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      Adipose tissue-derived factors: impact on health and disease.

      1 ,
      Endocrine reviews
      The Endocrine Society

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          Abstract

          The endocrine functions of the adipose organ are widely studied at this stage. The adipose organ, and in particular adipocytes, communicate with almost all other organs. Although some adipose tissue pads assume the functions as distinct "miniorgans," adipocytes can also be present in smaller numbers interspersed with other cell types. Although fat pads have the potential to have a significant systemic impact, adipocytes may also affect neighboring tissues through paracrine interactions. These local or systemic effects are mediated through lipid and protein factors. The protein factors are commonly referred to as adipokines. Their expression and posttranslational modifications can undergo dramatic changes under different metabolic conditions. Due to the fact that none of the mutations that affect adipose tissue trigger embryonic lethality, the study of adipose tissue physiology lends itself to genetic analysis in mice. In fact, life in the complete absence of adipose tissue is possible in a laboratory setting, making even the most extreme adipose tissue phenotypes genetically amenable to be analyzed by disruption of specific genes or overexpression of others. Here, we briefly discuss some basic aspects of adipocyte physiology and the systemic impact of adipocyte-derived factors on energy homeostasis.

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          Author and article information

          Journal
          Endocr Rev
          Endocrine reviews
          The Endocrine Society
          0163-769X
          0163-769X
          Dec 2006
          : 27
          : 7
          Affiliations
          [1 ] Departments of Cell Biology and Medicine, Diabetes Research and Training Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA.
          Article
          er.2006-0033
          10.1210/er.2006-0033
          17056740
          4214d317-7d16-40ac-b811-d51cfa2386c5
          History

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