Active clinical trials for "Insulin Resistance"

The purpose of this study is to investigate the effects of dietary exposure to artificial sweeteners on taste sensitivity, preference and brain response in adults. The investigators hypothesize that dietary exposure to artificial sweeteners (sucralose) will decrease sensitivity to taste, shift preference of sweet and savory taste to a higher dose, and reduce brain response in amygdala to sweet taste compared to sucrose.

To determine if consumption of different diet plans that both are nutritionally-adequate and provide energy to maintain body weight, alters fasting insulin concentrations, shifts other common clinical markers of metabolic disease risk, and affects metabolomic profiles that reflect glucose, lipid, and amino acid metabolism.

Context and Rationale: Uninterrupted sitting is associated with increased risk of diabetes, heart disease, and death, even among people who are physically active. These relationships are likely due to increases in post-meal blood sugar observed when people sit for long periods (e.g. > 1 hour) without interruption. In contrast to sitting, standing results in large reductions in post-meal blood sugar levels. Our group has recently shown that sit-stand desks result in large (e.g. 2.5 hour/day) reductions in occupational sitting time. Taken together, these findings suggest that sit-stand desks may help to reduce post-meal blood sugar levels. However, this has yet to be examined in the field. Theoretical Approach and Objectives: The objective of this randomized crossover study is to determine whether people have lower blood sugar when using a sit-stand desk, in comparison to a desk that can only be used while sitting. Methods and Procedures: Sixteen participants will be asked to wear a continuous glucose monitor to measure their blood sugar levels during 2 separate conditions. During one condition, they will be asked to use a sit-stand desk to sit and/or stand as much as they like during 1 workday. During the other condition, they will be asked to work at a seated desk for 1 workday. Participants will be provided with identical meals to eat during each of the two conditions. We hypothesize that participants will have lower blood sugar levels on the day when they use the sit-stand desk, in comparison to the day using a traditional seated desk. Significance and Future Use: If our results support this hypothesis, this would suggest that sit-stand desks may be a useful way to reduce blood sugar levels in people at risk for diabetes. This could also lead to larger population-based interventions studying the health impact of sit-stand desks.

This is a single-center randomized crossover trial. The investigators will target completion of 15 adults (age 18-65 years) with Type 1 Diabetes who use an insulin pump. After completion of the Screening Visit, each subject will participate in a 28-day at home Data Collection Period while using their personal insulin pump, a personal glucometer, a study CGM, and a study activity tracker (i.e., Fitbit). This data collection period may be extended to obtain to gather more days of quality data, if needed per principal investigator judgement. Once the data has been collected and processed, subjects will participate in two 24-hour admissions (Experimental and Control Admission) in a semi-controlled environment (i.e., hotel), performed in the assigned random order. During both admissions, subjects will use the personal insulin pump and glucometer, and a study CGM. The exercise session will consist of three 15-minute bouts of moderate-intensity exercise (i.e., stationary bicycle). Subjects will be provided a controlled dinner; the SI-informed bolus calculator will be used in the Experimental Admission while standard therapy will be used in the Control Admission. Subjects will then be observed overnight and discharged in the following morning.

This study evaluates the existence of a day-night rhythm in skeletal muscle energy metabolism in prediabetic subjects. Subjects will stay at the research facility for 44 hours with a standardized living protocol during which several measurements of skeletal muscle and whole body energy metabolism will be performed.

Two important mechanisms play a major role in the pathogenesis of type 2 diabetes: insulin resistance of the target tissues and the impaired insulin secretion from pancreatic β-cells. Postprandial factors (such as insulin) are perceived by the human brain and induce signals that regulate glucose metabolism via the parasympathetic nervous system. Deep breathing exercise can increase parasympathetic nerve activity. Heart rate variability (HRV) in healthy people can be significantly increased by deep breathing maneuvers, indicating a shift from sympathetic activity to parasympathetic activity. The hypothesis is that this postprandial shift results in a change in peripheral glucose metabolism. In turn, the increased parasympathetic activity could potentially result in a change in postprandial insulin sensitivity or secretion. To test this hypothesis, this study investigates the effect of deep breathing exercise versus normal breathing on insulin sensitivity, on insulin secretion, glucose tolerance, resting energy expenditure, and on parasympathetic tone (analysis of heart rate variability).

Physical inactivity is a significant predictor of major non-communicable diseases such as type 2 diabetes (7%), cardiovascular disease (6%), musculoskeletal disorders and some cancers, and has been proposed to be the 4th leading cause of death worldwide. Reduced physical activity leads to an impaired function of the hormone insulin and increased adiposity. Thus, the elimination of physical inactivity would remove between 6% and 10% of the major non-communicable diseases and increase life expectancy. The aim of the study is to investigate the effects of a short-term (2-day) period of reduced physical activity, with and without a proportional decrease in energy intake, on the action of insulin to regulate blood sugar fluctuations, appetite, and cardiovascular parameters (heart rate, cardiac output, stroke volume, blood flow, arterial blood pressure, peripheral vascular resistance) in response to food ingestion.

Recently a common Greenlandic nonsense p.Arg684erTer variant (in which arginine is replaced by a termination codon) in the gene TBC1D4 was discovered. The variant has an allele frequency of 17%. Homozygous carriers of this TBC1D4 variant have impaired glucose tolerance and a 10-fold enhanced risk of developing type 2 diabetes (T2D). The investigators propose to carry out comprehensive metabolic phenotyping of adult Inuits carrying zero or two alleles of the TBC1D4 variant. The investigators hypothesise that regulation of TBC1D4 in skeletal muscle is pivotal in regulating glucose uptake during exercise, during physiological insulin stimulation, and for the ability of an acute bout of exercise to improve insulin sensitivity to regulate glucose metabolism in humans. The overall aims in the present project are to: Determine whether the TBC1D4 p.Arg684Ter variant affects the regulation of glucose uptake in skeletal muscle during exercise and during physiological insulin stimulation. Determine the effect of the TBC1D4 p.Arg684Ter variant for the ability of acute exercise to insulin sensitize skeletal muscle to regulate glucose metabolism. Define the metabolic pathways affected by the p.Arg684Ter variant in order to identify causal factors responsible for the diabetic phenotype of Inuit carriers. The knowledge generated will contribute to additional explanatory clues to the increased frequency of T2D in the carriers.

The purpose of this study is to investigate the effects of 5 weeks treatment with dapagliflozin in type 2 diabetes patients on how the hormone insulin acts on sugar uptake in muscles.

It is well known that the hormone insulin lowers blood glucose in part by acting directly on the liver and reducing hepatic glucose production. Animal studies have shown that the hormone insulin can act on the brain to indirectly lower glucose production by the liver. It has previously been shown that a nasal spray can deliver insulin directly to the brain without affecting circulating insulin concentration in humans. Intranasal spray of insulin suppressed hepatic glucose production in lean subjects. It is unknown whether this effects is blunted in subjects with insulin resistance.