Mouse CCKAR blocking peptide

Background: The feed conversion ratio (FCR) and residual feed intake (RFI) are common indexes in measuring feed efficiency for livestock RFI is a feed intake adjusted for requirements for maintenance and production so these two traits are related. Similarly, FCR is related to feed intake and weight gain because it is their ratio. Cholecystokinin type A receptor (CCKAR) plays an important role in animal digestive process. We examined the interplay of these three parameters in a local Chinese chicken population. Results: The feed intake (FI) and body weights (BW) of 1,841 individuals were monitored on a daily basis from 56 to 105 d of age. There was a strong correlation between RFI and average daily feed intake (ADFI) and a negative correlation between the FCR and daily gain (r(g) = -0.710). Furthermore, we identified 51 single nucleotide polymorphisms (SNPs) in the CCKAR and 4 of these resulted in amino acid mutations. The C334A mutation was specifically associated with Fl and the expected feed intake (EFI) (P < 0.01) and significantly associated with the average daily gain (ADG) (P < 0.05). G1290A was significantly associated with Fl and EFI (P < 0.05). Conclusion: FCR is apply to weight selecting, and RFI is more appropriate if the breeding focus is feed intake. And C334A and G1290A of the CCKAR gene can be deemed as candidate markers for feed intake and weight gain.

Type A cholecystokinin receptor (CCKAR) antagonists differing in blood-brain barrier permeability were used to test the hypothesis that satiety is mediated, in part, by CCK action at CCKARs located peripheral to the blood-brain barrier. At dark onset, non-food-deprived rats received a bolus injection of devazepide (2.5 mumol/kg iv), a 3-h infusion of A-70104 (1 or 3 mumol . kg(-1) . h(-1) iv), or vehicle either alone or coadministered with a 3-h infusion of CCK-8 (10 nmol . kg(-1) . h(-1) iv) or a 2-h intragastric infusion of peptone ( 1 g/h). Food intake was determined from continuous computer recordings of changes in food bowl weight. Devazepide penetrates the blood-brain barrier; A-70104, the dicyclohexylammonium salt of N-alpha-3-quinolinoyl-D- Glu-N,N-dipentylamide(A-65186), does not. CCK-8 inhibited 3-h food intake by more than 50% and both A-70104 and devazepide abolished this response. A-70104 and devazepide stimulated food intake and similarly attenuated the anorexic response to intragastric infusion of peptone. Thus endogenous CCK appears to act, in part, at CCKARs peripheral to the blood-brain barrier to inhibit food intake.