scispace - formally typeset
Search or ask a question

Why is my sugar level not going down even after taking insulin 20? 

Answers from top 10 papers

More filters
Papers (10)Insight
Even when medication, diet, and physical activity regimens are maintained, blood sugar levels might not be effectively controlled because stress triggers the release of sugar into the blood.
However, this high-dose insulin reduced the blood sugar significantly (p < 0.01), from 11.8 to 7.8 mM, probably by virtue of centrally administered insulin reaching the periphery.
The high levels of blood sugar are attributed to a decrease in the Insulin mRNA level in the pancreas that is caused by impaired islet development and the subsequent impairment of Insulin‐producing cell formation.
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.
The existence of a diurnal variation in the blood sugar after intravenous glucose load, as well as after glucagon, seems to be correlated to a simultaneous diurnal variation in the insulin response, suggesting decreased pancreatic beta-cell activity in the afternoon.
We suggest that the insulin sensitivity index may not accurately reflect the insulin effect as the plasma level of insulin was significantly increased during insulin infusion but not at 24 h, possibly because of alteration of distribution and/or degradation rate of exogenous insulin.
This seems to prove that this drop of blood sugar content is attributable to a sudden release of insulin.
Blood sugar levels from tested rats indicate that with increasing amount of insulin, blood sugar levels fall down.
These findings suggest that the rise in blood saccharidelevel per se after intravenous administration may not be the sole stimulus for insulin secretion but possibly a metabolite of the infused sugar is a stimulus.
These data suggest that added sugar consumed at the median American intake level does not produce changes in measures of insulin sensitivity or glucose tolerance and that no sugar has more deleterious effects than others.

Related Questions

What are the factors that affect blood glucose levels?5 answersFactors that affect blood glucose levels include excess weight, gender, age, physical pattern (Body Mass Index/BMI), physical activity, eating patterns (number of calories), analytical variables (intrinsic to glucometer and glucose strips), pre-analytical variables (pH of blood, hypoxia, hypotension, hematocrit), and work-related subjective stress. Additionally, the physical properties of consumed food such as temperature, viscosity, and water content can also influence postprandial glucose levels. Self-monitoring of blood glucose and glycated proteins like A1C are important measures to assess glycemic control and guide treatment decisions.
Does an unhealthy diet cause high blood sugar?4 answersAn unhealthy diet, specifically a high-sugar diet, has been associated with high blood sugar levels and the development of type 2 diabetes. Consuming foods that elicit a marked glycemic response, such as those high in glucose and fructose, can lead to insulin resistance and chronic inflammatory diseases. However, the relationship between dietary patterns and blood glucose levels is complex. While one study found no association between a Prudent diet and fasting blood glucose levels or type 2 diabetes, another study emphasized the importance of healthy eating, including high-fiber carbohydrates, lean protein sources, and reduced-fat dairy products, in managing blood glucose levels for individuals with diabetes. Further research is needed to fully understand the role of diet in blood glucose response and related health outcomes.
Even with very low intake of carbohydrate sugar level rises too much how much insulin one must take10 answers
Is insulin low after keeping seating for 48 hrs?9 answers
Post meal sugar is low then how to adjust insulin dose9 answers
Sugar level for insulin Ki Matra10 answers

See what other people are reading

How do beta cells becomes dysregulated in type 2 diabetes?
5 answers
Beta cells become dysregulated in type 2 diabetes due to various factors. Chronic hyperglycemia leads to the downregulation of transcription factors PDX1 and MAFA, which are important for beta-cell identity and insulin production. Additionally, defects in beta-cell function and mass contribute to the development and progression of diabetes. Recent studies suggest that beta-cell failure occurs mainly due to increased beta-cell dedifferentiation rather than limited proliferation or increased cell death. Furthermore, mitochondrial dysfunction plays a central role in the pathogenesis of type 2 diabetes, affecting the coupling between metabolism and exocytosis in beta cells. Hyperglycemia in diabetes leads to aberrant insertion of a mitochondrial ion channel in the plasma membrane of beta cells, resulting in suppression of insulin secretion. These findings highlight the complex mechanisms involved in beta-cell dysregulation in type 2 diabetes.
How does diabetes worsen with beta cell dysfunction?
3 answers
Diabetes 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 answers
Beta 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 answers
Beta 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 answers
Beta 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 answers
Beta 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 answers
Pancreatic 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 answers
Hyperglycaemia 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 answers
GPR27 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 answers
Hyperglycaemia 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 answers
Oxidative 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.