Visfatin, A "Belly Fat" Hormone, and Its Relationship to the Metabolic Syndrome

I recently learned in a New York Times article (see: When Sleep Leaves You Tired) that inadequate sleep can result in elevated levels of visfatin, a hormone about which I was unfamiliar. Here is the relevant quote from it:

Studies presented at the American Association of Sleep Medicine's annual meeting in Seattle this week also found that inadequate sleep is associated with lower GPAs among college students and with elevated levels of visfatin, a hormone secreted by belly fat that is associated with insulin resistance.

Having never heard of visfatin. I turned to the Wikipedia for more information about the protein. Here is a brief description of it:

Nampt, PBEF, and visfatin refer to an identical protein, as judged by its amino acid sequence, with multiple biological functions....This protein has also been reported to be a cytokine (PBEF) that promotes B cell maturation and inhibits neutrophil apoptosis....Nampt/PBEF was recently re-identified as a “new visceral fat-derived hormone” named visfatin. It is reported that visfatin is enriched in the visceral fat of both humans and mice and that its plasma levels increase during the development of obesity. Strikingly, visfatin is reported to exert insulin-mimetic effects in cultured cells and to lower plasma glucose levels in mice by binding to and activating the insulin receptor.

So visfatin is a cytokine, a class of proteins that are involved in cellular communication and whose concentrations in the body can increase dramatically with trauma or infection. As soon as a read about the link between visfatin and diabetes/belly fat, I thought about the metabolic syndrome and pre-diabetes about which I have posted previous notes. I had remarked previously that one can quickly recognize the metabolic syndrome because the patient's belly enters the examining room before the patient. Searching for a relationship between visfatin and the metabolic syndrome, I came across another reference (see: PBEF/Visfatin: A Role in Metabolic Syndrome, but What Is It?):

Another hypothesis [about the relationship between visfatin and the metabolic syndrome] notes that macrophages are more prevalent in obese adipose tissue, especially surrounding apoptotic adipocytes. Not only do the macrophages secrete the inflammatory mediators characteristic of metabolic syndrome, they also join adipocytes in producing PBEF/visfatin. Regardless of how a PBEF/visfatin differential is created, once it exists it has the potential to magnify the differential expression of other adipokines and lipolytic pathway molecules due to its ability to promote adipogenesis. What is the relationship between PBEF/visfatin and metabolic syndrome? Is it part of the cause, a compensatory response, or simply an intriguing marker?

So we now have a picture of belly fat as a possible home/factory for macrophages and adipocytes that secrete visfatin and other inflammatory mediators. These substances function as either markers for the metabolic syndrome, a cause of the disease, or a compensatory response. One confusing aspect of this brief analysis is that the NYT article describes visfatin as being associated with insulin resistance whereas the Wikipedia article describes it as having insulin-mimetic effects.

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