I am take 30 mg insulin in morning and 28 mg evening
Answers from top 9 papers
|But if the morning blood sugar values are clearly below 100 mg/dl, the cause may be nocturnal low blood sugar levels and the evening insulin dose should, therefore, be reduced.|
01 Jul 2008-Archives of Gerontology and Geriatrics
|We propose two treatment schemes: (i) The first one consists of three administrations of rapid insulin with the meals, and on dose of slow insulin 2h after the last meal in the evening.|
|This indicates that high morning blood sugar levels result from the dawn phenomenon and require a higher evening dose of slow-release insulin.|
01 Jan 2004-Current Pharmaceutical Design
|Provided that the dose is slowly increased it is generally well tolerated and safe up to 20 and 30 mg per day, with intake preferably in the morning.|
01 Oct 2006-Clinical Therapeutics
|The results of this study in patients whose type 2 DM was poorly controlled with > or =1 OAD suggest that insulin detemir QD in the morning or evening can be used to improve glycemic control.|
|The IST is sensitive and allows clear insulin dose effects to be demonstrated with 100 mU/kg requiring 355.0 +/- 14.3 mg/kg over 30 min and 50 mU/kg requiring 198.7 +/- 11.1 mg/kg.|
01 Mar 2003-Fertility and Sterility
|Oral low-dose E(2) 1 mg/NETA 0.5 mg regimen did not impair carbohydrate metabolism, but seemed to improve insulin sensitivity in healthy postmenopausal women.|
|If blood glucose levels cannot be maintained in the normal range (fasting < 95 mg/dl and 1 h after meals < 140 mg/dl) insulin therapy should be initiated as first choice.|
Open access•Journal Article•DOI
01 Oct 2001-Journal of Lipid Research
|Interestingly, plasma insulin levels decreased 40% during the 30 mg/kg treatment period, suggesting improvement in insulin sensitivity.|
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How does diabetes worsen with beta cell dysfunction?
3 answersDiabetes worsens with beta cell dysfunction because beta cells are responsible for producing and secreting insulin, which helps regulate blood glucose levels. When beta cells become dysfunctional, they are unable to produce enough insulin, leading to elevated blood glucose levels. This dysfunction is observed in both type 1 and type 2 diabetes. In type 2 diabetes, beta cells initially adapt to insulin resistance by increasing insulin secretion, but over time, they become exhausted and their mass decreases. This decrease in beta cell mass and function contributes to the progression of diabetes and the worsening of glycemic control. It is important to preserve or recover beta cell functional mass in the management of type 2 diabetes, as beta cell regenerative capacity is limited in humans. Lifestyle modifications, such as weight loss and reducing beta cell workload, are effective strategies for preserving beta cell function and managing type 2 diabetes.How are beta cells involved in type 2 diabetes pathology?
5 answersBeta cells play a crucial role in the pathology of type 2 diabetes. The dysfunction and reduced mass of beta cells contribute to the onset and progression of the disease. In type 2 diabetes, beta cells exhibit impaired insulin secretion and pathology findings. The underlying mechanisms for beta cell dysfunction include defects in insulin secretory machinery, disruption of the insulin secretory machinery, and a decrease in beta cell volume. Lipotoxic injury and inflammation also contribute to beta cell damage and dysfunction. Additionally, altered mitochondrial structure and function in beta cells lead to impaired coupling between metabolism and insulin secretion. These findings highlight the importance of beta cell dysfunction in type 2 diabetes and provide insights for potential therapeutic strategies targeting beta cells to improve the treatment of the disease.What changes happen in beta cells in t2dm?
5 answersBeta cells in type 2 diabetes (T2DM) undergo changes in gene expression, reverting to a more immature state and in some cases transdifferentiating into other islet cell types. These changes are associated with alterations in β-cell identity and mass, as well as changes in metabolism and intracellular signaling. The defects in β-cells leading to T2DM vary among individuals and include variations in β-cell mass, development, expansion, responses to stress, insulin production and secretion, and intracellular signaling pathways. Some β-cells undergo dedifferentiation without dying in T2DM, suggesting potential strategies to revive these cells and restore their functionality.How are beta cells involved in pathogenesis of type 2 diabetes?
5 answersBeta cells are involved in the pathogenesis of type 2 diabetes through various mechanisms. One important factor is the downregulation of arginase 2 (ARG2) in human pancreatic beta cells, which regulates the synthesis of polyamines that are involved in beta cell function and pancreas development. Additionally, alpha cells within the islets of Langerhans play a significant role in glucose homeostasis and communicate with other cells through glucagon action, contributing to the bi-hormonal model of type 2 diabetes. Furthermore, beta cell dysfunction and reduced beta cell mass with aging are associated with the development of type 2 diabetes, suggesting a role for beta cell senescence in the pathogenesis of the disease. Insulin resistance, which is a major cause of type 2 diabetes, leads to elevated free fatty acid levels that can disrupt lipid metabolism and contribute to decreased beta cell function and lipotoxicity. Epigenetic modifications, such as DNA methylation, have also been found to play a significant role in the development of beta cell dysfunction in type 2 diabetes.What goes wrong with beta cells in type 2 diabetes?
5 answersBeta cell dysfunction in type 2 diabetes is caused by compromised beta-cell identity, decreased beta-cell mass, and impaired beta-cell function. Chronic hyperglycemia leads to the downregulation of transcription factors PDX1 and MAFA, which are critical regulators of insulin production and beta-cell identity. In addition, beta-cell apoptosis and dedifferentiation contribute to the decrease in beta-cell mass and function. Mitochondrial dysfunction also plays a role in beta-cell dysfunction, as reduced ATP production impairs insulin secretion. Furthermore, defects in insulin secretion and pathology findings in beta cells are observed in type 2 diabetes, highlighting the importance of understanding the underlying mechanisms for better prevention and treatment.How do pancreatic beta cells secrete insulin?
3 answersPancreatic beta cells secrete insulin through a dynamic and highly regulated process. Insulin secretion is influenced by multiple regulatory layers that allow beta cells to adapt to changes in nutrient availability and metabolic demand. The process involves the regulation of histone modifications, which play a role in acute adaptations to fasting and feeding cycles. Cholesterol homeostasis also plays a crucial role in beta cell function, including early steps of insulin synthesis and secretion. Insulin secretion is triggered by an increase in intracellular ATP concentration, leading to the closure of KATP channels, depolarization of the cell, and opening of voltage-gated calcium channels. Insulin secretion occurs in a pulsatile manner, with oscillatory pulses superimposed on a basal secretion rate. Understanding the mechanisms of insulin secretion and the factors that regulate it is important for the development of therapeutic interventions for metabolic disorders such as diabetes.How does hyperglycaemia affect insulin release?
5 answersHyperglycaemia affects insulin release by reducing insulin secretion. This reduction in insulin secretion is independent of abnormalities in islet morphology, beta cell mass, and pancreatic insulin content. In patients with type 2 diabetes, hyperglycaemia is associated with a reduction in postprandial insulin secretion, specifically through a reduction in insulin pulsatility. Long-term exposure of fetal beta cells to high plasma glucose levels in utero suppresses or alters further insulin secretory response not only to glucose but also to other nutrient secretagogues. The presence of glucose can enhance the glucose-responsive insulin release from certain copolymers, leading to the release of loaded insulin.Is GPR27 deorphanised?
4 answersGPR27 is an orphan G protein-coupled receptor (GPCR) that has been studied in various contexts. In the context of energy metabolism, GPR27 has been found to play a role in lipid metabolism, insulin signaling, and glucose homeostasis. In pancreatic beta cells, GPR27 has been implicated in insulin transcription and glucose-stimulated insulin secretion. Additionally, GPR27 has been linked to insulin secretion in the central nervous system. In the context of hepatocellular carcinoma (HCC), GPR27 has been shown to affect the proliferation of HCC cells through the MAPK/ERK pathway. However, despite these findings, GPR27 remains an orphan receptor as no confirmed ligands have been identified for it.How does hyperglycaemia affect insulin secretion?
5 answersHyperglycaemia affects insulin secretion by reducing insulin secretion. This reduction in insulin secretion is independent of abnormalities in islet morphology, beta cell mass, and pancreatic insulin content. Chronic hyperglycaemia induces adaptation and upregulation of glucose- and arginine-stimulated insulin secretion by enhancing β-cell function rather than increasing β-cell mass. In addition to impaired glucose-induced insulin secretion, impaired glucagon-like peptide (GLP)1-induced insulin secretion has been identified in subjects with diabetes and impaired glucose tolerance. Hyperglycaemia in type 2 diabetes is associated with a reduction in postprandial insulin secretion, specifically through a reduction in insulin pulsatility. These findings suggest that hyperglycaemia impairs insulin secretion and that the plasticity of insulin secretion is essential to maintain insulin action during insulin resistance and prevent diabetes.Oxidative stress ?
5 answersOxidative stress is a condition characterized by an imbalance between the production of reactive oxygen species (ROS) and the body's ability to detoxify them. It has been implicated in the development and progression of various diseases, including cardiovascular diseases, neurodegenerative diseases, diabetes, cancer, and liver diseases. Oxidative stress can be caused by both endogenous factors, such as metabolic processes, and exogenous factors, including pollution, alcohol, and certain drugs. It can lead to damage of biomolecules, inflammation, and structural defects in DNA. Mitochondria play a significant role in the production of ROS and oxidative stress, and their dysfunction can contribute to the development of metabolic disorders and insulin resistance. While oxidative stress is generally harmful to the body, it can also be exploited as a therapeutic approach in certain clinical conditions, such as cancer. Understanding the mechanisms of oxidative stress is important for the prevention, treatment, and surveillance of various diseases.What does high albumin/creatinine indicate?
3 answersHigh albumin/creatinine ratio (ACR) is an indicator of microvascular damage, renal disease, and kidney dysfunction. It has been linked to cardiovascular events, including stroke. A high ACR at admission may predict a poor outcome in patients with acute ischemic stroke. In a primary prevention population, a high-normal urine ACR (>6 mg/g) independently predicts an increased risk of mortality. The urine ACR is a reliable predictor of mortality and improves the predictive ability of traditional biomarkers and risk scores. A high ACR is associated with a higher risk of hypertension, type 2 diabetes, and stroke. It is also related to older age, lower high-density lipoprotein cholesterol level, higher total cholesterol level, higher systolic blood pressure, higher prevalence of current smoking, higher prevalence of diabetes, and higher anti-hypertensive medication use.