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      Vitamin A Metabolism and Adipose Tissue Biology

      review-article
      Author(s): , *
      Publication date (Electronic):
      Journal: Nutrients
      Publisher: MDPI
      Keywords: retinol, retinoic acid, adipose tissue, cellular retinol-binding protein, beta-carotene, adipogenesis

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          Abstract

          In recent years, the importance of vitamin A in adipose tissue biology, obesity and type II diabetes has become apparent. This review focuses on recent developments within the area of vitamin A and adipose tissue biology. Adipose tissue has an active vitamin A metabolism as it not only stores vitamin A but retinol is also converted to its active metabolite retinoic acid. Several mouse models point to a relationship between vitamin A metabolism and the development of adiposity. Similarly, in vitro studies provide new molecular mechanisms for the function of different forms of vitamin A and retinol- or retinoic acid-binding proteins in adipose tissue.

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          Adipocytes as regulators of energy balance and glucose homeostasis.

          Evan Rosen, Bruce M Spiegelman (2006)
          Adipocytes have been studied with increasing intensity as a result of the emergence of obesity as a serious public health problem and the realization that adipose tissue serves as an integrator of various physiological pathways. In particular, their role in calorie storage makes adipocytes well suited to the regulation of energy balance. Adipose tissue also serves as a crucial integrator of glucose homeostasis. Knowledge of adipocyte biology is therefore crucial for understanding the pathophysiological basis of obesity and metabolic diseases such as type 2 diabetes. Furthermore, the rational manipulation of adipose physiology is a promising avenue for therapy of these conditions.
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            Retinol-binding protein 4 and insulin resistance in lean, obese, and diabetic subjects.

            Timothy Graham, Qin Yang, Matthias Blüher … (2006)
            Insulin resistance has a causal role in type 2 diabetes. Serum levels of retinol-binding protein 4 (RBP4), a protein secreted by adipocytes, are increased in insulin-resistant states. Experiments in mice suggest that elevated RBP4 levels cause insulin resistance. We sought to determine whether serum RBP4 levels correlate with insulin resistance and change after an intervention that improves insulin sensitivity. We also determined whether elevated serum RBP4 levels are associated with reduced expression of glucose transporter 4 (GLUT4) in adipocytes, an early pathological feature of insulin resistance. We measured serum RBP4, insulin resistance, and components of the metabolic syndrome in three groups of subjects. Measurements were repeated after exercise training in one group. GLUT4 protein was measured in isolated adipocytes. Serum RBP4 levels correlated with the magnitude of insulin resistance in subjects with obesity, impaired glucose tolerance, or type 2 diabetes and in nonobese, nondiabetic subjects with a strong family history of type 2 diabetes. Elevated serum RBP4 was associated with components of the metabolic syndrome, including increased body-mass index, waist-to-hip ratio, serum triglyceride levels, and systolic blood pressure and decreased high-density lipoprotein cholesterol levels. Exercise training was associated with a reduction in serum RBP4 levels only in subjects in whom insulin resistance improved. Adipocyte GLUT4 protein and serum RBP4 levels were inversely correlated. RBP4 is an adipocyte-secreted molecule that is elevated in the serum before the development of frank diabetes and appears to identify insulin resistance and associated cardiovascular risk factors in subjects with varied clinical presentations. These findings provide a rationale for antidiabetic therapies aimed at lowering serum RBP4 levels. Copyright 2006 Massachusetts Medical Society.
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              Regulation of lipolysis in adipocytes.

              Robin Duncan, Maryam Ahmadian, Kathy Jaworski … (2007)
              Lipolysis of white adipose tissue triacylglycerol stores results in the liberation of glycerol and nonesterified fatty acids that are released into the vasculature for use by other organs as energy substrates. In response to changes in nutritional state, lipolysis rates are precisely regulated through hormonal and biochemical signals. These signals modulate the activity of lipolytic enzymes and accessory proteins, allowing for maximal responsiveness of adipose tissue to changes in energy requirements and availability. Recently, a number of novel adipocyte triacylglyceride lipases have been identified, including desnutrin/ATGL, greatly expanding our understanding of adipocyte lipolysis. We have also begun to better appreciate the role of a number of nonenzymatic proteins that are critical to triacylglyceride breakdown. This review provides an overview of key mediators of lipolysis and the regulation of this process by changes in nutritional status and nutrient intakes.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Nutrients
                Journal ID (publisher-id): nutrients
                Title: Nutrients
                Publisher: MDPI
                ISSN (Electronic): 2072-6643
                Publication date (Electronic): 06 January 2011
                Publication date Collection: January 2011
                Volume: 3
                Issue: 1
                Pages: 27-39
                Affiliations
                Department of Medicine and the Institute of Human Nutrition, Columbia University, 630 W 168th Street, P&S 1512, New York, NY 10032, USA; Email: mail@ 123456simonefrey.de
                Author notes
                [* ]Author to whom correspondence should be addressed; Email: sv98@ 123456columbia.edu ; Tel.: +1-212-305-4808; Fax: +1-212-305-3079.
                Article
                Publisher ID: nutrients-03-00027
                DOI: 10.3390/nu3010027
                PMC ID: 3257733
                PubMed ID: 22254074
                SO-VID: 1685ecf1-e35a-4650-a063-7e2747f63081
                Copyright © © 2011 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 20 November 2010
                Date revision received : 14 December 2010
                Date accepted : 05 January 2011
                Categories
                Subject: Review

                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: adipose tissue,retinoic acid,beta-carotene,adipogenesis,cellular retinol-binding protein,retinol
                Data availability:
                ScienceOpen disciplines: Nutrition & Dietetics
                Keywords: adipose tissue, retinoic acid, beta-carotene, adipogenesis, cellular retinol-binding protein, retinol

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