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Overview

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Metabolism of Human Diseases

Abstract

Adipose tissue has evolved into a highly specialized tissue for storing energy in the form of triglycerides (TGs, also called triacylglycerols, or “fat”). It is heterogeneous in cellular composition, location, and function – reflecting its complex role in normal physiology and disease [1]. It is comprised not only of different types of adipocytes (ranging from white to brown) but also other non-adipocyte cell types (such as stromal vascular and immune cells) to form a true multicellular organ [2]. Unlike other organs, adipose tissue is distributed throughout the body where it exhibits location-specific properties. Furthermore, its functions extend well beyond its role in fat storage to a variety of other processes necessary for physiological homeostasis including energy homeostasis, immune homeostasis, and reproductive function [3]. The heterogeneity of adipose tissue is reflected by the variety of clinical disorders that result from adipose tissue dysfunction [4, 5]. Indeed, both adipose tissue excess (obesity) and deficiency (lipodystrophy) result in profound physiological impairments that promote the metabolic syndrome (see chapter “Metabolic syndrome”) and cardiovascular disease (see chapter “Atherosclerotic heart disease”). Adipose tissue dysfunction or excess also contributes to a myriad of other diseases affecting virtually all organ systems including liver disease, i.e., fatty liver and cirrhosis (see chapter “Cirrhosis”); kidney disease, e.g., diabetic and hypertensive nephropathy (see chapters “Diabetes mellitus” and “Hypertension”); pulmonary disease, e.g., sleep apnea; musculoskeletal disease, i.e., arthritis (see chapters “Osteoarthritis” and “Rheumatoid arthritis”) and back pain; reproductive disease, i.e., infertility; psychological disease, i.e., depression (see chapter “Major depressive disorder”); and even cancer (see chapter “Overview” under the part “Cancer”) [6]. Thus, adipose tissue is not simply an inert tissue for storing fat, but a highly dynamic tissue required for health and survival. By understanding the unique characteristics of adipose tissue, can we begin to exploit its complexities to treat or prevent disease.

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References

  1. Gesta S, Tseng YH, Kahn CR (2007) Developmental origin of fat: tracking obesity to its source. Cell 131:242–256

    Article  CAS  PubMed  Google Scholar 

  2. Cinti S (2012) The adipose organ at a glance. Dis Model Mech 5:588–594

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  3. Kershaw EE, Flier JS (2004) Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 89:2548–2556

    Article  CAS  PubMed  Google Scholar 

  4. Garg A (2011) Lipodystrophies: genetic and acquired body fat disorders. J Clin Endocrinol Metab 96:3313–3325

    Article  CAS  PubMed  Google Scholar 

  5. Herbst KL (2012) Rare adipose disorders (RADs) masquerading as obesity. Acta Pharmacol Sin 33:155–172

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  6. Malnick SD, Knobler H (2006) The medical complications of obesity. QJM 99:565–579

    Article  CAS  PubMed  Google Scholar 

  7. Cypess AM, Lehman S, Williams G, Tal I, Rodman D, Goldfine AB, Kuo FC, Palmer EL, Tseng YH, Doria A, Kolodny GM, Kahn CR (2009) Identification and importance of brown adipose tissue in adult humans. N Engl J Med 360:1509–1517

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Wu J, Cohen P, Spiegelman BM (2013) Adaptive thermogenesis in adipocytes: is beige the new brown? Genes Dev 27:234–250

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Bickel PE, Tansey JT, Welte MA (2009) PAT proteins, an ancient family of lipid droplet proteins that regulate cellular lipid stores. Biochim Biophys Acta 1791:419–440

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Karastergiou K, Mohamed-Ali V (2010) The autocrine and paracrine roles of adipokines. Mol Cell Endocrinol 318:69–78

    Article  CAS  PubMed  Google Scholar 

  11. Cinti S, Mitchell G, Barbatelli G, Murano I, Ceresi E, Faloia E, Wang S, Fortier M, Greenberg AS, Obin MS (2005) Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans. J Lipid Res 46:2347–2355

    Article  CAS  PubMed  Google Scholar 

  12. Gregor MF, Hotamisligil GS (2011) Inflammatory mechanisms in obesity. Ann Rev Immunol 29:415–445

    Article  CAS  Google Scholar 

  13. Mantzoros CS, Magkos F, Brinkoetter M, Sienkiewicz E, Dardeno TA, Kim SY, Hamnvik OP, Koniaris A (2011) Leptin in human physiology and pathophysiology. Am J Physiol Endocrinol Metab 301:E567–E584

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Turer AT, Scherer PE (2012) Adiponectin: mechanistic insights and clinical implications. Diabetologia 55:2319–2326

    Article  CAS  PubMed  Google Scholar 

  15. Wajchenberg BL (2000) Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome. Endocr Rev 21:697–738

    Article  CAS  PubMed  Google Scholar 

  16. Flier JS (2004) Obesity wars: molecular progress confronts an expanding epidemic. Cell 116:337–350

    Article  CAS  PubMed  Google Scholar 

  17. Malik VS, Willett WC, Hu FB (2013) Global obesity: trends, risk factors and policy implications. Nat Rev Endocrinol 9:13–27

    Article  PubMed  Google Scholar 

  18. O'Rahilly S (2009) Human genetics illuminates the paths to metabolic disease. Nature 462:307–314

    Article  PubMed  Google Scholar 

  19. Magkos F, Yannakoulia M, Chan JL, Mantzoros CS (2009) Management of the metabolic syndrome and type 2 diabetes through lifestyle modification. Annu Rev Nutr 29:223–256

    Article  CAS  PubMed  Google Scholar 

  20. Grun F, Blumberg B (2009) Endocrine disrupters as obesogens. Mol Cell Endocrinol 304:19–29

    Article  PubMed  PubMed Central  Google Scholar 

  21. McAllister EJ, Dhurandhar NV, Keith SW, Aronne LJ, Barger J, Baskin M, Benca RM, Biggio J, Boggiano MM, Eisenmann JC, Elobeid M, Fontaine KR, Gluckman P, Hanlon EC, Katzmarzyk P, Pietrobelli A, Redden DT, Ruden DM, Wang C, Waterland RA, Wright SM, Allison DB (2009) Ten putative contributors to the obesity epidemic. Crit Rev Food Sci Nutr 49:868–913

    Article  PubMed  PubMed Central  Google Scholar 

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Correspondence to Erin E. Kershaw .

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Schoiswohl, G., Aljammal, J., Kershaw, E.E. (2014). Overview. In: Lammert, E., Zeeb, M. (eds) Metabolism of Human Diseases. Springer, Vienna. https://doi.org/10.1007/978-3-7091-0715-7_29

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