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Insulin Tolerance Test Mice

The Cb1 Antagonist Rimonabant Decreases Insulin Hypersecretion In Rat Pancreatic Islets

The Cb1 Antagonist Rimonabant Decreases Insulin Hypersecretion In Rat Pancreatic Islets

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In Vivo Analysis Of The Contribution Of Bone Resorption To The Control Of Glucose Metabolism In Mice - Sciencedirect

In Vivo Analysis Of The Contribution Of Bone Resorption To The Control Of Glucose Metabolism In Mice - Sciencedirect

Volume 2, Issue 4 , November 2013, Pages 498-504 In vivo analysis of the contribution of bone resorption to the control of glucose metabolism in mice Author links open overlay panel JulieLacombe1 Osteocalcin is a hormone produced in bones by osteoblasts and regulating energy metabolism. While osteocalcin exists in two forms, -carboxylated and undercarboxylated only the latter appears to function as a hormone in vivo. It has been proposed recently that osteoclasts, the bone-resorbing cells, are responsible of decarboxylating, i.e. activating osteocalcin. To address the role of osteoclasts in the maintenance of energy metabolism we analyzed mutant mouse strains harboring either an increase or a decrease in osteoclasts number. Osteoprotegerin-deficient mice that are characterized by an increase in the number of osteoclasts demonstrate an increase in serum levels of undercarboxylated osteocalcin and are significantly more glucose tolerant than WT animals. Conversely, osteoclasts ablation in mice results in a decrease in serum undercarboxylated osteocalcin levels and in reduced glucose tolerance. These results support the notion that osteoclasts are controlling glucose metabolism at least in part through the regulation of osteocalcin decarboxylation. Continue reading >>

Age-dependent Onset Of Insulin Resistance In Insulin-resistant Mice

Age-dependent Onset Of Insulin Resistance In Insulin-resistant Mice

Age-Dependent Onset of Insulin Resistance in Insulin-Resistant Mice Department of Clinical Pharmaceutics & Pharmacy Practice, Graduate School of Pharmaceutical Sciences, University of Shizuoka Department of Clinical Pharmaceutics & Pharmacy Practice, Graduate School of Pharmaceutical Sciences, University of Shizuoka Department of Clinical Pharmaceutics & Pharmacy Practice, Graduate School of Pharmaceutical Sciences, University of Shizuoka Department of Clinical Pharmaceutics & Pharmacy Practice, Graduate School of Pharmaceutical Sciences, University of Shizuoka Volume 38 (2015) Issue 12 Pages 1925-1934 Released on J-STAGE: December 01, 2015 [Advance Publication] Released: - Received: July 31, 2015 Revised: - Accepted: September 11, 2015 We have previously isolated spontaneous insulin-resistant mice (ddY-H) and non-insulin-resistant mice (ddY-L) from ddY mice. In the present study, age-dependent onset of insulin resistance in obese ddY-H mice was investigated by comparing with lean ddY-L mice. In ddY-H mice fed a standard diet, an increase in elevation of glucose-stimulated plasma insulin level, glucose intolerance in an intraperitoneal glucose tolerance test, and a reduction of hypoglycemic action of insulin were found at 9 weeks of age, but not at 6 weeks of age. When ddY-H mice were administered nateglinide, a greater elevation of plasma insulin level and a less decrease of serum glucose level were observed at 9 weeks of age. These changes developed progressively with age. These findings suggest that insulin resistance is induced at 9 weeks of age. The age-related change in insulin resistance was correlated with reductions in mRNA expression and protein content of the insulin receptor (InsR), and insulin receptor substrate (IRS)-1 and IRS-2 in the epididymal adipose 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 >>

Insulin Tolerance Test And Hyperinsulinemic-euglycemic Clamp

Insulin Tolerance Test And Hyperinsulinemic-euglycemic Clamp

Human insulin (Eli Lilly, Indianapolis, IN) [3-3H] glucose (Perkin Elmer, catalog number: NET331A250UC ) 2-deoxy-D-[1-14C] glucose (2-[14C]DG) (PerkinElmer, catalog number: NET328250UC ) C57BL/6J mice were fasted for 6 h and then injected intraperitoneally with insulin (1 U per kg of body weight), and blood glucose concentrations were monitored over time using a Contour blood glucometer on a drop of blood from the tip of the tail. Mice were cannulated in the lateral cerebral ventricle and catheterized in the right internal jugular vein for the hyperinsulinemic-euglycemic clamp (Figure 1)(Thrivikraman et al., 2002). Intravenous infusion of [3-3H] glucose (5 Ci bolus, 0.05 Ci/min) was used. Human insulin (16 mU/kg) was injected intravenously as a bolus, followed by continuous infusion at 2.5 mU/kg/min. Tail blood glucose was measured by glucometer at 10 min intervals, and 20% glucose was infused to maintain blood glucose at euglycemic levels (120 to 140 mg/dl of plasma glucose levels). After steady state had been maintained for 1 h, the glucose uptake in various tissues was determined by injecting 2-deoxy-D-[1-14C] glucose (2-[14C]DG) (10 mCi) 45 min before the end of clamps (the catheter was used for the injection). During the final 50 min of basal and clamp infusions, 20 l blood samples were collected at 10 min intervals for measurement of [3H] glucose, [3H] H2O and 2-[14C]DG from the tail vein. Samples were stored in -20 C. Figure 1. Right internal jugular vein catheterization. A catheter is placed in the right jugular vein for the infusion of glucose and insulin. This protocol has been adapted from our previously published paper: Paschos et al. (2012). The work during the development of the protocol was supported by the US National Institutes of Health (NIH) grant RO Continue reading >>

Amelioration Of Insulin Resistance In Streptozotocin Diabetic Mice By Transgenic Overexpression Of Glut4 Driven By An Adipose-specific Promoter

Amelioration Of Insulin Resistance In Streptozotocin Diabetic Mice By Transgenic Overexpression Of Glut4 Driven By An Adipose-specific Promoter

In diabetic rodents and humans, glucose transporter 4 (GLUT4) expression is suppressed in adipocytes in association with insulin resistance. Transgenic mice overexpressing GLUT4 selectively in fat have enhanced glucose disposal in vivo and massively increased glucose transport in adipocytes. To determine whether overexpression can be maintained in diabetes and whether it can prevent insulin resistance, we rendered wild-type and transgenic mice diabetic with streptozotocin. After 1214 days, blood glucose was more than 21.4 mm and plasma insulin was 1.06 ng/ml or less in both diabetic groups in the fed state. Body weight was reduced and gonadal fat pad weight and adipocyte size were 5275% smaller in both nontransgenic and transgenic diabetic mice, compared with nondiabetic. Basal and maximally-stimulated rates of lipolysis were similar in adipocytes from nontransgenic and transgenic mice, but the ED50 for isoproterenol stimulation was 50% lower in transgenic mice. There was no difference in the sensitivity to insulin to inhibit lipolysis. In adipocytes of nontransgenic diabetic mice, GLUT4 protein was reduced 34%, with a 46% reduction in insulin stimulated glucose transport. In contrast, in adipocytes of transgenic diabetic mice, GLUT4 remained 21-fold overexpressed, resulting in 21-fold increased basal and 10-fold increased insulin stimulated glucose transport. Injection of insulin (0.7 mU/g BW) resulted in a 35% decrease in blood glucose in transgenic diabetic mice (P < 0.05), with no effect in nontransgenic diabetic mice. Thus, high-level overexpression of GLUT4 driven by a fat specific promoter can be maintained with insulinopenic diabetes, even when fat cell metabolism is markedly altered. Overexpression of GLUT4 in adipocytes prevents insulin resistant glucose tran 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 >>

Glucose And Insulin Tolerance Tests In The Mouse

Glucose And Insulin Tolerance Tests In The Mouse

Glucose and Insulin Tolerance Tests in the Mouse Part of the Methods in Molecular Biology book series (MIMB, volume 1339) In vivo metabolic tests are highly valuable to determine whether atherosclerosis progression in mouse models is accompanied by carbohydrate metabolism alterations such as glucose intolerance and insulin resistance. In this chapter, we describe protocols to perform in the mouse glucose and insulin tolerance tests, two metabolic assays which evaluate the glucose tolerance and the insulin sensitivity, respectively. InsulinGlucoseMetabolismIntraperitoneal injectionMetabolic test This is a preview of subscription content, log in to check access Springer Nature is developing a new tool to find and evaluate Protocols. Learn more This work was supported by grants from the Carlos III Health Institute (CP10/00555, PI13/00834) and from the European Regional Development Fund (FEDER). H. Gonzlez-Navarro is a Miguel Servet Program researcher, and A. Vinu received salary support from Proyecto Paula. Benetos A, Thomas F, Pannier B et al (2008) All-cause and cardiovascular mortality using the different definitions of metabolic syndrome. Am J Cardiol 102:188191 CrossRef PubMed Google Scholar Zambon S, Zanoni S, Romanato G et al (2009) Metabolic syndrome and all-cause and cardiovascular mortality in an Italian elderly population: the Progetto Veneto Anziani (Pro.V.A.) Study. Diabetes Care 32:153159 PubMedCentral CrossRef PubMed Google Scholar Beckman JA, Creager MA, Libby P (2002) Diabetes and atherosclerosis: epidemiology, pathophysiology, and management. JAMA 287:25702581 CrossRef PubMed Google Scholar Nunn AV, Bell JD, Guy GW (2009) Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe? Nutr Metab (Lond) 6:16 C Continue reading >>

Jci -transgenic Mice Overexpressing Insulin-like Growth Factor-ii In Cells Develop Type 2 Diabetes

Jci -transgenic Mice Overexpressing Insulin-like Growth Factor-ii In Cells Develop Type 2 Diabetes

During embryonic development, insulin-like growth factor-II (IGF-II) participates in the regulation of islet growth and differentiation. We generated transgenic mice (C57BL6/SJL) expressing IGF-II in cells under control of the rat Insulin I promoter in order to study the role of islet hyperplasia and hyperinsulinemia in the development of type 2 diabetes. In contrast to islets from control mice, islets from transgenic mice displayed high levels of IGF-II mRNA and protein. Pancreases from transgenic mice showed an increase in -cell mass (about 3-fold) and in insulin mRNA levels. However, the organization of cells within transgenic islets was disrupted, with glucagon-producing cells randomly distributed throughout the core. We also observed enhanced glucose-stimulated insulin secretion and glucose utilization in islets from transgenic mice. These mice displayed hyperinsulinemia, mild hyperglycemia, and altered glucose and insulin tolerance tests, and about 30% of these animals developed overt diabetes when fed a high-fat diet. Furthermore, transgenic mice obtained from the N1 backcross to C57KsJ mice showed high islet hyperplasia and insulin resistance, but they also developed fatty liver and obesity. These results indicate that local overexpression of IGF-II in islets might lead to type 2 diabetes and that islet hyperplasia and hypersecretion of insulin might occur early in the pathogenesis of this disease. Continue reading >>

Methods And Models For Metabolic Assessment In Mice

Methods And Models For Metabolic Assessment In Mice

Journal of Diabetes Research Volume 2013 (2013), Article ID 986906, 8 pages 1Metabolic Unit, ISIB CNR, 35127 Padova, Italy 2Department of Medicine, Lund University, 221 84 Lund, Sweden Academic Editor: Daisuke Koya Copyright © 2013 G. Pacini et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The development of new therapies for the treatment of type 2 diabetes requires robust, reproducible and well validated in vivo experimental systems. Mice provide the most ideal animal model for studies of potential therapies. Unlike larger animals, mice have a short gestational period, are genetically similar, often give birth to many offspring at once and can be housed as multiple groups in a single cage. The mouse model has been extensively metabolically characterized using different tests. This report summarizes how these tests can be executed and how arising data are analyzed to confidently determine changes in insulin resistance and insulin secretion with high reproducibility. The main tests for metabolic assessment in the mouse reviewed here are the glucose clamp, the intravenous and the oral glucose tolerance tests. For all these experiments, including some commonly adopted variants, we describe: (i) their performance; (ii) their advantages and limitations; (iii) the empirical formulas and mathematical models implemented for the analysis of the data arising from the experimental procedures to obtain reliable measurements of peripheral insulin sensitivity and beta cell function. Finally, a list of previous applications of these methods and analytical techniques is provided to better comprehend their use a 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 >>

Improved Insulin Sensitivity And Resistance To Weight Gain In Mice Null For The Ahsg Gene

Improved Insulin Sensitivity And Resistance To Weight Gain In Mice Null For The Ahsg Gene

Fetuin inhibits insulin-induced insulin receptor (IR) autophosphorylation and tyrosine kinase activity in vitro, in intact cells, and in vivo. The fetuin gene (AHSG) is located on human chromosome 3q27, recently identified as a susceptibility locus for type 2 diabetes and the metabolic syndrome. Here, we explore insulin signaling, glucose homeostasis, and the effect of a high-fat diet on weight gain, body fat composition, and glucose disposal in mice carrying two null alleles for the gene encoding fetuin, Ahsg (B6, 129-Ahsgtm1Mbl). Fetuin knockout (KO) mice demonstrate increased basal and insulin-stimulated phosphorylation of IR and the downstream signaling molecules mitogen-activated protein kinase (MAPK) and Akt in liver and skeletal muscle. Glucose and insulin tolerance tests in fetuin KO mice indicate significantly enhanced glucose clearance and insulin sensitivity. Fetuin KO mice subjected to euglycemic-hyperinsulinemic clamp show augmented sensitivity to insulin, evidenced by increased glucose infusion rate (P = 0.077) and significantly increased skeletal muscle glycogen content (P < 0.05). When fed a high-fat diet, fetuin KO mice are resistant to weight gain, demonstrate significantly decreased body fat, and remain insulin sensitive. These data suggest that fetuin may play a significant role in regulating postprandial glucose disposal, insulin sensitivity, weight gain, and fat accumulation and may be a novel therapeutic target in the treatment of type 2 diabetes, obesity, and other insulin-resistant conditions. Worldwide prevalence data indicate that type 2 diabetes has reached epidemic proportions (1). Parallel to the rise in type 2 diabetes is a rapid expansion of obesity, associated with consumption of a high-fat diet (2). Insulin resistance is central to the Continue reading >>

Insulin Tolerance Test

Insulin Tolerance Test

Glucose Test Strips - AccuChek Comfort Curve or equivalent echoMRI if the mice differ in body fat levels (see below) 0.1 U/mL humulin in PBS (make as 10uL of 100 U/mL in 10 mL, sterile filtered). This will correspond to 1 U/kg injections. If you are using a higher or lower dose of insulin, add more or less to the 10 mL of PBS, so that injections are 10 uL/g of mass. This may need to be adjusted depending on the insulin sensitivity of the mice, and this is based on a normal C57BL/6J mouse on chow. In general for insulin resistant mice, such as those >40g on a high fat diet or such, increase the dose to 2 or 2.5U/kg. In general you want the insulin to decrease blood glucose by about 60-70% in the most responsive of your too group so if your response is <20% of >70% change in blood glucose you will probably have to change your dose and retry. The insulin is diluted from Humulin R-100 and is purchased through the veterinary staff. Remove food from mice for about 6h by putting them in a fresh cage. Add do not feed tag to cages, or ideally move cage to procedure room. Try to make sure that the mice are in a quiet, undisturbed temperature controlled room with the lights on. Typically starve the mice at 8AM and aim to start injections at 2PM Prepare a 1 g/10mL solution of glucose in case some animals become hypoglyemic. Weigh mice, mark tails if necessary with different colors for rapid identification and take fasting glucose measurement via a tail clip. Prepare insulin syringes with 10 uL per g mouse weight (ie for a 30g mouse, 300 uL). At approximately 1 min intervals, inject appropriate amount of insulin into interperitoneal cavity of the mouse. Immobilize mouse and restrain tail with one hand Aim needle between the midline and the hip bone Insert syringe (do not inject) in 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 >>

Standard Operating Procedures For Describing And Performing Metabolic Tests Of Glucose Homeostasis In Mice

Standard Operating Procedures For Describing And Performing Metabolic Tests Of Glucose Homeostasis In Mice

Standard operating procedures for describing and performing metabolic tests of glucose homeostasis in mice 1Vanderbilt-NIH Mouse Metabolic Phenotyping Center, Nashville, TN 37232, USA 2Sanford-Burnham Medical Research Institute at Lake Nona, Orlando, FL 32827, USA 1Vanderbilt-NIH Mouse Metabolic Phenotyping Center, Nashville, TN 37232, USA 2Sanford-Burnham Medical Research Institute at Lake Nona, Orlando, FL 32827, USA 3Yale-NIH Mouse Metabolic Phenotyping Center, New Haven, CT 06520, USA 4University of Washington-NIH Mouse Metabolic Phenotyping Center, Seattle, WA 98109, USA 5University of Cincinnati-NIH Mouse Metabolic Phenotyping Center, Cincinnati, OH 45267, USA 6Case Western Reserve University-NIH Mouse Metabolic Phenotyping Center, Cleveland, OH 44106, USA *Author for correspondence ( [email protected] ) This article has been cited by other articles in PMC. The Mouse Metabolic Phenotyping Center (MMPC) Consortium was established to address the need to characterize the growing number of mouse models of metabolic diseases, particularly diabetes and obesity. A goal of the MMPC Consortium is to propose standard methods for assessing metabolic phenotypes in mice. In this article, we discuss issues pertaining to the design and performance of various tests of glucose metabolism. We also propose guidelines for the description of methods, presentation of data and interpretation of results. The recommendations presented in this article are based on the experience of the MMPC Consortium and other investigators. The miniaturization of metabolic techniques for use in the mouse has resulted in important advances in our understanding of the pathophysiology of diabetes and its associated complications. An important goal of the Mouse Metabolic Phenotyping Center (MMPC) Co Continue reading >>

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