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      Magnetic Resonance Imaging of Changes in Abdominal Compartments in Obese Diabetics during a Low-Calorie Weight-Loss Program

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          Abstract

          Objectives

          To investigate changes in the fat content of abdominal compartments and muscle area during weight loss using confounder-adjusted chemical-shift-encoded magnetic resonance imaging (MRI) in overweight diabetics.

          Methods

          Twenty-nine obese diabetics (10/19 men/women, median age: 59.0 years, median body mass index (BMI): 34.0 kg/m 2) prospectively joined a standardized 15-week weight-loss program (six weeks of formula diet exclusively, followed by reintroduction of regular food with gradually increasing energy content over nine weeks) over 15 weeks. All subjects underwent a standardized MRI protocol including a confounder-adjusted chemical-shift-encoded MR sequence with water/fat separation before the program as well at the end of the six weeks of formula diet and at the end of the program at 15 weeks. Fat fractions of abdominal organs and vertebral bone marrow as well as volumes of visceral and subcutaneous fat were determined. Furthermore, muscle area was evaluated using the L4/L5 method. Data were compared using the Wilcoxon signed-rank test for paired samples.

          Results

          Median BMI decreased significantly from 34.0 kg/m 2 to 29.9 kg/m 2 (p < 0.001) at 15 weeks. Liver fat content was normalized (14.2% to 4.1%, p < 0.001) and vertebral bone marrow fat (57.5% to 53.6%, p = 0.018) decreased significantly throughout the program, while fat content of pancreas (9.0%), spleen (0.0%), and psoas muscle (0.0%) did not (p > 0.15). Visceral fat volume (3.2 L to 1.6 L, p < 0.001) and subcutaneous fat diameter (3.0 cm to 2.2 cm, p < 0.001) also decreased significantly. Muscle area declined by 6.8% from 243.9 cm 2 to 226.8 cm 2.

          Conclusion

          MRI allows noninvasive monitoring of changes in abdominal compartments during weight loss. In overweight diabetics, weight loss leads to fat reduction in abdominal compartments, such as visceral fat, as well as liver fat and vertebral bone marrow fat while pancreas fat remains unchanged.

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          Most cited references28

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          Visceral fat adipokine secretion is associated with systemic inflammation in obese humans.

          Luigi Fontana, J Christopher Eagon, Maria E Trujillo … (2007)
          Although excess visceral fat is associated with noninfectious inflammation, it is not clear whether visceral fat is simply associated with or actually causes metabolic disease in humans. To evaluate the hypothesis that visceral fat promotes systemic inflammation by secreting inflammatory adipokines into the portal circulation that drains visceral fat, we determined adipokine arteriovenous concentration differences across visceral fat, by obtaining portal vein and radial artery blood samples, in 25 extremely obese subjects (mean +/- SD BMI 54.7 +/- 12.6 kg/m(2)) during gastric bypass surgery at Barnes-Jewish Hospital in St. Louis, Missouri. Mean plasma interleukin (IL)-6 concentration was approximately 50% greater in the portal vein than in the radial artery in obese subjects (P = 0.007). Portal vein IL-6 concentration correlated directly with systemic C-reactive protein concentrations (r = 0.544, P = 0.005). Mean plasma leptin concentration was approximately 20% lower in the portal vein than in the radial artery in obese subjects (P = 0.0002). Plasma tumor necrosis factor-alpha, resistin, macrophage chemoattractant protein-1, and adiponectin concentrations were similar in the portal vein and radial artery in obese subjects. These data suggest that visceral fat is an important site for IL-6 secretion and provide a potential mechanistic link between visceral fat and systemic inflammation in people with abdominal obesity.
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            Mechanisms of disease: is osteoporosis the obesity of bone?

            Clifford Rosen, Mary Bouxsein (2006)
            Osteoporosis and obesity, two disorders of body composition, are growing in prevalence. Interestingly, these diseases share several features including a genetic predisposition and a common progenitor cell. With aging, the composition of bone marrow shifts to favor the presence of adipocytes, osteoclast activity increases, and osteoblast function declines, resulting in osteoporosis. Secondary causes of osteoporosis, including diabetes mellitus, glucocorticoids and immobility, are associated with bone-marrow adiposity. In this review, we ask a provocative question: does fat infiltration in the bone marrow cause low bone mass or is it a result of bone loss? Unraveling the interface between bone and fat at a molecular and cellular level is likely to lead to a better understanding of several diseases, and to the development of drugs for both osteoporosis and obesity.
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              Pancreatic fat content and beta-cell function in men with and without type 2 diabetes.

              Maarten E. Tushuizen, Mathijs Bunck, Petra Pouwels … (2007)
              Insulin resistance, associated with increased lipolysis, results in a high exposure of nonadipose tissue to lipids. Experimental data indicate that fatty infiltration of pancreatic islets may also contribute to beta-cell dysfunction, but whether this occurs in humans in vivo is unknown. Using proton magnetic resonance spectroscopy and oral glucose tolerance tests, we studied the association of pancreatic lipid accumulation in vivo and various aspects of beta-cell function in 12 insulin-naive type 2 diabetic and 24 age- and BMI-matched nondiabetic men. Patients versus control subjects had higher A1C, fasting plasma glucose, and insulin and triglyceride levels and lower HDL cholesterol, but similar waist circumference. Median (interquartile range) pancreatic fat content in patients and control subjects was 20.4% (13.4-43.6) and 9.7% (7.0-20.2), respectively (P = 0.032). Pancreatic fat correlated negatively with beta-cell function parameters, including the insulinogenic index adjusted for insulin resistance, early glucose-stimulated insulin secretion, beta-cell glucose sensitivity, and rate sensitivity (all P < 0.05), but not potentiation. However, these associations were significantly affected by the diabetic state, such that a significant association of pancreatic fat with beta-cell dysfunction was only present in the nondiabetic group (all P < 0.01), suggesting that once diabetes occurs, factors additional to pancreatic fat account for further beta-cell function decline. In control subjects, the association of pancreatic fat and beta-cell function remained significant after correction for BMI, fasting plasma glucose, and triglycerides (P = 0.006). These findings indicate that pancreatic lipid content may contribute to beta-cell dysfunction and possibly to the subsequent development of type 2 diabetes in susceptible humans.
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                Author and article information

                Contributors
                François Blachier: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 25 April 2016
                Publication date Collection: 2016
                Volume: 11
                Issue: 4
                Electronic Location Identifier: e0153595
                Affiliations
                [1 ]Department of Medicine A, University Medicine Greifswald, Greifswald, Germany
                [2 ]Institute of Community Medicine, University Medicine Greifswald, Greifswald, Germany
                [3 ]Department of Radiology and Neuroradiology, University Medicine Greifswald, Greifswald, Germany
                National Institute of Agronomic Research, FRANCE
                Author notes

                Competing Interests: Two authors of this manuscript declare relationships with the following companies: LJV and JK received a Gerhard Domagk scholarship from University Medicine Greifswald made possible through an unrestricted educational grant from Baxter Deutschland GmbH (Unterschleissheim, Germany), Medinal GmbH (Greven, Germany) and Nutricia GmbH (Erlangen, Germany). This does not alter the authors' adherence to PLOS ONE policies on sharing data and materials. In addition, this study has received funding by Nestlé HealthCare Science GmbH. Nestlé HealthCare Science GmbH supported the study by granting study participants a 15% discount for the formula diet.

                Conceived and designed the experiments: LJV AS JPK MML AAA. Performed the experiments: LJV AS JPK SG JK. Analyzed the data: LJV JPK PJM. Contributed reagents/materials/analysis tools: LJV JPK. Wrote the paper: LJV AS JPK MML JM NH RK AAA MLK.

                Article
                Publisher ID: PONE-D-15-28027
                DOI: 10.1371/journal.pone.0153595
                PMC ID: 4844151
                PubMed ID: 27110719
                SO-VID: 9adea894-b94d-47f6-8371-8d16d47f83be
                Copyright © © 2016 Vogt et al
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 26 June 2015
                Date accepted : 31 March 2016
                Page count
                Figures: 5, Tables: 3, Pages: 14
                Funding
                Two authors of this manuscript declare relationships with the following companies: LJV and JK received a Gerhard Domagk scholarship from University Medicine Greifswald made possible through an unrestricted educational grant from Baxter Deutschland GmbH (Unterschleissheim, Germany), Medinal GmbH (Greven, Germany) and Nutricia GmbH (Erlangen, Germany). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The other authors have no conflict of interests. In addition, this study has received funding by Nestlé HealthCare Science GmbH. The standardized weight-loss program OPTIFAST ® was used with the consent of Nestlé HealthCare Science GmbH. Nestlé HealthCare Science GmbH supported the study by granting study participants a 15% discount for the formula diet.
                Categories
                Subject: Research Article
                Subject: Biology and Life Sciences
                Subject: Biochemistry
                Subject: Lipids
                Subject: Fats
                Subject: Medicine and Health Sciences
                Subject: Diagnostic Medicine
                Subject: Diagnostic Radiology
                Subject: Magnetic Resonance Imaging
                Subject: Research and Analysis Methods
                Subject: Imaging Techniques
                Subject: Diagnostic Radiology
                Subject: Magnetic Resonance Imaging
                Subject: Medicine and Health Sciences
                Subject: Radiology and Imaging
                Subject: Diagnostic Radiology
                Subject: Magnetic Resonance Imaging
                Subject: Medicine and Health Sciences
                Subject: Endocrinology
                Subject: Endocrine Disorders
                Subject: Diabetes Mellitus
                Subject: Medicine and Health Sciences
                Subject: Metabolic Disorders
                Subject: Diabetes Mellitus
                Subject: Biology and Life Sciences
                Subject: Physiology
                Subject: Physiological Parameters
                Subject: Body Weight
                Subject: Weight Loss
                Subject: Medicine and Health Sciences
                Subject: Physiology
                Subject: Physiological Parameters
                Subject: Body Weight
                Subject: Weight Loss
                Subject: Biology and Life Sciences
                Subject: Physiology
                Subject: Immune Physiology
                Subject: Bone Marrow
                Subject: Medicine and Health Sciences
                Subject: Physiology
                Subject: Immune Physiology
                Subject: Bone Marrow
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune System
                Subject: Bone Marrow
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Immune System
                Subject: Bone Marrow
                Subject: Biology and Life Sciences
                Subject: Physiology
                Subject: Physiological Parameters
                Subject: Body Weight
                Subject: Obesity
                Subject: Medicine and Health Sciences
                Subject: Physiology
                Subject: Physiological Parameters
                Subject: Body Weight
                Subject: Obesity
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Endocrine System
                Subject: Pancreas
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Endocrine System
                Subject: Pancreas
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Exocrine Glands
                Subject: Pancreas
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Exocrine Glands
                Subject: Pancreas
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Musculoskeletal System
                Subject: Muscles
                Subject: Abdominal Muscles
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Musculoskeletal System
                Subject: Muscles
                Subject: Abdominal Muscles
                Custom metadata
                Data Availability All relevant data are within the paper and its Supporting Information files.

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