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Glucose Tolerance Test Vs Insulin Tolerance Test

Evaluating The Glucose Tolerance Test In Mice

Evaluating The Glucose Tolerance Test In Mice

Evaluating the glucose tolerance test in mice The objective of this study was to determine the optimal conditions under which to assess glucose tolerance in chow- and high-fat-fed C57BL/6J mice. Mice were fed either chow or high-fat diet for 8 wk. Variables tested were fasting duration (0-, 3-, 6-, and 24-h and overnight fasting), route of administration (intraperitoneal vs. oral) load of glucose given (2, 1, or 0.5 g/kg and fixed 50-mg dose), and state of consciousness. Basal glucose concentrations were increased in high-fat- compared with chow-fed mice following 6 h of fasting (9.1 0.3 vs. 7.9 0.4 mmol/l P = 0.01). Glucose tolerance was most different and therefore significant (P = 0.001) in high-fat-fed mice after 6 h of fasting (1,973 96 vs. 1,248 83 mmoll1120 min1). The difference in glucose tolerance was greater following an OGTT (142%), in contrast to an IPGTT, with a 127% difference between high fat and chow. We also found that administering 2 g/kg of glucose resulted in a greater level of significance (P = 0.0008) in glucose intolerance in high-fat- compared with chow-fed mice. A fixed dose of 50 mg glucose regardless of body weight was enough to show glucose intolerance in high-fat- vs. chow-fed mice. Finally, high-fat-fed mice showed glucose intolerance compared with their chow-fed counterparts whether they were tested under conscious or anesthetized conditions. We conclude that 2 g/kg glucose administered orally following 6 h of fasting is best to assess glucose tolerance in mice under these conditions. type 2 diabetes is characterized by glucose intolerance, which is contributed to by peripheral (muscle, fat, and liver) insulin resistance as well as islet -cell dysfunction ( 17 ). The glucose tolerance test is used in clinical practice and research to iden Continue reading >>

Melior Discovery: Insulin Tolerance Test

Melior Discovery: Insulin Tolerance Test

The Insulin Tolerance Test (ITT) is designed to determine the sensitivity of insulin receptors in tissue by measuring blood glucose levels before and after insulin administration.This is a standard test to determine the diabetic status in humans and experimental animals. This test is used to assess the efficacy of insulin-like compounds and pharmacological agents that can modify insulin responsiveness. The graph above illustrates the difference in response to an insulin challenge (ITT) in insulin-depleted (streptozotocin-treated) mice administered insulin, insulin+MLR-1023 or MLR-1023 alone. This study shows that MLR-1023 significantly extended the duration and magnitude of the insulin response. Data are mean SEM, *p<0.05, ***p<0.001 compared to vehicle. MLR-1023 is a potential "next-generation" insulin sensitizer that works independently of a PPAR mechanism. This compound improves glycemic control by directly and selectively activating the enzyme Lyn kinase. Lyn kinase has been previously shown to modulate the insulin-signaling pathway. MLR-1023 is the first described specific and direct activator of Lyn kinase that elicits glycemic control activity through potentiation of insulin activity. For more information on MLR-1023, please visitour sister site, Melior Pharmaceuticals . In addition to MLR-1023 studies, Melior routinely performs ITT studies in mice fed a "Western diet" that is designed to approximate the "typical" human diet of North Americaand Europe. The "Western diet" contains greater than five times more fat than the normal diet. In this study, mice were fasted four hours prior to study commencement. Insulin tolerance test. A baseline glucose measurement was evaluated one hour prior to dosing. At time 0 minutes, mice received either insulin or vehicle (no in Continue reading >>

Is Oral Glucose Tolerance Test Is Preferred Or Ip Glucose Tolerance Test Is Preferred?

Is Oral Glucose Tolerance Test Is Preferred Or Ip Glucose Tolerance Test Is Preferred?

I would say that if you can OGTT is more physiologic. You just have to be sure that you doesn't stress too much the animal during the oral "gavage". Concerning the blood sampling, you should first contact the ethical committee in charge of the animal experiment. To see what you are allow or not to do on a non-anesthetized animal. Another things is that you could help yourself the day of the experiment with a glucometer (to see if nothing is going wrong), but to have better results you should probably reanalyzed the glucose with a proper assay. This is particularly true for the insulin tolerance test, with the glucometer you can see the animal doing a big hypoglycaemia (then you should warm them, and feed them back quickly). If your groups are big enough, you could try to do one half for ogtt, and one other half for ITT, to avoid repetitive stress of the same animal (which will play on insulin/glc metabolism, then give you bad results). I can add just some words to mentioned above from my expertise. The way you choose the method of introducing a glucose depends on your expectation, For example, you know for sure that substance X act in GI tract but you want to see clear effect of glucose and your X on pancreas that I would go with IPGTT. But I agree that OGTT is preferred in over 90% of publications as a more natural way for glucose delivery. We always fast mice 6 hours: 8AM to 2PM. Longer time is called starvation and can affect you results. At the time of OGTT we use glucometer to measure blood glucose and collect blood enough to get some plasma for insulin ELISA. (45mkL of blood per 5mkL of EDTA. next final concetration should be [Ins x 0.1+Ins] because of dilution). The way you get a blood depends on you institutional rules and regulations. There are many way how to Continue reading >>

Insulin Secretory Deficiency And Glucose Intolerance In Rab3a Null Mice*

Insulin Secretory Deficiency And Glucose Intolerance In Rab3a Null Mice*

The EasyTagTMExpre35S35S protein labeling mix from PerkinElmer Life Sciences, containing 73% ofl-[35S]methionine, was used for islet protein synthesis radiolabeling. Uridine 5-[-32P]trisphosphate (3000 Ci/mmol) was purchased from Amersham Biosciences.d-[U-14C]glucose (250360 mCi/mmol) was purchased from PerkinElmer Life Sciences. GLP-1736was purchased from Bachem Inc. (King of Prussia, PA). Rab3A polyclonal antibody was from Santa Cruz Biotechnology Inc. (Santa Cruz, CA), and VAMP-2 antibody was from Calbiochem. The anti-rabbit IgG-horseradish peroxidase conjugate was from Jackson ImmunoResearch (West Grove, PA). All other reagents were of analytical grade and obtained from either Sigma or Fisher. The Rab3A+/+ on a B6 background (B6129SF2/J) and Rab3A/ mice were obtained from The Jackson Laboratory (Bar Harbor, ME). Mice were housed on a 12-h light/dark cycle and were allowed free access to standard mouse food and water. Mice were used at 1220 weeks of age. Glucose, Arginine, and Insulin Tolerance Tests Glucose (1 mg/g), arginine (1 mg/g), and insulin (0.75 milliunits/g) tolerance tests were performed on 1517-week-old Rab3A/ and Rab3A+/+ mice after an overnight fast by intraperitoneal injection dose relative to body weight as described ( 14 ). Blood samples were obtained from the tail vein at the times indicated after the glucose injection. Blood glucose concentrations were measured with a HemoCue blood glucose analyzer (HemoCue AB, ngelholm, Sweden), and plasma insulin levels measured by enzyme-linked immunosorbent assay (Crystal Chem, Chicago, IL). Islet Isolation and in Vitro Insulin Secretion Analysis Pancreatic mouse islets were isolated by collagenase digestion, and insulin secretory activity examined in static or perifusion incubation studies of isolated islets Continue reading >>

Oral Glucose Tolerance Test

Oral Glucose Tolerance Test

Tweet The Glucose Tolerance Test (GTT), also referred to as the Oral Glucose Tolerance Test (OGTT), is a method which can help to diagnose instances of diabetes mellitus or insulin resistance. The test is a more substantial indicator of diabetes than finger prick testing. What is an OGT test? The test is used to determine whether the body has difficulty metabolising intake of sugar/carbohydrate. The patient is asked to take a glucose drink and their blood glucose level is measured before and at intervals after the sugary drink is taken. Why is an oral glucose tolerance test done? This can be a useful test in helping to diagnose: Pre-diabetes Gestational diabetes in pregnant women Insulin resistance Reactive hypoglycemia How is the test performed? Before the test you will be asked not to eat, or drink certain fluids, for up to 8 to 12 hours before the test. You may be asked to not take certain medications in the lead up to the test, but only if these would affect the test results. For the test itself, you will first have blood taken to measure your blood glucose level before the test. The next stage is to take a very sweet tasting, glucose drink. Further blood samples will then be taken either at regular intervals of say 30 or 60 minutes or a single test after 2 hours. The test could take up to 3 hours. Between blood tests you will need to wait so it’s best to have some reading material, or something else to keep you occupied, with you. What should the OGTT results be? People without diabetes Fasting value (before test): under 6 mmol/L At 2 hours: under 7.8 mmol/L People with impaired glucose tolerance (IGT) Fasting value (before test): 6.0 to 7.0 mmol/L At 2 hours: 7.9 to 11.0 mmol/L Diabetic levels Fasting value (before test): over 7.0 mmol/L At 2 hours: over 11.0 mm Continue reading >>

Aldosterone Synthase Inhibition Improves Glucose Tolerance In Zucker Diabetic Fatty (zdf) Rats

Aldosterone Synthase Inhibition Improves Glucose Tolerance In Zucker Diabetic Fatty (zdf) Rats

Aldosterone Synthase Inhibition Improves Glucose Tolerance in Zucker Diabetic Fatty (ZDF) Rats Division of Vascular Endothelium and Microcirculation (A.H., C.B., J.M., F.E., H.M., Technische Universitt Dresden, 01307 Dresden, Germany Search for other works by this author on: Division of Vascular Endothelium and Microcirculation (A.H., C.B., J.M., F.E., H.M., Technische Universitt Dresden, 01307 Dresden, Germany Search for other works by this author on: Division of Clinical Neurochemistry (M.P., G.E.), Technische Universitt Dresden, 01307 Dresden, Germany Search for other works by this author on: University Hospital Carl Gustav Carus Dresden, and Institute of Physiology (M.M., A.D.), Technische Universitt Dresden, 01307 Dresden, Germany Search for other works by this author on: Division of Vascular Endothelium and Microcirculation (A.H., C.B., J.M., F.E., H.M., Technische Universitt Dresden, 01307 Dresden, Germany Search for other works by this author on: Department of Cardiac Surgery (A.J.), Herzzentrum Dresden, Medical Faculty, Technische Universitt Dresden, 01307 Dresden, Germany Search for other works by this author on: Division of Vascular Endothelium and Microcirculation (A.H., C.B., J.M., F.E., H.M., Technische Universitt Dresden, 01307 Dresden, Germany Search for other works by this author on: Department of Cardio Metabolic Diseases (N.F.B., S.M.W.), Boehringer Ingelheim Pharmaceuticals Inc, Ridgefield, Connecticut 06877 Search for other works by this author on: Department of Cardio Metabolic Diseases (N.F.B., S.M.W.), Boehringer Ingelheim Pharmaceuticals Inc, Ridgefield, Connecticut 06877 Search for other works by this author on: Department of Cardio Metabolic Diseases (J.H., R.S.), Boehringer Ingelheim Pharma GmbH and Co KG, 88400 Biberach, Germany Search for Continue reading >>

Nrc Research Press

Nrc Research Press

Accepted Manuscript - Manuscripts that have been selected for publication. They have not been typeset and the text may change before final publication. Uncorrected Proof - Articles that are not yet finalized and that will be corrected by the author(s). The text could change before final publication. (Uncorrected proofs may be temporarily unavailable for production reasons) Corrected Proof - Articles containing author corrections will usually remain unchanged and possible further corrections are fairly minor. Typically the only difference with the final published article is that specific issue and page numbers have not yet been assigned. Although these articles do not have all bibliographic details available yet, they can be cited using the year of online publication and the DOI as follows: Author(s), Article title, Publication (year), DOI. Please consult the journal's reference style for the exact appearance of these elements, abbreviation of journal names, and use of punctuation. Continue reading >>

The One Test Your Doctor Isn’t Doing That Could Save Your Life

The One Test Your Doctor Isn’t Doing That Could Save Your Life

Insulin resistance doesn’t happen overnight. When most of your diet includes empty calories and an abundance of quickly absorbed sugars, liquid calories, and carbohydrates like bread, pasta, rice, and potatoes, your cells slowly become resistant to the effects of insulin. Your body increasingly demands more insulin to do the same job of keeping your blood sugar even. Eventually your cells become resistant to insulin’s call, resulting in insulin resistance. The higher your insulin levels are, the worse your insulin resistance. Your body starts to age and deteriorate. In fact, insulin resistance is the single most important phenomenon that leads to rapid, premature aging and all its resultant diseases, including heart disease, stroke, dementia, and cancer. Insulin resistance and the resulting metabolic syndrome often comes accompanied by increasing central obesity, fatigue after meals, sugar cravings, high triglycerides, low HDL, high blood pressure, problems with blood clotting, as well as increased inflammation. Even without these warning signs, one test can determine high insulin levels years or even decades before diabetes develops. Early detection can help you reverse these symptoms, yet doctors rarely use this crucial test that can detect high insulin levels. Why Doctors Miss the Initial Warning Sign of Insulin Resistance Doctors have been trained to measure a person’s fasting blood sugar, or the glucose levels present in your blood, at least eight hours after your last meal. Most don’t express concern until results show blood sugar levels reaching 110 mg/dl. That’s when they start “watching it.” Then, once your blood sugar reaches 126 mg/dl, your doctor will diagnose you with diabetes and put you on medication. The important thing to note is that bloo Continue reading >>

Impaired Glucose Tolerance And Predisposition To The Fasted State In Liver Glycogen Synthase Knock-out Mice*

Impaired Glucose Tolerance And Predisposition To The Fasted State In Liver Glycogen Synthase Knock-out Mice*

Conversion to glycogen is a major fate of ingested glucose in the body. A rate-limiting enzyme in the synthesis of glycogen is glycogen synthase encoded by two genes, GYS1, expressed in muscle and other tissues, and GYS2, primarily expressed in liver (liver glycogen synthase). Defects in GYS2 cause the inherited monogenic disease glycogen storage disease 0. We have generated mice with a liver-specific disruption of the Gys2 gene (liver glycogen synthase knock-out (LGSKO) mice), using Lox-P/Cre technology. Conditional mice carrying floxed Gys2 were crossed with mice expressing Cre recombinase under the albumin promoter. The resulting LGSKO mice are viable, develop liver glycogen synthase deficiency, and have a 95% reduction in fed liver glycogen content. They have mild hypoglycemia but dispose glucose less well in a glucose tolerance test. Fed, LGSKO mice also have a reduced capacity for exhaustive exercise compared with mice carrying floxed alleles, but the difference disappears after an overnight fast. Upon fasting, LGSKO mice reach within 4 h decreased blood glucose levels attained by control floxed mice only after 24 h of food deprivation. The LGSKO mice maintain this low blood glucose for at least 24 h. Basal gluconeogenesis is increased in LGSKO mice, and insulin suppression of endogenous glucose production is impaired as assessed by euglycemic-hyperinsulinemic clamp. This observation correlates with an increase in the liver gluconeogenic enzyme phosphoenolpyruvate carboxykinase expression and activity. This mouse model mimics the pathophysiology of glycogen storage disease 0 patients and highlights the importance of liver glycogen stores in whole body glucose homeostasis. After ingestion of a meal, glucose is cleared from the bloodstream primarily by conversion t Continue reading >>

Glucose Tolerance Test

Glucose Tolerance Test

The glucose tolerance test (intraperitoneal or oral) is commonly used in the diagnosis of diabetes in both humans and rodents. The ability to quickly normalize the hyperglycemic episode following administration of a glucose bolus provides integrated information about glucose-induced insulin secretion by the pancreatic B cells and insulin sensitivity in the liver and peripheral organs. In addition, an oral (versus intraperitoneal) administration of glucose stimulates intestinal secretion of powerful insulinotropic hormones, the incretins, GLP-1 and GIP. Diabetes is associated with alterations in several physiological functions. Thus, the glucose tolerance test is generally coupled with other tests in order to dissect out the contribution of each individual alteration. For example, a primary defect at the level of incretin secretion or action is diagnosed with an impaired oral glucose tolerance in face of a normal intraperitoneal glucose tolerance. An impaired intraperitoneal glucose tolerance will suggest impairments in either insulin secretion or insulin sensitivity (or both together). It is, therefore, often coupled with an insulin tolerance test. Whenever a defect in insulin secretion is suspected, B cell function can be further assessed in vivo by a glucose-stimulated insulin secretion (GSIS) test, a hyperglycemic clamp , or ex vivo in isolated islets during static infusions or perifusions experiments . A minimum of 10 mice per group should be sent to our facility, one week prior to the experiment. Preitner F, Ibberson M, Franklin I, Binnert C, Pende M, Gjinovci A, Hansotia T, Drucker DJ, Wollheim C, Burcelin R, Thorens B. Gluco-incretins control insulin secretion at multiple levels as revealed in mice lacking GLP-1 and GIP receptors. J Clin Invest. 2004 Feb;113(4): Continue reading >>

Glucose And Insulin Measurements From The Oral Glucose Tolerance Test And Mortality Prediction

Glucose And Insulin Measurements From The Oral Glucose Tolerance Test And Mortality Prediction

OBJECTIVE—To verify what information from oral glucose tolerance tests (OGTTs) independently predicts mortality. RESEARCH DESIGN AND METHODS—A total of 1,401 initially nondiabetic participants from the Baltimore Longitudinal Study of Aging aged 17–95 years underwent one or more OGTTs (median 2, range 1–8), with insulin and glucose measurements taken every 20 min over the course of 2 h included in this study. Proportional hazards using the longitudinally collected data and Bayesian model averaging were used to examine the association of OGTT measurements individually and grouped with mortality, adjusting for covariates. RESULTS—Participants were followed for a median 20.3 years (range 0.5–40). The first-hour OGTT glucose and insulin levels increased only modestly with age, whereas levels during the second hour increased 4% per decade. Individually, 100- and 120-min glucose measures and fasting and 100-min insulin levels were all independent predictors of mortality. When all measures were considered together, only higher 120-min glucose was a significant independent risk factor for mortality. CONCLUSION—The steeper rise with age of the OGTT 2-h glucose values and the prognostic primacy of the 120-min glucose value for mortality is consistent with previous reports and suggests the value of using the OGTT in clinical practice. Many but not all studies have found a nearly linear association between fasting plasma glucose levels >100 mg/dl and mortality (1). Plasma glucose 2 h after an oral glucose load is also a strong predictor of mortality regardless of fasting plasma glucose level (2,3) and may actually be a better predictor of mortality than the fasting level (4). It has been proposed that in early stages of glucose metabolism dysregulation, fasting and 2-h Continue reading >>

Insulin Tolerance Test

Insulin Tolerance Test

An insulin tolerance test (ITT) is a medical diagnostic procedure during which insulin is injected into a patient's vein, after which blood glucose is measured at regular intervals. This procedure is performed to assess pituitary function, adrenal function, and sometimes for other purposes. An ITT is usually ordered and interpreted by endocrinologists. Insulin injections are intended to induce extreme hypoglycemia below 2.2 mmol/l (40 mg/dl). Patient must have symptomatic neuroglycopenia to trigger counter-regulatory cascade. Glucose levels below 2.2 nmol/L are insufficient absent symptoms. The brain must register low glucose levels. In response, adrenocorticotropic hormone (ACTH) and growth hormone (GH) are released as a part of the stress mechanism. ACTH elevation causes the adrenal cortex to release cortisol. Normally, both cortisol and GH serve as counterregulatory hormones, opposing the action of insulin, i.e. acting against the hypoglycemia.[1] Thus ITT is considered to be the gold standard for assessing the integrity of the hypothalamic–pituitary–adrenal axis. Sometimes ITT is performed to assess the peak adrenal capacity, e.g. before surgery. It is assumed that the ability to respond to insulin induced hypoglycemia translates into appropriate cortisol rise in the stressful event of acute illness or major surgery.[2] This test is potentially very dangerous and must be undertaken with great care, because it can iatrogenically induce the equivalent of a diabetic coma. A health professional must attend it at all times. Other provocation tests which cause much less release of growth hormone include the use of glucagon, arginine and clonidine. Side effects[edit] Side effects include sweating, palpitations, loss of consciousness and rarely convulsions due to severe Continue reading >>

Usefulness Of The Insulin Tolerance Test In Patients With Type 2 Diabetes Receiving Insulin Therapy

Usefulness Of The Insulin Tolerance Test In Patients With Type 2 Diabetes Receiving Insulin Therapy

Usefulness of the insulin tolerance test in patients with type 2 diabetes receiving insulin therapy 1Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita City, Osaka, Japan *Corresponding author. Kohei Okita Tel.: +81668793732 Fax: +81668793739 Email address: pj.ca.u-akaso.dem.temdne@iko Received 2013 Mar 13; Revised 2013 Jun 13; Accepted 2013 Jul 30. Copyright 2014 Asian Association for the Study of Diabetes and Wiley Publishing Asia Pty Ltd Copyright 2013 The Authors. Journal of Diabetes Investigation published by Asian Association of the Study of Diabetes (AASD) and Wiley Publishing Asia Pty Ltd This is an open access article under the terms of the Creative Commons AttributionNonCommercialNoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is noncommercial and no modifications or adaptations are made. To establish the validity of the plasma glucose disappearance rate (KITT), derived from an insulintolerance test (ITT), for evaluating the insulin sensitivity of patients with type 2 diabetes after insulin therapy. In the first arm of the study, 19 patients with poorly controlled diabetes were treated with insulin and underwent an ITT and a euglycemic clamp test (clampIR). The relationship between the insulin resistance index, as assessed by both the clampIR and KITT tests, was examined. In the second arm of the study, the relationships between KITT values and various clinical parameters were investigated in 135 patients with poorly controlled diabetes, after achieving glycemic control with insulin. In study 1, a close correlation between KITT and the average glucose infusion rate during the last 30min of the standard clampIR test (Mvalue) was noted (P<0.001). In stu Continue reading >>

Assessment Of Methods And Indexes Of Insulin Sensitivity

Assessment Of Methods And Indexes Of Insulin Sensitivity

Insulin resistance contributes to the pathophysiology of diabetes and is a hallmark of obesity, metabolic syndrome, and many cardiovascular diseases. Therefore, quantifying insulin sensitivity/resistance in humans and animal models is of great importance. Various methods are used to assess insulin sensitivity both in individuals and in study populations. Validity, reproducibility, cost, and degree of subject burden are important factors for both clinicians and researchers to consider when weighing the merits of a particular method. Some methods rely on steady-state analysis of glucose and insulin, whereas others rely on dynamic testing. Each of these methods has distinct advantages and limitations. Thus, optimal choice and employment of a specific method depend on the nature of the studies being performed. Established direct methods for measuring insulin sensitivity in vivo are relatively complex. Finally, simple surrogate indexes for insulin sensitivity/resistance are available that are derived from blood insulin and glucose concentrations under fasting conditions (steady state) or in the postprandial state (dynamic). This article highlight merits, limitations, and appropriate use of current in vivo measures of insulin sensitivity/resistance and presents the advantages and disadvantages of each. A resistência à insulina contribui para a fisiopatologia da diabetes e é uma característica marcante da obesidade, da síndrome metabólica, e de doenças cardiovasculares. Assim, quantificar a sensibilidade à insulina vs resistência à insulina em humanos e em modelos animais é de grande importância. Existem vários métodos para avaliar a sensibilidade à insulina, tanto em indivíduos, como em populações de estudo. A validade, reprodutibilidade, custo e envolviment Continue reading >>

Metabolic Phenotyping Guidelines: Assessing Glucose Homeostasis In Rodent Models

Metabolic Phenotyping Guidelines: Assessing Glucose Homeostasis In Rodent Models

Introduction The incidence of diabetes mellitus, particularly obesity-related type 2 diabetes, is increasing at an alarming rate in the developed world, and this epidemic is driving numerous research programmes into the causes of, and new treatment regimens for, this metabolic disorder. The complex hormonal control of nutrient homeostasis involves numerous tissues and organs, including liver, skeletal muscle, adipose, endocrine pancreas and CNS. While in vitro studies can provide cellular mechanistic insights, it is inevitable that in vivo models are needed to study the integrated control systems. Many animal models for the study of diabetes already exist, with various mechanisms for inducing either type 1 or type 2 diabetes (King 2012). Furthermore, genetically modified mouse models in which genes are up- or down-regulated either globally or in a tissue-specific manner are increasingly used to assess the physiological role of a potential target in glucose homeostasis and the development of diabetes. Consequently, techniques for accurately assessing glucose homeostasis in vivo in rodents are essential tools in current diabetes research. Mice and rats are by far the two most commonly used species for experimental studies of glucose homeostasis, and both models have specific advantages and disadvantages. The primary advantage of using a rat model is a technical consideration in that the larger size of the rat facilitates complex surgical procedures such as catheterisation, and the larger blood volume allows the sampling of more frequent and/or larger blood samples to enable detailed and simultaneous monitoring of multiple plasma hormone levels. Surgical techniques developed in the rat have been successfully miniaturised for use in mouse models, although they are technical Continue reading >>

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