Active clinical trials for "Insulin Resistance"

The aim of the study is to isolate the direct effects of endotoxin on glucose, lipid and protein metabolism. Eight healthy volunteers are enrolled. The hypothesis is that endotoxin will induce insulin resistance, lypolysis and proteolysis acutely.

The combination of impaired insulin sensitivity and insulin secretion is thought to be the basis of type 2 diabetes. Increased free fatty acids levels impair insulin action in muscle and liver, but also systemic inflammation processes play a role in the development of insulin resistance. This study compares the effects of fat and inflammation on insulin sensitivity, systemic inflammation, energy metabolism, vascular system and neural function in healthy humans.

In parallel with the increasing prevalence of obesity worldwide, type 2 diabetes mellitus (T2DM) has reached epidemic proportions. Despite a multitude of available therapies, only bariatric surgery (e.g., roux-en-Y gastric bypass (GBP)) has proven to be an effective long term treatment modality for morbid obesity. Moreover, the majority of T2DM patients who undergo GBP experience normalization of their blood glucose and are able to discontinue their anti-diabetes medications soon after the procedure. The insulin resistant state commonly seen in non-diabetic obese subjects also improves after GBP. Evidence from recent animal studies suggests that the rapid return to euglycemia seen in T2DM patients after GBP might in part result from excluding the duodenum from the flow of nutrients. With the use of enteral feeding tubes, we hope to better understand the factors in the human gut that may predispose obese individuals to the development of insulin resistance and T2DM.

An increase of plasma free fatty acids impairs insulin secretion and insulin sensitivity, thereby playing an important role in causing type 2 diabetes. Lipotoxicity plays an important role in the progression from normal glucose tolerance to fasting hyperglycemia and coversion to frank type 2 diabetes. A recent publication in the journal Science showed that buphenyl, when given to obese diabetic mice, resulted in normalization of hyperglycemia, restoration of systemic insulin sensitivity, resolution of fatty liver disease and inhancement of insulin action in liver, muscle and adipose tissue. the mechanism of action is believed to be due to reduction of endoplasmic reticulum (ER) stress. Buphenyl is currently approved for the treatment of rare inherited disorders of the urea cycle. We plan to administer Buphenyl orally to humans at a dose far lower than that used for the treatment of urea cycle disorders for 2 weeks prior to the testing of pancreatic function. One potential mechanism whereby chromically elevated plasma FFAs and glucose impairment beta cell function and insuln sensitivity is by ER stress and this can be prevented by administeration of buphenyl.

The purpose of this study is to examine the effects of a physiological bolus of growth hormone on insulin signaling pathways in muscle tissue in healthy lean men.

Introduction: Patients with DM2 have chronic hyperglycemia derived from a decrease in insulin sensitivity, cause of comorbidities such as bone demineralization, decreasing quality of life and increasing mortality. This could be related to changes in the serum levels of carboxylated Osteocalcin and Insulin, together with the deficit the daily consumption of vitamins D3 and K, which is crucial for the process of mineralization of the bone matrix. Research question: What is the effect of supplementation with Vitamins D3 and K2 on serum levels of Carboxylated Osteocalcin and Insulin in patients with Type 2 Diabetes mellitus? Hypothesis: Supplementation with Vitamins D3 and K2 modifies the serum levels of Carboxylated Osteocalcin and Insulin in patients with Type 2 Diabetes mellitus. General Objectives: To assess the effect of supplementation with Vitamins D3 and K2 on serum levels of Carboxylated and Non-Carboxylated Osteocalcin in patients with Type 2 Diabetes mellitus. Material and Methods: Clinical trial, double blind, randomization, 40 patients with DM2, 35-65 years, supplementation (3 months), clinical and laboratory determinations (uOC and Insulin). Group 1: Vitamin D3 1000UI + Placebo Group 2: Vitamin K2 100 mcg + Placebo Group 3 (Positive Control): Vitamins D3 1000UI + K2 100 mcg

Recently, it has been proposed that the consumption of non-nutritive sweeteners, including sucralose, it's not harmless and is related with metabolic effects. Some studies have reported that sucralose produces alterations in glucose homeostasis. In vitro studies indicate that sucralose is capable of interacting with sweet taste receptors (T1R2 and T1R3) in the intestine, thus increasing the expression of glucose transporters including the sodium-glucose cotransporter type 1 (SGLT1) and the glucose transporter 2 (GLUT2), increasing glucose absorption. This interaction with intestinal sweet taste receptors also generates an increase in the secretion of the incretins glucagon-like peptide type 1 (GLP-1) and the glucose-dependent insulinotropic polypeptide (GIP), which might enhance the postprandial insulin release. However, these results are preliminary and it's desirable to confirm if sucralose consumption is associated with glucose metabolism modifications using an appropriate methodological design and with gold standard methods. The aim of this triple-blind, placebo-controlled, parallel, randomized clinical trial is to confirm the changes in insulin sensitivity associated with sucralose consumption in humans, to identify whether these changes are in the liver or skeletal muscle and to investigate the pathophysiological mechanisms generating these changes. Specifically, we will investigate if sucralose generates a dysbiosis in the gut microbiota that could be related to insulin resistance by increasing concentrations of lipopolysaccharide, a toxin present in Gram-negative bacteria that triggers a low grade inflammation known as metabolic endotoxemia. In addition, the changes in postprandial concentrations of GLP-1, glucose, insulin and C-peptide due to the combination of sucralose with a mixed meal will be investigated. The results of this study will determine if sucralose consumption, frequently used as a non-nutritive sweetener, is associated to significant changes in glucose homeostasis in humans.

The subject of doctoral dissertation: Assessment of the effects of a meatless, ketogenic restrictive diet on body composition, strength capacity, oxidative stress and immune response During planning of research and topic of the doctoral dissertation, it was considered how to modify a standard ketogenic diet rich in saturated fatty acids so that the use of this model of nutrition has the most anti-inflammatory effect. Therefore, it was decided to conduct a research to check whether a diet rich in omega-3 polyunsaturated fatty acids will show such an effect when following a high-fat diet. Hypotheses: 1. The ketogenic diet reduces systemic inflammation. 2.The ketogenic diet reduces oxidative stress. 3. The ketogenic diet reduces body fat. 4. A ketogenic diet does not worsen strength performance.

The purpose of this study is to assess the metabolic effects of plant based diet on healthy young adults.

The study aimed at assessing the effect of a decaffeinated green coffee extract, rich in hydroxycinnamates, oat beta-glucans or the combination of both bioactive compounds on overweight/obese subjects with hyperglycemia.