Adiponectin: More Than Just Another Fat Cell Hormone

Recent research has shown that adipose tissue is not simply an inert storage depot for lipids but is also an important endocrine organ that plays a key role in the integration of endocrine, metabolic, and inflammatory signals for the control of energy homeostasis.

The view of the adipocyte as simply a storage depot for fat is no longer tenable. Among the various “adipocytokines,” adiponectin, which is an abundant circulating protein synthesized solely in adipose tissue, appears to play a very important role in carbohydrate and lipid metabolism and vascular biology. Adiponectin appears to be a major modulator of insulin action and its levels are reduced in type 2 diabetes, which could contribute to peripheral insulin resistance in this condition. It has significant insulin-sensitizing as well as anti-inflammatory properties that include suppression of macrophage phagocytosis and TNF-α secretion and blockage of monocyte adhesion to endothelial cells in vitro. To date, however, adiponectin’s putative antiatherogenic potential in humans remains substantially weaker and less well studied than its insulin-sensitizing effects.

Although further investigations are required, adiponectin administration, as well as regulation of the pathways controlling its production, represents a promising target for managing obesity, hyperlipidemia, insulin resistance, type 2 diabetes, and vascular inflammation.

Numerous important questions about adiponectin await further study. The mechanisms by which adiponectin is synthesized and secreted need to be elucidated, as do the signals that reduce adiponectin expression in adipocytes with increasing adiposity. Similarly, the role and regulation of adiponectin oligomerization need to be defined. The molecular mechanisms by which adiponectin exerts its multiple functions and whether its actions are receptor mediated still remain a mystery. Is the primary activity of adiponectin antiatherosclerotic, or is it principally a modulator of lipid metabolism and regulator of insulin sensitivity—or is it all of the above? The answers to these and other intriguing questions will undoubtedly provide additional insight into the metabolic roles of this new adipocyte hormone.

The domain structure of Acrp30: signal sequence, species-specific variable region, collagenous domain, and globular trimerization domain. Modified with permission from Berg et al. (23).

Model for assembly of adiponectin complexes. Three monomers form a trimer through associations between their globular domains. Four to six trimers associate noncovalently through their collagenous domains to form high-molecular-weight oligomers, which circulate in the plasma. Modified with permission from Berg et al. (23).

Hypothetical model for the actions of adiponectin. In skeletal muscle, adiponectin increases tyrosine phosphorylation of the insulin receptor. This effect may contribute to increased insulin sensitivity. It also increases fatty acid oxidation, probably by activation of 5′-AMP kinase, with resultant decreased intramyocellular steatosis. In the liver, the decreased free fatty acid influx and increased fatty acid oxidation contribute to reduced hepatic glucose output and VLDL triglyceride synthesis. In vascular endothelium, adiponectin decreases monocyte adhesion to endothelium, suppresses macrophage-to-foam cell transformation, and inhibits vascular smooth muscle cell proliferation and migration.


  1. Manju Chandran, MD1,
  2. Susan A. Phillips, MD2,
  3. Theodore Ciaraldi, PHD1 and
  4. Robert R. Henry, MD1

-Author Affiliations

  1. 1Division of Diabetes, Endocrinology and Metabolism, University of California, San Diego School of Medicine
  2. 2Division of Pediatric Endocrinology, University of California, San Diego School of Medicine, and VA San Diego Health Care System, San Diego, California

Day after day I felt it couldn't continue to burn myself out. I looked up at the sky and begged for silence, rest and peace.

I was fatally tired and the last straw had manifest; my partner abandoned me and moved on. Shortly after, circumstances took their toll and I collapsed..

Read more

All in all, I spent 6 months in total isolation and silence. During this time, I went through absolute mental and physical fasting. I also met twice with the other side, which was the scariest moments in my life, but allowed me to experience a deeper insight - a sense of enlightenment.

In other words, I gathered my desire and the last willpower and after 100% focus on myself and my healing:

- I walked out of bed after 2 months in 5 days;
- I was healed from illness in 4 months;
- I was recovered and restored my body power in 6 months;
- I was all clear and I changed my life to 180°!

Within the healing time, I had to go through all my unsolved pain and injuries from the past and worked with that at the same time in order to allow myself to naturally heal, no drugs or experiments involved.

To be fully healed and feel no more pain or suffering we have to give it enough focus to ascertain the roots thereof!

Today I am infinitely grateful for the blessings I received and I am now, in turn, to inspired to use my gifts to help and heal others!


I'll help you find a way out of worry, stress, crisis, loneliness, burnout, phobia, conflict, domestic violence, anxiety, anxiety disorder, panic attacks or physical illness to reunite with your lost Self and return to your inner peace and well-being.
The method I use will help you overcome difficulties, learn from my similar experiences, receive guidance and support to cope with your story, achieve healing, recovery, peace and happiness.



I'll help you find a way out of suffering from Stress, Crisis, Loneliness, Burnout, Phobia, Conflict, Domestic Violence, Anxiety- and Panic Disorder, Body Illness, generally, whatever the case may be.

Blueprints One-By-One
Check Out The
Special Offers On Etsy

Substance-induced anxiety disorder
Irisin in metabolic diseases

Write first comment

Email again: