The number of molecules controlling appetite and body weight continues to grow! A new satiety-inducing molecule, secreted by the hypothalamus, has been identified and named ‘nesfatin-1’ (short for: NEFA/nucleobindin2-encoded satiety- and fat-influencing protein).
An article published last year described a new appetite suppressing peptide hormone, obestatin (see previous blog and reference here). One interesting feature about this peptide is that it appears to be derived from the same precursor as ghrelin, the hunger hormone elevated in PWS. Thus ghrelin and obestatin were proposed to originate from the same molecule, but have opposing effects - a Yin and Yang of the appetite world.
A new paper out in the Journal of Pediatrics looks at Ghrelin levels in young children with Prader-Willi syndrome - Erdie-Lalena CR, Holm VA, Kelly PC, Frayo RS, Cummings DE. J Pediatrics, 149:199-204, 2006). This study adds to the existing literature on ghrelin in PWS, and raises the possibility that ghrelin in low is young children with PWS, but increases with age.
Here’s an intriguing new study about ghrelin and seizures (go figure…), showing that people with epilepsy have significantly higher serum ghrelin levels than healthy individuals. The authors propose that high ghrelin levels may indicate a predisposition to seizure activity.
OK, so who out there thinks their child with PWS, despite having some learning difficulties, has a memory like an elephant? And is pretty good at spatial tasks? Well, one possible explanation is provided by Dr. Horvath’s study, link below.
As many of you know, leptin is the signal released from fat cells that relays a message to the brain that the fat cells are 'full' and it's time to stop eating. It has also been discovered that leptin works directly on the fat cells themselves, decreasing their fat-storing ability.
A new hormone involved in controlling hunger has been reported. Obestatin is a derivative of the precursor to ghrelin that has an opposing effect (ie, stopping hunger).
Here is an article in which the authors investigated why people with PWS have high levels of ghrelin in their blood. They wondered if perhaps it had something to do with growth hormone (GH) deficiency, which is common in PWS.
Below a link to an article recently published in the International Journal of Molecular Medicine. The first author is Dr. Talebizadeh, who was supported by an FPWR grant and the last author is Dr. Butler, who many of you know is very active in PWS research and clinical studies. Here, the investigators examined expression of hunger hormones (ghrelin and PYY) and their respective receptors in brain tissue specimens.
Two recent papers look at the obesity due to hypothalamic damage (hypothalamic obesity-HO, which can occur, for example, after treatment for a brain tumor), and one directly compares that condition to PWS. Based on these papers (abstract link below) it looks like the molecular basis for obesity due to HO is at least somewhat different than in PWS.
