Appeal 2006-1223
Application 10/214,009
from their having been individually taught in [the] prior art” (Kerkhoven,
626 F.2d at 850, 205 USPQ at 1072; Answer 4).
Appellants additionally argue that Portman’s “long chain fatty acids
by themselves would not produce [ ] increased satiety” (Br. 4), because “to
increase satiety there has to be some kind of negative feedback mechanism
of CCK release” (id.).
We have carefully considered this argument, but it does not persuade
us that the Examiner’s prima facie case is in error. According to Portman,
“[w]hen food is consumed, CCK releasing protein (CCKRP) is released in
the small intestine. CCKRP stimulates CCK release from intestinal cells.
The release of CCK generates the behavioral symptoms associated with
satiety and at the same time activates a number of negative feedback
mechanisms to turn off the CCK response” (Portman, col. 1, l. 63 to col. 2, l.
1). For example, CCK “stimulates gallbladder contraction causing bile acids
to be released into the intestinal lumen” and “[b]ile acids are powerful
regulators of CCK, inhibiting its release” (id. at col. 2, ll. 6-9).
To counteract this effect and extend satiety, Portman’s composition
includes fiber to bind bile acids, thereby “block[ing] the negative feedback
mechanism of CCK release” (id. at col. 5, ll. 64-65; and col. 6, ll. 27-31).
We note that claim 1 on appeal is not closed to the inclusion of fiber in the
composition, that certain dependent claims explicitly recite that the
composition contains fiber (e.g., claim 17), and finally, that the exemplary
compositions set forth in Examples 1-14 of the present specification all
contain fiber. That being the case, the fact the Portman teaches that CCK
release normally initiates a negative feedback mechanism does not persuade
6
Page: Previous 1 2 3 4 5 6 7 8 9 10 Next
Last modified: September 9, 2013