects will be studied. Study subjects will receive a continuous glucagon infusion for 12 hours. Following glucagon infusion, subjects will receive prime-continuous tracer infusions for additional 4 hours to measure adipocyte metabolism. Within 6-8 weeks, subjects will return for a repeat study with normal saline as a control group. Methods: All subjects will have an oral glucose tolerance test prior to participation to confirm they are normal glucose tolerant. Subjects will be admitted to the CRC at 4 PM and will receive a continuous glucagon for 12 hours. At 6 AM on the following morning, subjects will receive prime-continuous tracer infusions of the following for 4 hours (14C-glycerol, 3-3H glucose, and D2O). At 10 AM continuous indirect calorimetry will be performed to determine rates of energy expenditure and glucose/lipid oxidation for 40 minutes. At 6 AM a surgical biopsy of abdominal adipose tissue will be performed for measurement of adipocyte metabolism. At 8 AM, the study team will infuse insulin/glucose to test for insulin sensitivity. Clinical Relevance: The results of this study will help the study team to further understand the pathophysiology of metabolic disturbances that is induced by hyperglucagonemia in type 2 diabetes patients.

The aim of this intervention clinical study are: evaluation the effect of vitamin D supplementation on anti-oxidant status, inflammation, insulin resistance in patients type 2 diabetes mellitus. The research question is how the effect of vitamin D supplementation for 3 and 6 months on anti-oxidant status, inflammation and insulin resistance in patients type 2 diabetes mellitus. The main tasks participants will be asked to do: interviews, filling the questionnaires, and giving informed consent after receiving an explanation by the researcher about the purpose of the research taking blood for screening examination which includes examination of Serum Glutamic Pyruvic Transaminase (SGPT), albumin, creatinine and blood Ca. participant who meet the inclusion and exclusion criteria, performed a physical examination (height and weight) and blood collection for examination 25(OH)D. Subjects/participant with vitamin D deficiency and insufficiency will be included in randomization, two groups: the group that received vitamin D3 5,000 IU and the group that received a placebo. Vitamin D 5000 IU and placebo taken daily for 6 months. Observations for 3 months and 6 months from the first time supplementation was given. Treatments they'll be given: During the study, the subject's clinical condition will be monitored. Subject observations are monitored by telephone or google form to subject or their families

This is a two-center proof-of-concept study, ancillary to the MetACTIV study, whose objective is to define immune activation profiles from the data of individuals followed by the Caisse Primaire d'Assurance Maladie du Gard (health insurance fund). The IRACTIV study will include a subset of volunteers from the MetACTIV study for whom a blood sample will be taken as part of the IRACTIV study.

Insulin promotes the clearance of sugars from the blood into skeletal muscle and fat cells for use as energy; it also promotes storage of excess nutrients as fat. Type 2 diabetes occurs when the cells of the body become resistant to the effects of insulin, and this causes high blood sugar and contributes to a build-up of fat in muscle, pancreas, liver, and the heart. Understanding how insulin resistance occurs will pave the way for new therapies aimed at preventing and treating type 2 diabetes. Mitochondria are cellular structures that are responsible for turning nutrients from food, into the energy that our cells run on. As a result, mitochondria are known as "the powerhouse of the cell." Mitochondria are dynamic organelles that can move within a cell to the areas where they are needed, and can fuse together to form large, string-like, tubular networks or divide into small spherical structures. The name of this process is "mitochondrial dynamics" and the process keeps the cells healthy. However, when more food is consumed compared to the amount of energy burned, mitochondria may become overloaded and dysfunctional resulting in a leak of partially metabolized nutrients that can interfere with the ability of insulin to communicate within the cell. This may be a way for the cells to prevent further uptake of nutrients until the current supply has been exhausted. However, long term overload of the mitochondria may cause blood sugar levels to rise and lead to the development of type 2 diabetes. This study will provide information about the relationship between mitochondrial dynamics, insulin resistance and type 2 diabetes.

The purpose of this study is to provide information regarding potential factors underlying metabolic dysfunction, insulin resistance, and loss of muscle mass in aging muscle.

Objective: To show that a 1-2 day reduction of caloric intake can reduce the insulin resistance produced by several days of overnutrition. Approach: Healthy volunteers will be admitted to the Clinical Research Center and undergo a baseline euglycemic-hyperinsulinemic clamp study to assess their insulin resistance. Subjects will then start on an overnutrition program for 4 days consisting of 3 meals and 3 snacks containing ~6,000 Kcal/24hours. A second clamp study will be performed on day 5 to demonstrate the overnutrition induced increase in insulin resistance. Starting on day 5 the subject's caloric intake will be reduced to ~1,000 Kcal for 2 days (day 5 and 6). After that on the morning of day 7, a third hyperinsulinemic-euglycemic clamp will be performed to determine whether the reduced caloric intake did reduce insulin resistance and the volunteer will be discharged from the Clinical Research Center.

The current protocol plans to enroll participants with youth-onset Type 2 Diabetes (T2D) as well as obese and lean controls from the Renal-HEIR - Renal Hemodynamics, Energetics and Insulin Resistance in Youth Onset Type 2 Diabetes Study (n=100) [COMIRB #16-1752] in a prospective investigation that seeks to 1) define the changes in kidney function by gold standard techniques and energetics by functional Magnetic Resonance Imaging (MRI) in adolescents with and without T2D as they transition to young adulthood; 2) quantify kidney oxidative metabolism by 11C-acetate Positron Emission Tomography (PET) in a subset of participants who are ≥18 years of age with youth-onset T2D and/or obesity; 3) determine peripheral arterial stiffness by SphygmoCor. Mechanistic insight will be provided by transcriptomic analyses of repeat biopsies 3-years after their initial biopsy for eligible participants with youth-onset T2D, as well as molecular analysis of tissue obtained from J-wire endovascular biopsies. This study will also leverage this well-characterized cohort of youths to define youth-onset T2D-related changes in brain morphology and function by structural MRI and resting-state functional MRI and through the assessment of cognitive function (fluid and crystallized intelligence) using the NIH Toolbox Cognitive Battery (NIHTB-CB), as an exploratory objective. All enrollees in Renal-HEIR have consented to be contacted for future research opportunities.