CCK knockout mice were resistant to high-fat diet-induced obesity — paradoxically, losing the satiety hormone CCK protected against weight gain, suggesting CCK has complex metabolic roles beyond simple meal termination.
Key findingCCK knockout mice were resistant to high-fat diet-induced obesity — paradoxically, losing the satiety hormone CCK protected against weight gain, sugge
What the researchers found
CCK knockout mice were resistant to high-fat diet-induced obesity — paradoxically, losing the satiety hormone CCK protected against weight gain, suggesting CCK has complex metabolic roles beyond simple meal termination.
Why it matters
Relevant for peptide research.
How the study worked
research study.
What this study cannot tell us
See abstract.
How to read the evidence
emerging evidence.
When this study was published
Published in 2010.
The bigger picture
Advances peptide research.
Questions still open
- Further research needed.
Common questions
What was studied?
What was found?
Read the original research
Cholecystokinin knockout mice are resistant to high-fat diet-induced obesity.
Gastroenterology, 138(5), 1997-2005
Citation
Lo, Chun-Min; King, Alexandra; Samuelson, Linda C; Kindel, Tammy Lyn; Rider, Therese; Jandacek, Ronald J; Raybould, Helen E; Woods, Stephen C; Tso, Patrick. (2010). Cholecystokinin knockout mice are resistant to high-fat diet-induced obesity.. Gastroenterology, 138(5), 1997-2005. https://doi.org/10.1053/j.gastro.2010.01.044