Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liraglutide is a long-acting analog of GLP-1, being developed by Novo Nordisk and currently undergoing regulatory review for the treatment of type 2 diabetes. Upon injection, liraglutide binds non-covalently to albumin, giving it a pharmacokinetic profile suitable for once-daily administration. In clinical trials of up to 1 year duration, liraglutide has been demonstrated to have beneficial effects on islet cell function, leading to improvements in glycemic control. Both fasting and postprandial glucose concentrations are lowered, and are associated with lasting reductions in HbA1c levels. Liraglutide is effective as monotherapy and in combination therapy with oral antidiabetic drugs, and reduces HbA1c by up to approximately 1.5% from baseline (8.2%-8.4%). Because of the glucose-dependency of its action, there is a low incidence of hypoglycemia. Liraglutide is associated with body weight loss, and reductions in systolic blood pressure have been observed throughout the clinical trials. The most common adverse events reported with liraglutide are gastrointestinal (nausea, vomiting and diarrhea). These tend to be most pronounced during the initial period of therapy and decline with time. Further clinical experience with liraglutide will reveal its long-term durability, safety and efficacy.
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PMID:Potential of liraglutide in the treatment of patients with type 2 diabetes. 1943 48

Gastric emptying is frequently abnormal in patients with long-standing type 1 and type 2 diabetes mellitus. Symptoms commonly associated with disordered gastric emptying include nausea, vomiting, bloating and epigastric pain, while patients are also at risk of malnutrition, weight loss, impaired drug absorption, disordered glycaemic control and poor quality of life. Although often attributed to the presence of irreversible autonomic neuropathy, acute hyperglycaemia represents a potentially reversible cause of gastric dysfunction in diabetes. Scintigraphy represents the gold standard for measuring gastric emptying. The management of diabetic gastroparesis is less than optimal, partly because the pathogenesis has not been clearly defined. Treatment approaches include dietary modification and optimization of glycaemia, and the use of prokinetic drugs, while novel therapies such as gastric electrical stimulation are the subject of ongoing investigation.
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PMID:Diabetic gastroparesis: diagnosis and management. 1949 27

It is long known that both type 1 and type 2 diabetes can be associated with changes in gastric emptying; a number of publications have linked diabetes to delayed gastric emptying of variable severity and often with poor relationship to gastrointestinal symptomatology. In contrast, more recent studies have reported accelerated gastric emptying when adjusted for glucose concentration in patients with diabetes, indicating a reciprocal relationship between gastric emptying and ambient glucose concentrations. This review proposes that gastroparesis or gastroparesis diabeticorum, a severe condition characterized by a significant impairment of gastric emptying accompanied by severe nausea, vomiting, and malnutrition, is often overdiagnosed and not well contrasted with delays in gastric emptying. The article offers a clinically relevant definition of gastroparesis that should help differentiate this rare condition from (often asymptomatic) delays in gastric emptying. The fact that delayed gastric emptying can also be observed in non-diabetic individuals under experimental conditions in which hyperglycaemia is artificially induced suggests that a delay in gastric emptying rate when blood glucose concentrations are high is actually an appropriate physiological response to hyperglycaemia, slowing further increases in blood glucose. The article discusses the strengths and weaknesses of various methodologies for assessing gastric emptying, especially with respect to the diabetes population, and reviews newer diabetes therapies that decelerate the rate of gastric emptying. These therapies may be a beneficial tool in managing postprandial hyperglycaemia because they attenuate rapid surges in glucose concentrations by slowing the delivery of meal-derived glucose.
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PMID:Diabetes mellitus and gastric emptying: questions and issues in clinical practice. 1961 Jan 28

Lixisenatide, under development by sanofi-aventis, is a novel human glucagon-like peptide-1 receptor (GLP-1R) agonist for the treatment of type 2 diabetes mellitus (T2DM; non-insulin dependent diabetes). The structure of lixisenatide, based on exendin-4(1-39) modified C-terminally with six Lys residues, is able to withstand physiological degradation by dipeptidyl peptidase IV. In vitro, lixisenatide bound to human GLP-1R with a greater affinity than native human GLP-1 (7-36 amide). In various in vitro and in vivo models of T2DM, lixisenatide improved glycemic measures and demonstrated promising pancreatic beta-cell-preserving actions. In patients with T2DM, subcutaneously administered lixisenatide displayed linear pharmacokinetics. In two phase II clinical trials, lixisenatide improved glucose tolerance, resulted in weight loss and lowered HbA1C, thereby causing significantly more patients to achieve target HbA1C levels compared with placebo. Lixisenatide exhibited well-established GLP-1-related gastrointestinal side effects, with mild nausea occurring most frequently; a low frequency of hypoglycemia was also reported. The results of phase III trials are awaited for confirmation of the anticipated effects of lixisenatide on glycemic measures and weight; favorable results would place lixisenatide for consideration among other GLP-1R agonists in the treatment armamentarium for T2DM.
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PMID:Lixisenatide, a novel GLP-1 receptor agonist for the treatment of type 2 diabetes mellitus. 1962 85

Liraglutide (Victoza) is an acylated analogue of glucagon-like peptide-1 (GLP-1) indicated for the treatment of type 2 diabetes mellitus. In phase III studies, once-daily subcutaneous liraglutide improved glycaemic control compared with placebo or active comparator in adult patients with type 2 diabetes, both as monotherapy and in combination with one or two oral antidiabetic drugs such as metformin, sulfonylureas or thiazolidinediones. Liraglutide provided significantly better glycaemic control than rosiglitazone or insulin glargine in combination trials. At appropriate dosages, liraglutide was noninferior to glimepiride with respect to glycaemic control in a combination trial, but provided significantly better control than glimepiride or glibenclamide in monotherapy trials. Liraglutide improved pancreatic beta-cell function, generally led to weight loss, and was associated with a low risk of hypoglycaemia. Liraglutide was generally well tolerated, with the most common adverse events being gastrointestinal events, such as nausea, which decreased over time. Thus, liraglutide is an effective treatment option for use in patients with type 2 diabetes mellitus.
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PMID:Liraglutide: a review of its use in type 2 diabetes mellitus. 1974 13

Recently, the European Medicines Agency (EMEA) Committee for Medicinal Products for Human Use (CHMP) adopted a positive opinion, recommending to grant a marketing authorization for liraglutide for the treatment of type 2 diabetes mellitus. Liraglutide is the first human glucagon-like peptide-1 (GLP-1) analog, based on the structure of native GLP-1, with pharmacokinetic properties suitable for once-daily dosing. In the phase III Liraglutide Effect and Action in Diabetes (LEAD) program, liraglutide has been shown to lower glycated hemoglobin to the same extent or more than other antidiabetic drugs including insulin. Liraglutide determines favorable changes in the global cardiovascular risk profile because its use is associated with weight loss, blood pressure reduction, as well as improvements of several cardiovascular risk biomarkers. Liraglutide is generally well tolerated, the most frequently reported adverse effect is transient nausea, and it does not seems to have significant interactions with medications commonly used for cardiovascular prevention. This article reviews, for the practicing cardiologist, the results of the LEAD program and explores liraglutide potentials for cardiovascular prevention in type 2 diabetes mellitus.
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PMID:[Drug therapy of type 2 diabetes and cardiovascular prevention: potentials for liraglutide]. 1976 Nov 1

There is only limited community-based practice safety information available regarding antidepressant use in pediatric patients. This study identifies the factors associated with incident neuroendocrine-related metabolic, digestive, and sexual/reproductive adverse events in children and adolescents treated with antidepressants. A retrospective cohort design evaluating Medicaid medical and pharmacy claims between January, 1996 and December, 2005 was employed for 11970 children and adolescents prescribed an antidepressant medication, and a random sample of 4500 children not treated with psychotropic medications. Incident obesity/weight gain, Type 2 diabetes mellitus, and dyslipidemia were more likely for those prescribed selective serotonin reuptake inhibitors (SSRIs) (OR = 1.49; 1.37; 1.44), whereas Type 2 diabetes mellitus and dyslipidemia were more likely for those prescribed weight-inducing antidepressants (ORs = 1.26; 1.24), and those with pre-existing endocrinopathies (ORs = 3.96; 1.90), controlling for the effects of co-prescribed mood stabilizers or antipsychotics. Incident nausea/vomiting was less likely for those taking SSRIs (OR = 0.78). Females and children under 12 years of age were more likely to develop these adverse effects. Practitioners need to carefully consider the neuroendocrine- related adverse effects of SSRI antidepressant agents in particular, especially in individuals with comorbid endocrine conditions, and those co-prescribed other classes of psychotropic medications.
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PMID:Neuroendocrine-related adverse events associated with antidepressant treatment in children and adolescents. 1976 98

Liraglutide is a new glucagon-like peptide-1 (GLP-1) receptor agonist and a true GLP-1 analogue. After successful phase 2 studies, liraglutide was assessed in a series of phase 3 trials [(Liraglutide Effect and Action in Diabetes (LEAD)] designed to demonstrate efficacy and safety across the continuum of type 2 diabetes antihyperglycaemic care, both as monotherapy and in combination with commonly used oral antidiabetic drugs (OADs). The LEAD programme also compared liraglutide with other OADs. As a monotherapy, liraglutide demonstrated significant improvements in glycaemic control in comparison with glimepiride. When combined with one or two OADs, reductions in haemoglobin A1c, fasting plasma glucose and postprandial glucose were generally greater with liraglutide than with comparators. Throughout the trials, liraglutide was associated with weight reduction; in most instances, the reduction from baseline was significantly greater than that seen with comparators. Improvements in assessments of beta-cell function were consistently shown with liraglutide treatment across all trials. Furthermore, reductions in systolic blood pressure were reported. Liraglutide was associated with a low risk of hypoglycaemia and was generally well tolerated. The majority of adverse effects were gastrointestinal, the most frequent of which was nausea.
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PMID:The safety and efficacy of liraglutide with or without oral antidiabetic drug therapy in type 2 diabetes: an overview of the LEAD 1-5 studies. 1987 59

This is a retrospective analysis of medical records in 4 Belgian diabetes centres of 3 cohorts of patients with type 2 diabetes, with data available, respectively, after 3 months < or =163 patients exposed), 6 months (n=77) and 9 months (n=28) with exenatide therapy. This analysis mainly focuses on the 3 and 6 month cohorts. The mean HbA1 level at baseline averaged 9% and decreased by -1.3% and -1.4% at 3 and 6 months, respectively (-1.5% at 9 months). Neither the duration of diabetes nor initial body weight did influence the metabolic response. The decrease in HbA(1c) at 6 months was greater in patients with higher baseline HbA(1c):-0.5%, -1.4% and -2.4% for a baseline HbA(1c) level <8%, 8-10% and >10%, respectively. At 6 months, the composite criterion of a reduction of HbA(1c) by >1% or a final level <7% was reached by 69% of the cohort. Body weight decreased continuously over time, with a mean reduction of -2.1 kg at 3 months and -3.0 kg at 6 months (-4.9 kg at 9 months). The greater the baseline body weight, the greater the weight loss at final evaluation. Minor nausea and more rarely vomiting were observed, essentially during the first months of exenatide treatment. According to this observational study in routine practice, exenatide may be a valuable alternative to insulin for intensification of treatment of patients with type 2 diabetes after failure of oral drug combination, independently of baseline HbA(1c), body weight and duration of diabetes.
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PMID:[Improved glucose control and weight loss with exenatide in patients with type 2 diabetes: results of a retrospective observational multicentre Belgian study]. 1991 61

Pramlintide (Symlin), a synthetic analog of a neurohormone amylin, was approved by the US Food and Drug Administration for use along with premeal insulin in patients with type 1. In patients with type 2 diabetes, pramlintide is approved for addition to pre-meal insulin in those patients who are either only on pre-meal insulin or those receiving the combination of insulin and metformin and/or a sulfonylurea. This article reviews the pharmacology, pharmacokinetics, dosing, clinical trials, safety, contraindications, and drug interactions of pramlintide therapy. A search for published clinical trials and therapeutic reviews in the English language was done in the following databases: Iowa Drug Information Service (1966 to July 2008), MEDLINE (1966 to July 2008), and International Pharmaceutical Abstracts (1970 to July 2008). Pramlintide and amylin were used as keywords and title words. References of key articles were also reviewed to identify additional publications. Amylin is a 37 amino acid peptide neurohormone co-secreted from the beta cells of the pancreas, along with insulin, in response to meals. Amylin lowers serum glucose by decreasing glucagon release, slowing gastric emptying and decreasing food intake. Pramlintide, a synthetic analog of amylin, reduces 2-hour postprandial blood glucose between 3.4 and 5 mmol/L, reduces A1C by 0.2% to 0.7% and has no effect on fasting glucose levels. The use of pramlintide was associated with up to a 1.6 kg weight loss. Nausea was the most commonly reported adverse event. Pramlintide is an amylin analog that was FDA approved for the treatment of type 1 and type 2 diabetes. Its use results in modest reduction of A1C and the most frequent side effects are hypoglycemia and nausea.
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PMID:Review of pramlintide as adjunctive therapy in treatment of type 1 and type 2 diabetes. 1992 Sep 7


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