Chewing gum drug could help curb obesity?
I came across a news headline: “Chewing gum drug could help curb obesity.” I couldn’t help but be intrigued, so I decided to dig a little deeper. The news release, as it turns out, is based upon the work of professor Steven R. Blum, a British researcher who is a consultant for many major pharmaceutical companies (Merck, GSK, Roche, Novartis, Pfizer, Astra-Zeneca, J&J and others). In addition to owning stock in Thiakis, a new biopharmaceutical company created in 2004, the professor has just received 19 million dollars in VC money (and a 5 million dollar grant from the Wellcome Trust) to further investigate the use of pancreatic polypeptide – an appetite suppressing hormone – for the treatment of obesity.
The amount of money flowing into Blum’s research tells me one thing for sure – Big Pharma is placing a bet on gut hormones as the next big breakthrough in obesity management. Whether this is money well spent, I’m not sure. Leptin (an appetite suppressant hormone produced by fat cells) proved to be a big disappointment to researchers, as obese individuals proved to be resistant to leptin. Pancreatic polypeptide also has a flaw that may prove to limit its use: it is rapidly broken down in the blood stream by enzymes, causing its appetite suppressing effects to be quite transitory.
Evidence to date is limited in humans (as far as I can tell previous studies have mostly focused on mice – I’ll let my GI colleagues correct me here) and Bloom cites a study in which 17 obese adults ate ~15 -25% less at a buffet after being injected with pancreatic polypeptide (compared to 18 others who were injected with saline).
I’d like to believe that gut hormones will lead to an appetite suppressing pill that will reverse or slow our obesity epidemic. But I remain skeptical at this point. What do other people think about this?
This post originally appeared on Dr. Val’s blog at RevolutionHealth.com.
Pancreatic polypeptide (PP) has a number of inhibitory actions that are believed to be important for both pancreatic and gastrointestinal function. Because many of its actions are local, it has been difficult to assess the magnitude of PP’s effects in the pancreas; however, it is well recognized to inhibit pancreatic function. In addition, PP has inhibitory effects on gut motility, and may influence food intake, and energy metabolism.
The pancreatic polypeptide family clearly has a role in feeding behavior. However, regulation of appetite is complex and involves many interacting components, including a number of signaling mechanisms. Work in humans has been limited, and although promising, has a long way to go before it is ready for “prime time”
I wish we didn’t have to rely on studies by “Big Pharma” for the information we need to cure our obesity epidemic!
A study was published in Diabetes 2005 54:3198-3204 entitled “Peptide YY(3–36) Inhibits Morning, but Not Evening, Food Intake and Decreases Body Weight in Rhesus Macaques.” They concluded that these results show that endogenous PYY(3–36) may alter morning but not evening meal intake, and supraphysiological doses give twice a day by intravenous infusion are required for effective suppression of food intake. I suspect Thiakis is well aware of these limitations of using PPY 3 36 and has a synthetic analog that they can patent and which is not affectd by salivary enzymes.
Thiakis’ web site lists another analog they are studing. Professor Steve Bloom and his research group at Imperial College London have identified analogues of oxyntomodulin that are more potent and/or have a longer duration of effect than the native form of oxyntomodulin. These analogues are exclusively licensed to Thiakis.