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Basal Insulin Secretion

Elevated Basal Insulin Secretion In Type 2 Diabetes Caused By Reduced Plasma Membrane Cholesterol

Elevated Basal Insulin Secretion In Type 2 Diabetes Caused By Reduced Plasma Membrane Cholesterol

Type-2 diabetes (T2D) develops when the pancreatic β-cells fail to increase insulin secretion to compensate for systemic insulin resistance. This condition is also characterized by increased levels of plasma cholesterol, a general disorder of lipid metabolism and increased basal insulin secretion. However, it remains incompletely elucidated how this affects cholesterol levels in the endocrine pancreatic islets from individuals with diabetes and its consequences for insulin section and pathophysiology of T2D. Membrane rafts are specialized platforms enriched in cholesterol and glycosphingolipids. Several important biological functions have been associated with membrane raft integrity including hormone release in pancreatic β-cells (1,–5). Membrane raft microdomains in neuroendocrine and epithelial cells determine the spatial organization of important exocytotic regulatory proteins such as soluble N-ethylmaleimide-sensitive fusion protein attachment protein receptor (SNARE) protein, syntaxin 1, vesicle-associated membrane protein, and the Ca2+ sensor synaptotagmin 1 (6,–8). Important β-cell ion channels like L-type Cav1.2 Ca2+ channels and Kv2.1 potassium channels are also suggested to colocalize with membrane rafts in both clonal pancreatic β-cells and rodent islets (9,–11). Membrane rafts can be manipulated in terms of their cholesterol content by different compounds (12). Methyl β-cyclodextrin (MβCD) extracts membrane cholesterol using its hydrophobic core (13). Longer incubations with MβCD suppress the genes that control the endogenous cholesterol efflux ability of the cells, which could pose potential problems with cell viability (13,–16). MβCD treatment is also known to cause selective release of some important membrane proteins such as Glycosylphosp Continue reading >>

Basal And 24-h C-peptide And Insulin Secretion Rate In Normal Man

Basal And 24-h C-peptide And Insulin Secretion Rate In Normal Man

King's College Hospital NHS Foundation Trust An understanding of the metabolic abnormalities rising from inappropriate insulin delivery in diabetic patients demands a knowledge of 24-h and basal insulin secretion rates in normal man. We have used biosynthetic human C-peptide to determine its kinetic parameters in 10 normal subjects and applied these to measurements of plasma concentrations in the same subjects to determine pancreatic secretion rate. Metabolic clearance rate measured by stepped primed infusion of biosynthetic human C-peptide at rates of 10, 19 and 26 nmol/h was 4.7 +/- 0.7 (+/- SD) ml X kg-1 X min-1, and was independent of infusion rate. Fractional clearance (T1/2, 26 +/- 3 min) and distribution volume (0.178 +/- 0.039 l/kg) were calculated from the decline in concentration after cessation of the highest rate infusion. Basal insulin secretion calculated from the C-peptide metabolic clearance rate and plasma concentrations for the period 02.00 to 07.00 hours was 1.3 +/- 0.4 U/h. Over 24 h total insulin secretion on a standard high carbohydrate diet was 63 +/- 15 U, calculated from the area under the C-peptide concentration curve. Basal insulin secretion, therefore, accounted for 50 +/- 8% of total insulin secretion. Although only 5.6 +/- 1.1% of C-peptide was detected in 24-h urine collections, urinary C-peptide excretion was significantly related to 24-h C-peptide secretion (r = 0.74, p less than 0.02). Do you want to read the rest of this article? ... Of the total renal insulin clearance, 60% clearance occurs by glomerular filtration and 40% is extracted from peritubular vessels [9]. The endogenous insulin has a shorter mean plasma half-life (3-5 min), is not bound to plasma proteins and cleared from the circulation within 10-15 min [10,11]. Most of th Continue reading >>

Insulin Basics

Insulin Basics

Diabetics need insulin therapy because they can't make their own. Insulin therapy tries to mimic natural insulin secretion — what happens automatically in non-diabetics. The ultimate goal of insulin therapy is to mimic normal insulin levels. Unfortunately, current insulin replacement therapy can only approximate normal insulin levels. Insulin therapy for type 2 diabetes ranges from one injection a day to multiple injections and using an insulin pump (continuous subcutaneous insulin infusion – CSII). The more frequent the insulin injections, the better the approximation of natural or normal insulin levels. Discuss with your medical provider the insulin regimen that is best for you. On this page you will learn about: Normal or Non-diabetic blood sugar levels and insulin release from the pancreas Natural insulin (i.e. insulin released from your pancreas) keeps your blood sugar in a very narrow range. Overnight and between meals, the normal, non-diabetic blood sugar ranges between 60-100mg/dl and 140 mg/dl or less after meals and snacks. See the picture below of blood sugar levels throughout the day in someone who does not have diabetes. To keep the blood sugar controlled overnight, fasting and between meals, your body releases a low, background level of insulin. When you eat, there is a large burst of insulin. This surge of insulin is needed to dispose of all the carbohydrate or sugar that is getting absorbed from your meal. All of this happens automatically! More About Natural Insulin Release Insulin is continuously released from the pancreas into the blood stream. Although the insulin is quickly destroyed (5-6 minutes) the effect on cells may last 1-1/2 hours. When your body needs more insulin, the blood levels quickly rise, and, the converse – when you need less, Continue reading >>

Increased Basal Insulin Secretion In Pdzd2-deficient Mice

Increased Basal Insulin Secretion In Pdzd2-deficient Mice

Volume 315, Issues 12 , 5 February 2010, Pages 263-270 Increased basal insulin secretion in Pdzd2-deficient mice Author links open overlay panel S.W.Tsanga D.Shaob K.S.E.Cheaha K.Okuseb P.S.Leungc K.-M.Yaoa Get rights and content Expression of the multi-PDZ protein Pdzd2 (PDZ domain-containing protein 2) is enriched in pancreatic islet cells, but not in exocrine or cells, suggesting a role for Pdzd2 in the regulation of pancreatic -cell function. To explore the in vivo function of Pdzd2, Pdzd2-deficient mice were generated. Homozygous Pdzd2 mutant mice were viable and their gross morphology appeared normal. Interestingly, Pdzd2-deficient mice showed enhanced glucose tolerance in intraperitoneal glucose tolerance tests and their plasma insulin levels indicated increased basal insulin secretion after fasting. Moreover, insulin release from mutant pancreatic islets was found to be twofold higher than from normal islets. To verify the functional defect in vitro, Pdzd2 was depleted in INS-1E cells using two siRNA duplexes. Pdzd2-depleted INS-1E cells also displayed increased insulin secretion at low concentrations of glucose. Our results provide the first evidence that Pdzd2 is required for normal regulation of basal insulin secretion. Continue reading >>

Reactive Oxygen Species Stimulate Insulin Secretion In Rat Pancreatic Islets: Studies Using Mono-oleoyl-glycerol

Reactive Oxygen Species Stimulate Insulin Secretion In Rat Pancreatic Islets: Studies Using Mono-oleoyl-glycerol

Reactive Oxygen Species Stimulate Insulin Secretion in Rat Pancreatic Islets: Studies Using Mono-Oleoyl-Glycerol Contributed equally to this work with: Marylana Saadeh, Thomas C. Ferrante Affiliation Department of Medicine, Obesity Research Center, School of Medicine, Boston University, Boston, Massachusetts, United States of America Contributed equally to this work with: Marylana Saadeh, Thomas C. Ferrante Affiliation Department of Medicine, Obesity Research Center, School of Medicine, Boston University, Boston, Massachusetts, United States of America Affiliation Department of Medicine, Obesity Research Center, School of Medicine, Boston University, Boston, Massachusetts, United States of America Affiliation Department of Medicine, Obesity Research Center, School of Medicine, Boston University, Boston, Massachusetts, United States of America Affiliation Department of Medicine, Obesity Research Center, School of Medicine, Boston University, Boston, Massachusetts, United States of America Affiliation Department of Medicine, Obesity Research Center, School of Medicine, Boston University, Boston, Massachusetts, United States of America Continue reading >>

Handbook Of Diabetes, 4th Edition, Excerpt #4: Normal Physiology Of Insulin Secretion And Action

Handbook Of Diabetes, 4th Edition, Excerpt #4: Normal Physiology Of Insulin Secretion And Action

Insulin is synthesized in and secreted from the β-cells within the islets of Langerhans in the pancreas. The normal pancreas has about 1 million islets, which constitute about 2-3% of the gland’s mass. All of the islet cell types are derived embryologically from endodermal outgrowths of the fetal gut. The islets can be identified easily with various histological stains, such as hematoxylin and eosin (Figure 5.1), with which the cells react less intensely than does the surrounding exocrine tissue. The islets vary in size from a few dozen to several thousands of cells and are scattered irregularly throughout the exocrine pancreas…. The main cell types of the pancreatic islets are β-cells that produce insulin, α-cells that secrete glucagon, δ cells that produce somatostatin and PP cells that produce pancreatic polypeptide. The different cell types can be identified by immunostaining techniques, in situ hybridization for their hormone products (using nucleotide probes complementary to the target mRNA) and the electron microscope appearance of their secretory granules. The β-cells are the most numerous cell type and are located mainly in the core of the islet, while α and δ cells are located in the periphery (Figure 5.2). Islet cells interact with each other through direct contact and through their products (e.g. glucagon stimulates insulin secretion and somatostatin inhibits insulin and glucagon secretion) (Figure 5.3). The blood flow within the islets is organized centrifugally so that the different cell types are supplied in the sequence β → α → δ . Insulin also has an ‘autocrine’ (self-regulating) effect that alters the transcription of insulin and glucokinase genes in the β cell. The pancreatic islets are densely innervated with autonomic and pept Continue reading >>

Insulin Oscillation

Insulin Oscillation

Insulin release from pancreas is pulsatile with a period of 3-6 minutes.[1] The insulin concentration in blood increases after meals and gradually returns to basal levels during the next 1–2 hours. However, the basal insulin level is not stable. It oscillates with a regular period of 3-6 min. After a meal the amplitude of these oscillations increases but the periodicity remains constant.[1] The oscillations are believed to be important for insulin sensitivity by preventing downregulation of insulin receptors in target cells.[1] Such downregulation underlies insulin resistance, which is common in type 2 diabetes. It would therefore be advantageous to administer insulin to diabetic patients in a manner mimicking the natural oscillations.[1] The insulin oscillations are generated by pulsatile release of the hormone from the pancreas. Insulin originates from beta cells located in the islets of Langerhans. Since each islet contains up to 2000 beta cells and there are one million islets in the pancreas it is apparent that pulsatile secretion requires sophisticated synchronization both within and among the islets of Langerhans. Pulsatile insulin release from single beta cells is synchronized in each islet of Langerhans as well as among all islets in the pancreas. Mechanism[edit] Pulsatile insulin secretion from individual beta cells is driven by oscillation of the calcium concentration in the cells. In beta cells lacking contact, the periodicity of these oscillations is rather variable (2-10 min). However, within an islet of Langerhans the oscillations become synchronized by electrical coupling between closely located beta cells that are connected by gap junctions, and the periodicity is more uniform (3-6 min).[1] Coordination of pulsatile insulin release. In addition to gap Continue reading >>

Control Of Basal Insulin Secretion, With Special Reference To The Diagnosis Of Insulinomas

Control Of Basal Insulin Secretion, With Special Reference To The Diagnosis Of Insulinomas

Abstract Estimation of plasma glucose and immunoreactive insulin concentrations in normal subjects after an overnight fast showed that subjects with high basal plasma glucose levels tended to have high plasma insulin concentrations. A similar correlation between glucose and insulin levels was seen in patients with obesity and various endocrine disorders. The suppression of plasma insulin levels associated with hypoglycaemia was used to derive an “amended insulin-glucose ratio,” which appeared to be a good discriminant for the diagnosis of insulinomas. In normal subjects the ratio was less than 30 μU insulin/mg glucose, in obese subjects less than 50 μU/mg, and most of the patients with insulinomas had values over 200 μU/mg. Continue reading >>

Stevioside Does Not Cause Increased Basal Insulin Secretion Or Beta-cell Desensitization As Does The Sulphonylurea, Glibenclamide: Studies In Vitro.

Stevioside Does Not Cause Increased Basal Insulin Secretion Or Beta-cell Desensitization As Does The Sulphonylurea, Glibenclamide: Studies In Vitro.

Abstract We have shown that stevioside (SVS) enhances insulin secretion and thus may have a potential role as antihyperglycemic agent in the treatment of type 2 diabetes mellitus. However, whether SVS stimulates basal insulin secretion (BIS) and/or cause desensitization of beta cells like sulphonylureas (SU), e.g. glibenclamide (GB), is not known. To explore and compare the effects of SVS pretreatment with those of GB and glucagon-like peptide-1 (GLP-1), we exposed isolated mouse islets to low or high glucose for 1 h after short-term (2 h) or long-term (24 h) pretreatment with SVS, GB or GLP-1, respectively. BIS at 3.3 or 5.5 mM glucose were not changed after short-term pretreatment with SVS (10(-7) M), while it increased about three folds after pretreatment with GB (10(-7) M). Glucose stimulated insulin secretion (GSIS) (16.7 mM) increased dose-dependently after long-term pretreatment with SVS at concentrations from 10(-7) to 10(-5) M. Pretreatment for 24 h with GB (10(-7) M) increased the subsequent BIS (3.3 mM glucose) (p < 0.001), but decreased GSIS (16.7 mM glucose) (p < 0.001). In contrast SVS (10(-7) M) and GLP-1 (10(-7) M) did not stimulate BIS but both enhanced the subsequent GSIS (16.7 mM glucose) (p < 0.05 and p < 0.05, respectively). While SVS pretreatment increased the intracellular insulin content, GB pretreatment decreased the insulin content. Our study suggests that SVS pretreatment does not cause a stimulation of BIS and does not desensitize beta-cells, i.e. SVS seems to have advantageous characteristics to GB as a potential treatment of type 2 diabetes. Continue reading >>

Basal And 24-h C-peptide And Insulin Secretion Rate In Normal Man

Basal And 24-h C-peptide And Insulin Secretion Rate In Normal Man

Summary An understanding of the metabolic abnormalities rising from inappropriate insulin delivery in diabetic patients demands a knowledge of 24-h and basal insulin secretion rates in normal man. We have used biosynthetic human C-peptide to determine its kinetic parameters in 10 normal subjects and applied these to measurements of plasma concentrations in the same subjects to determine pancreatic secretion rate. Metabolic clearance rate measured by stepped primed infusion of biosynthetic human C-peptide at rates of 10, 19 and 26nmol/h was 4.7±0.7 (±SD) ml·kg−1·min−1, and was independent of infusion rate. Fractional clearance (T1/2, 26±3 min) and distribution volume (0.178±0.039 l/kg) were calculated from the decline in concentration after cessation of the highest rate infusion. Basal insulin secretion calculated from the C-peptide metabolic clearance rate and plasma concentrations for the period 02.00 to 07.00 hours was 1.3±0.4U/h. Over 24h total insulin secretion on a standard high carbohydrate diet was 63±15 U, calculated from the area under the C-peptide concentration curve. Basal insulin secretion, therefore, accounted for 50±8% of total insulin secretion. Although only 5.6±1.1% of C-peptide was detected in 24-h urine collections, urinary C-peptide excretion was significantly related to 24-h C-peptide secretion (r=0.74,p<0.02). Continue reading >>

Decreased Basal Insulin Secretion From Pancreatic Islets Of Pups In A Rat Model Of Maternal Obesity

Decreased Basal Insulin Secretion From Pancreatic Islets Of Pups In A Rat Model Of Maternal Obesity

Decreased basal insulin secretion from pancreatic islets of pups in a rat model of maternal obesity E Zambrano, Departamento de Biologa de la Reproduccin., Instituto Nacional de Ciencias Mdicas y Nutricin Salvador Zubirn. , Mexico City, Mexico T Sosa-Larios, Departamento de Biologa de la Reproduccin., Instituto Nacional de Ciencias Mdicas y Nutricin Salvador Zubirn. , Mexico City , Mexico L Calzada, Departamento de Biologa de la Reproduccin., Instituto Nacional de Ciencias Mdicas y Nutricin Salvador Zubirn. , Mexico City , Mexico C Ibez, Departamento de Biologa de la Reproduccin., Instituto Nacional de Ciencias Mdicas y Nutricin Salvador Zubirn. , Mexico City , Mexico C Mendoza-Rodrguez, Faculty of Chemistry, National Autonomous University of Mexico, D.F., 04510, Mexico A Morales, Biologa de la Reproduccin, Instituto Nacional de Ciencias Mdicas y Nutricin Salvador Zubirn, D.F., Mexico S Morimoto, Departamento de Biologa de la Reproduccin., Instituto Nacional de Ciencias Mdicas y Nutricin Salvador Zubirn. , Mexico City , Mexico Correspondence: Sumiko Morimoto, Email: sumiko.morimotom{at}incmnsz.mx Maternal obesity (MO) is a deleterious condition that enhances susceptibility of adult offspring to metabolic diseases such as type 2 diabetes. Objective: To study the effect of MO on in vitro insulin secretion and pancreatic cellular population in offspring. We hypothesize that a harmful antenatal metabolic environment due to MO diminishes the basal glucose-responsive secretory function of pancreatic beta cells in offspring. Methods: Mothers were fed a control (C) or high fat diet from weaning through pregnancy (120 days) and lactation. At postnatal days (PNDs) 36 and 110, pups were killed, peripheral blood was collected, and pancreatic islets were isolated. Basal insulin sec Continue reading >>

Independent Influence Of Age On Basal Insulin Secretion In Nondiabetic Humans

Independent Influence Of Age On Basal Insulin Secretion In Nondiabetic Humans

Independent Influence of Age on Basal Insulin Secretion in Nondiabetic Humans Consiglio Nazionale delle Ricerche Institute of Clinical Physiology (P.I.), 56126 Pisa, Italy Address all correspondence and requests for reprints to: Patricia Iozzo, M.D., CNR Institute of Clinical Physiology, Via Savi, 8, 56126 Pisa, Italy. Search for other works by this author on: Consiglio Nazionale delle Ricerche Institute of Clinical Physiology (P.I.), 56126 Pisa, Italy Search for other works by this author on: Consiglio Nazionale delle Ricerche Institute of Clinical Physiology (P.I.), 56126 Pisa, Italy Search for other works by this author on: Consiglio Nazionale delle Ricerche Institute of Clinical Physiology (P.I.), 56126 Pisa, Italy Search for other works by this author on: Consiglio Nazionale delle Ricerche Institute of Clinical Physiology (P.I.), 56126 Pisa, Italy Search for other works by this author on: Consiglio Nazionale delle Ricerche Institute of Clinical Physiology (P.I.), 56126 Pisa, Italy Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 84, Issue 3, 1 March 1999, Pages 863868, Patricia Iozzo, Henning Beck-Nielsen, Markku Laakso, Ulf Smith, Hannele Yki-Jarvinen, Ele Ferrannini; Independent Influence of Age on Basal Insulin Secretion in Nondiabetic Humans, The Journal of Clinical Endocrinology & Metabolism, Volume 84, Issue 3, 1 March 1999, Pages 863868, Glucose tolerance deteriorates with aging. To test whether age per se impairs basal -cell function, we analyzed retrospective clamp data from a large group (n = 957) of nondiabetic Europeans over the 1885 yr age range (the European Group for the Study of Insulin Resistance database). In this cohort, the fasting posthepatic insulin delivery rate [IDR, obtained as the produc Continue reading >>

Elevated Basal Insulin Secretion In Type 2 Diabetes Caused By Reduced Plasma Membrane Cholesterol

Elevated Basal Insulin Secretion In Type 2 Diabetes Caused By Reduced Plasma Membrane Cholesterol

Elevated Basal Insulin Secretion in Type 2 Diabetes Caused by Reduced Plasma Membrane Cholesterol Department of Clinical Sciences Malm (V.N., A.S.K., J.H., C.L., S.B., P.B., T.M.R., E.Z., E.R.), Lund University Diabetes Centre, Lund University, SE-20502 Malm, Sweden Search for other works by this author on: Department of Clinical Sciences Malm (V.N., A.S.K., J.H., C.L., S.B., P.B., T.M.R., E.Z., E.R.), Lund University Diabetes Centre, Lund University, SE-20502 Malm, Sweden Search for other works by this author on: Department of Clinical Sciences Malm (V.N., A.S.K., J.H., C.L., S.B., P.B., T.M.R., E.Z., E.R.), Lund University Diabetes Centre, Lund University, SE-20502 Malm, Sweden Search for other works by this author on: Department of Clinical Sciences Malm (V.N., A.S.K., J.H., C.L., S.B., P.B., T.M.R., E.Z., E.R.), Lund University Diabetes Centre, Lund University, SE-20502 Malm, Sweden Search for other works by this author on: Department of Clinical Sciences Malm (V.N., A.S.K., J.H., C.L., S.B., P.B., T.M.R., E.Z., E.R.), Lund University Diabetes Centre, Lund University, SE-20502 Malm, Sweden Search for other works by this author on: Department of Clinical Sciences Malm (V.N., A.S.K., J.H., C.L., S.B., P.B., T.M.R., E.Z., E.R.), Lund University Diabetes Centre, Lund University, SE-20502 Malm, Sweden Search for other works by this author on: Department of Clinical Sciences Malm (V.N., A.S.K., J.H., C.L., S.B., P.B., T.M.R., E.Z., E.R.), Lund University Diabetes Centre, Lund University, SE-20502 Malm, Sweden Search for other works by this author on: Science for Life Laboratory (S.W.), KTH Royal Institute of Technology, SE-171 77 Stockholm, Sweden Search for other works by this author on: Department of Clinical Sciences Malm (V.N., A.S.K., J.H., C.L., S.B., P.B., T.M.R., Continue reading >>

Jci -quantitative Study Of Insulin Secretion And Clearance In Normal And Obese Subjects.

Jci -quantitative Study Of Insulin Secretion And Clearance In Normal And Obese Subjects.

Quantitative study of insulin secretion and clearance in normal and obese subjects. K S Polonsky, , T Karrison, E Van Cauter J Clin Invest. 1988; 81(2) :435-441. . The secretion and hepatic extraction of insulin were compared in 14 normal volunteers and 15 obese subjects using a previously validated mathematical model of insulin secretion and rate constants for C-peptide derived from analysis of individual decay curves after intravenous bolus injections of biosynthetic human C-peptide. Insulin secretion rates were substantially higher than normal in the obese subjects after an overnight fast (86.7 +/- 7.1 vs. 50.9 +/- 4.8 pmol/m2 per min, P less than 0.001, mean +/- SEM), over a 24-h period on a mixed diet (279.6 +/- 24.2 vs. 145.8 +/- 8.8 nmol/m2 per 24 h, P less than 0.001), and during a hyperglycemic intravenous glucose infusion (102.2 +/- 10.8 vs. 57.2 +/- 2.8 nmol/m2 per 180 min, P less than 0.001). Linear regression analysis revealed a highly significant relationship between insulin secretion and body mass index. Basal hepatic insulin extraction was not significantly different in the normal and obese subjects (53.1 +/- 3.8 vs. 51.6 +/- 4.0%). In the normal subjects, fasting insulin did not correlate with basal hepatic insulin extraction, but a significant negative correlation between fasting insulin and hepatic insulin extraction was seen in obesity (r = -0.63, P less than 0.02). This finding reflected a higher extraction in the six obese subjects with fasting insulin levels within the range of the normal subjects than [] Continue reading >>

Basal Bolus - Basal Bolus Injection Regimen

Basal Bolus - Basal Bolus Injection Regimen

Tweet A basal-bolus injection regimen involves taking a number of injections through the day. A basal-bolus regimen, which includes an injection at each meal, attempts to roughly emulate how a non-diabetic person’s body delivers insulin. A basal-bolus regimen may be applicable to people with type 1 and type 2 diabetes. What is a basal-bolus insulin regimen? A basal-bolus routine involves taking a longer acting form of insulin to keep blood glucose levels stable through periods of fasting and separate injections of shorter acting insulin to prevent rises in blood glucose levels resulting from meals. What is basal insulin? The role of basal insulin, also known as background insulin, is to keep blood glucose levels at consistent levels during periods of fasting. When fasting, the body steadily releases glucose into the blood to our cells supplied with energy. Basal insulin is therefore needed to keep blood glucose levels under control, and to allow the cells to take in glucose for energy. Basal insulin is usually taken once or twice a day depending on the insulin. Basal insulin need to act over a relatively long period of time and therefore basal insulin will either be long acting insulin or intermediate insulin. What is bolus insulin? A bolus dose is insulin that is specifically taken at meal times to keep blood glucose levels under control following a meal. Bolus insulin needs to act quickly and so short acting insulin or rapid acting insulin will be used. Bolus insulin is often taken before meals but some people may be advised to take their insulin during or just after a meal if hypoglycemia needs to be prevented. Your doctor will be able to advise you if you have any questions as to when your bolus insulin should be taken. Advantages of a basal-bolus regimen One of t Continue reading >>

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