Current Progress in Non-Invasive Imaging of Beta Cell Mass of the Endocrine Pancreas
Fabiola SouzaMatthew FreebyKristi HultmanNorman R. SimpsonAlan J. HerronPiotr WitkowskyEric LiuAntonella MaffeiPaul E. Harris
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The increasing incidence of diabetes requires a better understanding of the pathogenesis of the clinical disease. Studies in prevention and treatment have been hampered by the single end-point of diagnosis of diabetes and hyperglycemia. The common pathology in both type 1 and type 2 diabetes is insufficient beta-cell mass to meet the metabolic demand. Unfortunately, current diagnostic methods rely on metabolic responses that do not accurately reflect true beta-cell mass. Recent advances in beta-cell imaging have utilized multiple modalities in experimental and clinical settings. While no gold-standard exists to measure beta-cell mass, modalities such as single photon emission computed tomography, optical and fluorescent imaging, magnetic resonance imaging, and positron emission tomography have been used with mixed success. Many of the methods are limited by the inability to translate to the clinical setting, poor discrimination between the exocrine and endocrine pancreas, or a poor measurement of beta-cell mass. However, promising new neurofunctional imaging approaches have emerged as improved measures of beta-cell mass. We review the current understanding of the pathogenesis and evaluation of diabetes, as well as experimental approaches to assessing beta-cell mass.Keywords:
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Differentiation between neoplastic and nonneoplastic conditions magnetic resonance imaging (MRI) has established itself as one of the key clinical tools in evaluation of musculoskeletal pathology.However, MRI still has several key limitations which require supplemental information from additional modalities to complete evaluation of various disorders.This has led to the development hybrid positron emission tomography (PET)-MRI which is rapidly evolving to address key clinical questions by using the morphological strengths of MRI and functional information of PET imaging.In this article, we aim to review physical principles and techniques of PET-MRI and discuss clinical utility of functional information obtained from PET imaging and structural information obtained from MRI imaging for the evaluation of musculoskeletal pathology.More specifically, this review highlights the role of PET-MRI in musculoskeletal oncology including initial diagnosis and staging, treatment planning and posttreatment follow-up.Also we will review utility of PET-MRI in evaluating musculoskeletal infections (especially in the immunocompromised and diabetics) and inflammatory condition.Additionally, common pitfalls of PET-MRI will be addressed.
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A non-invasive method to image the mass and/or function of human pancreatic islets is needed to monitor the progression of diabetes, and the effect of therapeutic interventions. As yet, no method is available for this purpose, which could be applied to in situ human islets. Animal and in vitro studies have documented that manganese infusion could improve the magnetic resonance imaging (MRI) of the endocrine pancreas. Here, we have tested whether a similar approach could discriminate diabetic and non-diabetic patients. In vitro, human isolated islets readily incorporated manganese. In vivo, 243 manganese-enhanced magnetic resonance imaging (MEMRI) examinations were reviewed, including 41 examinations which were run on 24 patients with type 2 diabetes and 202 examinations which were run on 119 normoglycemic patients. The results show that MEMRI discriminates type 2 diabetics from non-diabetic patients, based on the signal enhancement of pancreas.
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Pancreatic beta-cell mass is a critical determinant of the progression of diabetes. The loss of beta-cells in various types of diabetes has been documented in comparison to age, sex and body mass index (BMI) matched control subjects. However, the underlying heterogeneity of beta-cell mass in healthy individuals has not been considered. In this study, the inter-individual heterogeneity in beta-cell/islet mass was examined among 10 cases of age-matched non-diabetic male subjects in relation to BMI, pancreas weight, and the percent ratio, volume and number of islets in the whole pancreas. Beta-cell/islet mass was measured using a large-scale unbiased quantification method. In contrast to previous studies, we found no clinically relevant correlation between beta-cell/islet mass and age, BMI or pancreas weight, with large differences in beta-cell/islet mass and islet number among the individuals. Our method extracts the comprehensive information out of individual pancreas providing multifaceted parameters to study the intrinsic heterogeneity of the human pancreas.
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A study was made of the possibility of preserving embryonal beta-cells of the human pancreas up to one year by subcultivation. High insulin-secreting activity of the cultures with many-layered foci in free-floating spherical colonies of beta-cells was recorded.
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Abstract Aims/hypothesis Type 2 diabetes is characterised by reduced beta cell mass (BCM). However, it remains uncertain whether the reduction in BCM in type 2 diabetes is due to a decrease in size or number of beta cells. Our aim was to examine the impact of beta cell size and number on islet morphology in humans with and without type 2 diabetes. Methods Pancreas samples were obtained from 64 Japanese adults with ( n = 26) and without ( n = 38) type 2 diabetes who underwent pancreatectomy. Using pancreatic tissues stained for insulin, we estimated beta cell size based on beta cell diameter. Beta cell number was estimated from the product of fractional beta cell area and pancreas volume divided by beta cell size. The associations of beta cell size and number with islet morphology and metabolic status were examined. Results Both beta cell size (548.7 ± 58.5 vs 606.7 ± 65.0 μm 3 , p < 0.01) and number (5.10 × 10 8 ± 2.35 × 10 8 vs 8.16 × 10 8 ± 4.27 × 10 8 , p < 0.01) were decreased in participants with type 2 diabetes compared with those without diabetes, with the relative reduction in beta cell number (37%) being greater than for beta cell size (10%). Beta cell number but not size was positively correlated with BCM in participants with and without type 2 diabetes ( r = 0.97 and r = 0.98, both p < 0.01) and negatively correlated with HbA 1c ( r = −0.45, p < 0.01). Conclusions/interpretation Both beta cell size and number were reduced in participants with type 2 diabetes, with the relative reduction in beta cell number being greater. Decrease in beta cell number appears to be a major contributor to reduced BCM in type 2 diabetes. Graphical abstract
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Background: Currently there are major efforts to develop strategies for the in vivo imaging of pancreatic beta cell mass as a clinical and investigational tool for detecting and tracking the loss of beta cells that underlies the progression of Type I diabetes. However, beta cells constitute only about 1% of pancreatic mass and are distributed throughout the pancreas within tiny islets of Langerhans that are each less than the spatial resolution of non-invasive imaging technologies. Methods: To estimate the requisite binding characteristics of a candidate beta cell imaging agent, calculations of the beta cell contribution to a positron emission tomography signal were made using simple equations. These were based on the relative population of beta cells and non–beta cells within the pancreas and surrounding tissue and an equation describing equilibrium ligand binding. Results: The calculations show that two criteria must be met: (1) The low-volume fraction of beta cells within the exocrine pancreas (about 1:100) requires that beta cells retain labeled imaging agents at least 1,000-fold more strongly than exocrine cells. (2) Agents that label cell surface receptors, even if beta cell-specific, must do so at a high enough level so that the imaging signal arising from unbound label retained in extracellular spaces must not overwhelm signals from labeled beta cells. Conclusions: The limits developed here can serve as criteria for identifying candidate imaging agents for the in vivo imaging of beta cell mass, thereby avoiding expensive preclinical development using compounds that have no chance of success.
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