View clinical trials related to Insulin Resistance.
Filter by:Many patients in the hospital who are malnourished or not eating received intravenous feeding or total parenteral nutrition (TPN). Despite improving nutrition, TPN may increase the risk of infections and hospital complications. We do not know why TPN increases hospital complications, but it may be caused by the high sugar or fat content in TPN solutions. The investigators believe that the high sugar and high fat content can limit the ability to fight infections and produce stiffness of blood vessels. This study will compare the effect of high sugar, high fat content or both on blood sugars, blood vessel function, on blood vessel function. The investigators will also compare the effect of different fats (olive oil and soybean) in the TPN solution on the risk of infection and blood vessel function on a total of 12 healthy subjects.
The present study aimed to evaluate the effect of a combination of insulin resistance reducing agents pre and post coronary artery bypass grafting surgery on post-operative blood glucose and oxidative stress regulation.
Our aim was to assess the effects of a hypocaloric diet, including diet fruit jelly with microencapsulated fish oil or conjugated linoleic acid or placebo, on anthropometry, body composition, insulin resistance and lipid profile in women with metabolic syndrome and genotype Pro12Pro in the PPAR gamma 2 gene.
Most new mothers in the United States will start off breastfeeding. For some mothers, despite following best practices, they are not able to meet their breastfeeding goals due to unexplained low milk supply. At the same time, nearly 1 in 4 new mothers are pre-diabetic (elevated blood sugar, but not yet diabetic). My progression of research suggests that the same metabolic factors causing pre-diabetes may also be causing low milk supply. Metformin is a widely prescribed drug to treat high blood sugar. This study is a preliminary, small scale randomized trial designed to test for a trend in the hypothesis that metformin is safe and potentially effective in treating low milk supply in insulin resistant and pre-diabetic mothers.
The study searched for answers to two questions 1. Is there endothelial dysfunction, inflammation and insulin resistance in patients with congenital hypogonadotropic hypogonadism? 2. What is the effect of testosterone replacement therapy on endothelial dysfunction, inflammation and insulin resistance?
Obesity is associated with low-grade inflammation, insulin resistance and low vitamin D status. Vitamin D has traditionally been known to involve in calcium homeostasis and prevent rickets; however, recently it has been recognized to inversely associate with many non-skeletal diseases and conditions including obesity and type 2 diabetes (T2DM). In vitro studies have demonstrated that vitamin D possesses anti-inflammatory properties. It remains unknown if the effect of vitamin D on insulin sensitivity is mediated by suppressing inflammation in human adipose tissues. The main objective of this study was to assess the association between vitamin D and insulin sensitivity and inflammation in morbidly obese pre-menopausal women. Obese women (n=76) were recruited from the University of Illinois at Chicago (UIC) Nutrition and Wellness Center and the UIC medical center bariatric surgery clinics. Insulin sensitivity/resistance was assessed by (1) Oral glucose insulin sensitivity (OGIS) index, derived from dynamic oral glucose tolerance test (OGTT), and (2) Homeostasis model of insulin resistance (HOMA-IR), calculated from fasting steady-state glucose and insulin. Also, to better understand the potential mechanism and the role circulating vitamin D (25OHD) plays in adipose tissue inflammation, we assessed messenger ribonucleic acid (mRNA) expression of vitamin D receptor (VDR) and various inflammatory genes in visceral (VAT) and subcutaneous adipose tissues (SAT) of obese women that underwent a restrictive bariatric procedure. We hypothesized that subjects with higher serum vitamin D levels would be less inflamed and more insulin sensitive and have increased expression of VDR and pro-inflammatory markers compared to those with lower serum vitamin D levels.
Vitamin D deficiency is extremely common in obese youth. In our obese population followed in the Endocrinology clinic at Children's Medical Center Dallas, vitamin D levels were inversely correlated with a measure of insulin resistance. We propose to show that correction of vitamin D levels in obese children and adolescents improves their insulin sensitivity. Obese youth presenting to the Center for Obesity and its Consequences on Health (COACH) clinic will be randomized to receive either the most recent Institute of Medicine (IOM) recommendations of minimum D3 dose of 600 IU/day (1), or receive higher doses of D3 such that the blood levels of vitamin D will be brought to a target level in either the low part or high part of the normal range. The goal is to determine if correction of vitamin D deficiency will improve insulin sensitivity in this group. Secondary goals include determining whether correction of vitamin D deficiency in obese adolescents and children results in less weight gain, and determining the amount of D3 required to correct vitamin D levels in this population. Our specific hypotheses are as follows: Hypothesis #1 Obese youth treated with Vitamin D3 who achieve low-normal 25-hydroxyvitamin D3 (OHD) levels (30-50 ng/mL) or high-normal 25-OHD levels (60-80 ng/mL) will have improved insulin resistance, as measured by Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), compared to those individuals with deficient 25-OHD levels (< 30 ng/mL). Hypothesis #2 Subjects with a higher BMI will have higher Vitamin D dose requirements than current IOM recommendations of 600 IU/day and will take a longer period of time to reach target 25-OHD levels. Hypothesis #3 Subjects with normal 25-OHD levels will demonstrate less weight gain compared to subjects on the control arm.
The purpose of this study is to help scientist better understand the effect of a 12-week single daily evening dose of ramelteon (Rozerem ©), a drug that has been approved by the U. S. Food and Drug Administration (FDA) for the treatment of insomnia (trouble falling asleep or staying asleep). The study will measure levels of inflammation, fasting insulin and fasting glucose (sugar) in subjects who are taking either ramelteon (8 mg) or placebo.
Magnesium is an essential mineral found in many foods; rich sources include whole grains, green leafy vegetables, coffee, and legumes. Magnesium is a critical cofactor in >300 enzymatic reactions, including those related to energy metabolism. Reduced magnesium intake and serum concentrations have been detected, both cross-sectionally and prospectively,in type 2 diabetes and insulin resistance, hypertension, dyslipidemia, and cardiovascular diseases. Different studies have reported inadequate magnesium intake and low serum magnesium concentrations may correlated also with metabolic syndrome, defined as a cluster of metabolic disorders including obesity, hypertension, dyslipidemia and impaired glucose tolerance or diabetes mellitus. Previous studies on this subject, however, reported contradicting results. Some investigations reported inadequate magnesium intake and low serum magnesium concentrations while others did not. To our knowledge, the epidemiological evidence on the relation between dietary magnesium intake and risk of metabolic syndrome has not yet been summarized.Therefore, the investigators will perform a systematic review and dose-response meta-analysis to assess the association between dietary and circulating magnesium level and risk of metabolic syndrome.
Main scientific question: A previous intervention with an anti-inflammatory multifunctional dietary portfolio (MFD) showed remarkable reductions in cardiometabolic (CM) risk markers compared with a well-designed control diet. The study was performed under weight maintenance conditions in healthy subjects in a 4w crossover design (Tovar et al., 2012). MFD consumption also resulted in improved cognitive performance after 4 weeks (Nilsson et al., 2013). The present project will further study the preventive potential of MFD, using its unique properties for identification of new biomarkers and to evaluate the potential role of alterations in the gut microbiota. MFD will be tested in healthy at risk subjects in a randomized parallel design in an eight-week intervention with the test or control diet, respectively, allowing for weight loss. Assessment of standard anthropometric/biochemical markers of CM risk, metabolomics analysis and appetite regulating hormone evaluation are also planned. Associations between the gut microbiota composition and measures of CM risk are also included. The project provides unique opportunities to identify mechanisms for the metabolic impact of MFD, for further exploitation in innovative food and/or dietary concepts. Central hypothesis: The CM-preventive potential of MFD may be boosted in a medium-term trial under conditions allowing for body weight reduction. Expected additional benefits may be recorded as reduced values for conventional CM-related parameters, markers of modified gut microbiota composition and specific changes in blood metabolite profiles. Objectives: - To further improve the effect of MFD on biochemical/anthropometric CM risk markers in healthy subjects by administering the diet under conditions allowing for weight reduction. - To identify MFD-related changes in the gut microbiota associated with improved CM risk markers. - To assess MFD-related modification in metabolic pathways, studied with a metabolomics approach, and to correlate them with conventional clinical outcomes, aiming to identify new markers of altered metabolic risk.