NUTRACORE, Glycaemic Index and Appetite
HyperglycemiaHyperglycemia4 moreIn recent decades, the world prevalence of obesity and type 2 diabetes (DMT2) has increased dramatically, resulting in a global epidemic. One of the aspects more connected to the etiology of these pathologies is undoubtedly the concept of the glycemic index (GI) and glycemic load (CG). It has been shown that, with the same CG, that is of carbohydrates contained in a food, a food with a higher GI tends to raise blood sugar more quickly (and consequently insulin), causing several negative effects on the body. We now have sufficient evidence to show that high GI diets are associated with increased incidence of DMT2, hyperlipoproteinemia, and cardiovascular disease. Although simple carbohydrates, namely sugars, have always been considered the major inducers of hyperglycemia and hyperinsulinemia, in reality also starches, or complex carbohydrates digestible by humans, may lead to an increase in blood sugar levels which is not as rapid but often equally harmful to health, since the GC is generally higher. The reason why a high GI diet is responsible for this increased risk of developing pathologies is not unambiguous. We can identify at least 4 probable mechanisms. Sudden hyperglycemia tends to cause insulin to rise beyond what is necessary, leading subsequently to the risk of hypoglycemia and thus an excessive feeling of hunger. Increased energy intake and obesity. Excess insulin secretion, aggravated by insulin resistance, represents an effort for the pancreas with the risk, over time, to arrive at a deficit of insulin-dependent diabetes type 2 insulin production Hyperinsulinemia is also associated with reduced lipolysis and increased lipogenesis obesity and hyperlipoproteinemia Fat accumulation, especially in the abdominal region, is associated with chronic inflammation and insulin resistance by type 2 diabetes tissues and metabolic syndrome In addition to these reasons, a high GI diet, typically called Western Diet, is also generally deficient in plant foods, rich in antioxidants and photo compounds with anti-inflammatory action, without which the process of chronic organic inflammation is accelerated, even in the absence of real obesity.
Contribution of Hyperinsulinemia vs. Hyperglycemia to Insulin Resistance in Type 1 Diabetes and...
Type 1 Diabetes MellitusMaturity-Onset Diabetes of the Young3 moreThe purpose of this study is to determine the key factors influencing insulin sensitivity in type 1 diabetes (T1DM) and maturity onset diabetes of the young, type 2 (MODY2). Our study tests the hypothesis that decreased insulin sensitivity is primarily driven by chronically elevated insulin levels in the blood rather than chronic elevations in blood sugar.
Reprometabolic Syndrome Mediates Subfertility in Obesity
ObesityInfertility2 moreObesity plays an adverse role at every stage of conception and pregnancy and mounting evidence implicates relative hypogonadotropic hypogonadism, and reduced menstrual cycle hormone secretion as likely contributors to the subfertility phenotype and possible contributors to complications of pregnancy and the developmental origin of adult diseases such as diabetes and cardiovascular disease. This study will be the first comprehensive investigation to tie together the patterns of hyperinsulinemia, hyperlipidemia and inflammation, characteristic of obesity and obesity-caused relative hypogonadotropic hypogonadotropism and its potential adverse reproductive outcomes. The investigators findings will be used to inform a subsequent clinical intervention to optimize reproductive outcomes for obese women and their offspring.
Vitamin E Supplementation in Hyperinsulinism/Hyperammonemia Syndrome
Hyperinsulinism-Hyperammonemia SyndromeInvestigators will assess the tolerability of oral Vitamin E supplementation in subjects with congenital hyperinsulinism (HI) and hyperammonemia (HA) syndrome.
Effect of Exendin-(9-39) on Glycemic Control in Subjects With Congenital Hyperinsulinism
Congenital HyperinsulinismThe purpose of this study is to determine if Exendin-(9-39), an antagonist of the glucagon-like peptide-1 (GLP-1) receptor with effects on the pancreatic beta cell, increases fasting blood glucose levels in subjects with congenital hyperinsulinism.
Evaluation of Single Ascending Doses of Subcutaneous Exendin 9-39 in Patients With Post-Bariatric...
Hyperinsulinemia HypoglycemiaThis study is designed to evaluate the safety, efficacy, and pharmacokinetic profile of single ascending doses of exendin 9-39 administered by subcutaneous route in subjects with post-bariatric hypoglycemia.
Inhibiting GABA Transaminase to Relieve Obesity Induced Hyperinsulinemia and Insulin Resistance...
HyperinsulinismInsulin Resistance3 more50% of Arizonans are diabetic or pre-diabetic resulting in $6.4 billion in health care and productivity costs. The severity and incidence of Type 2 Diabetes Mellitus (T2DM) is directly related to the hepatic lipid concentration. The degree of hepatic lipid accumulation is communicated by the hepatic vagal afferent nerve (HVAN) to regulate pancreatic insulin secretion and whole body insulin sensitivity. We have shown that obesity enhances expression of GABA-Transaminase (GABA-T) decreasing hepatic release of the excitatory neurotransmitter, aspartate, and increasing release of the inhibitor neurotransmitter, GABA. This enhanced inhibitory tone decreases hepatic vagal afferent nerve activity, increasing pancreatic insulin release and decreasing skeletal muscle glucose clearance/insulin sensitivity. Pharmacological inhibition of GABA-T robustly improves glucose homeostasis in diet induced obese mice. We propose 2 clinical objectives that will test the effect of GABA-T inhibition on glucose tolerance and insulin sensitivity in obese, hyperglycemic, hyperinsulinemic patients.
Effects Of Combined Cryolipolysis And High Intensity Interval Training On Insulin Resistance And...
Polycystic Ovary SyndromeHyperinsulinismthis study will be carried to investigate the effect of cryolipolysis and high intensity interval training on insulin resistance and body composition in pco women
Lanreotide Autogel Treatment of Patients With Congenital Hyperinsulinism of Infancy
Congenital HyperinsulinismThe purpose of our study is to evaluate the efficacy and safety of Lanreotide Autogel in children with congenital hyperinsulinism already treated with Octreotide by pump. Congenital hyperinsulinism is a genetic disorder characterized by inappropriate insulin secretion resulting in persistent hypoglycemia (low blood sugars. Patients exposed to recurrent hypoglycemic episodes are at increased risk of developmental disorders, so identification and prompt management of patients are essential. Many patients are treated with the somatostatin analog Octreotide which is administered by continuous infusion using a pump (we use an insulin pump). This treatment may pose a huge burden and be stressful for patients and families as it demands intensive daily care. In an effort to simplify the daily care of our patients and improve their quality of life we will study the efficacy and safety of Lanreotide Autogel - a long-acting somatostatin analog that can be administered by injection once a month
Maternal Lifestyle and Neonatal Hypoglycemia
HyperinsulinemiaMiscarriages3 moretPA has a pivotal role in placentation, mediationg activation of growth factors, such as vascular endothelial growth factor and brain-derived neurotrophic factor, degradation of extracellular matrix and basement membrane (directly or through activation of matrix metalloproteinases) and formation of hemidesmosomes. A high-carbohydrate intake combined with lack of physical activity provides a strong stimulus for maternal insulin production. In this scenario, either β-cells are dysfunctional and diabetes supervenes, or excessive amounts of insulin are produced, providing pathological stimulation of PAI-1 synthesis. Given that PAI-1 is a major tPA inhibitor, PAI-1 excess may affect placentation, increasing the risk of first trimester losses, preterm deliveries and intrauterine growth restriction. Our hypothesis was that prematurity was not the cause of neonatal hypoglycemia, but a parallel occurrence of a strong stimulus for maternal, fetal and neonatal production of insulin.