View clinical trials related to Insulin Resistance.
Filter by:To compare the effect of insulin sensitizing drugs (metformin and rosiglitazone) over glucose homeostasis (GH) in no diabetic metabolic syndrome individuals. A randomized blinded clinical trial did in patients with metabolic syndrome (n=30), without diabetes. Prior to detailed information and signature of informed consent by patients were done three treatment groups by randomized technique; a) Placebo, b) Metformin (850 mg/day), c) Rosiglitazone (4 mg/day), treatment was administered for 8 weeks. GH was measured before and after treatment using oral glucose tolerance test (OGTT), and IR-index (Homeostatic Model). Determination was performed on weight, size, body mass index, plicometry, blood pressure, fasting glucose levels, triglycerides, HDL-cholesterol and insulin.
This purpose of this study is to investigate whether lactation improves insulin sensitivity and increases lipolysis in women.
This is a research study to see if the addition of cinnamon to a provided food plan would improve insulin resistance in gynecological cancer patients. One study suggests that patients with gynecological cancers are more likely to be insulin resistant and/or have higher levels of fasting insulin. The study will be 24 weeks in length.
Type 2 diabetes is a chronic disease that has reached global epidemic proportions due to the growing number of patients in all countries; It has become the disease that causes more chronic and acute complications to patients, unfortunately, when the diagnosis of type 2 diabetes is made patients are identified at very advanced stages of the disease. For all the above, the best strategies will be those that are aimed at early stages of the disease, and the investigators are convinced that the use the combination of drugs with additive pathophysiological effect plus cardiovascular protection in early stages, will have better results, lasting and with greater results impact on the natural history of the disease that throws measures that may have an applicability in clinical practice, in order to contribute to the control of this pathology. Therefore, the combination of medications with different mechanisms of action, in low doses, could be a useful strategy not only to prevent type 2 diabetes, but also to prevent macro and microvascular complications early. The goal of this clinical trial is to evaluate the effect of low doses of linagliptin + metformin vs metformin alone on physiopathological parameters, such as glucose metabolism, insulin resistance, insulin secretion and pancreatic beta cell function in patients with impaired fasting glucose plus impaired glucose tolerance, during 12 months.
GLP-1 increases skeletal and cardiac microvascular perfusion and improves insulin's microvascular responses in human subjects with T1DM, leading to improved metabolic insulin responses, endothelial function, and increased muscle oxygenation
Counting Carbohydrates (CC) is the preferable method used to calculate the amount of insulin needed for a meal. This method is employed by patients with type 1 diabetes melitus (T1DM). the patients receive the general arithmetic calculation of how much insulin to inject for 15 grams/1 portion of carbohydrate (carb to insulin ratio (C:I) and insulin sensitivity (IS). However, Diabetes Educators are often confronted with difficulties guiding their T1DM patient when using this method and find patients get confused calculating the amount of carbs needed. The investigators sought to create a simple tool that would help our patients implement the CC method easily and properly.
Type 2 diabetes is a worldwide epidemic disease, and preventive strategies are needed to face this health problem. The goal of this trial is to evaluate the effect of empagliflozin + linagliptin + metformin + lifestyle on physiopathological parameters, sush as glucose metabolism, insulin resistance, pancreatic beta cell function and cardiovascular function in patients with impaired fasting glucose plus impaired glucose tolerance, during 12 months
The purposes of this study are: 1) to determine the mechanisms responsible for the development of cardiometabolic complications in some, but not all people with obesity; 2) determine the best dietary approach for cardiometabolic health; and 3) understand why some people have a stable metabolic phenotype over time whereas cardiometabolic health improves or worsens in others.
Previous work of the investigators demonstrated the anti-obesity and anti-steatosis potential of the Amazonian fruit camu-camu (CC) in a mouse model of diet-induced obesity [1]. It was demonstrated that the prebiotic role of CC was directly linked to higher energy expenditure stimulated by the fruit since fecal transplantation from CC-treated mice to germ-free mice was sufficient to reproduce the effects. The full protection against hepatic steatosis observed in CC-treated mice is of particular importance since nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease. Thirty percent of adults in developed countries have excess fat accumulation in the liver, and this figure can be as high as 80% in obese subjects. NAFLD is an umbrella term encompassing simple steatosis, as well as non-alcoholic steatohepatitis which can lead to cirrhosis and hepatocellular carcinoma in up to 20% of cases. Up to now, except for lifestyle changes, no effective drug treatment are available. Previous work has suggested that CC possesses anti-inflammatory properties and could acutely reduce blood pressure and glycemia after a single intake. While CC could represent a promising treatment for obesity and fatty liver, no studies have thoroughly tested this potential in humans. Therefore, a robust clinical proof of concept study is needed to provide convincing evidence for a microbiome-based therapeutic strategy to counteract obesity and its associated metabolic disorders. The mechanism of action of CC could involve bile acid (BA) metabolism. BA are produced in the liver and metabolized in the intestine by the gut microbiota. Conversely, they can modulate gut microbial composition. BA and particularly, primary BA, are powerful regulators of metabolism. Indeed, mice treated orally with the primary BA α, β muricholic (αMCA, βMCA) and cholic acids (CA) were protected from diet-induced obesity and hepatic lipid accumulation. Interestingly, the investigators reported that administration of CC to mice increased the levels of αMCA, βMCA and CA. Primary BA are predominantly secreted conjugated to amino acids and that deconjugation rely on the microbial enzymatic machinery of gut commensals. The increased presence of the deconjugated primary BA in CC-treated mice indicate that a cluster of microbes selected by CC influence the BA pool composition. These data therefore point to an Interplay between BA and gut microbiota mediating the health effects of CC. Polyphenols and in particular procyanidins and ellagitannins in CC can also be responsible for the modulation of BA that can impact on the gut microbiota. Indeed, it has been reported that ellagitannins containing food like walnuts modulate secondary BA in humans whereas procyanidins can interact with farnesoid X receptors and alter BA recirculation to reduce hypertriglyceridemia. These effects are likely mediated by the remodeling of the microbiota by the polyphenols. In accordance with the hypothesis that the ultimate effect of CC is directly linked to a modification of the microbiota, fecal transplantation from CC-treated mice to germ-free mice was sufficient to recapitulate the lower weight gain and the higher energy expenditure seen in donor mice.
Hardening of the blood vessels, called arterial stiffness, is a risk factor for future heart disease and its causes are unclear. The proposed study will 1) randomly assign adolescents at high risk of stiffening blood vessels to take a protein supplement called carnitine and study its effects on arterial stiffening and 2) study carnitine related genes for their effect on arterial stiffening. The study will definitively establish a role for carnitine action as a cause of stiffening blood vessels and signal a way to treat or prevent stiffening.