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A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood
Published on: April 28, 2016
Dietary unsaturated fatty acids increase plasma glucagon-like peptide-1 and cholecystokinin and may decrease premeal
B J Bradford1, K J Harvatine, M S Allen
1Department of Animal Science, Michigan State University, East Lansing 48824, USA.
Journal of Dairy Science
|March 20, 2008
Summary
Dietary unsaturated fats reduce feed intake in dairy cows by increasing gut peptides cholecystokinin (CCK) and glucagon-like peptide 1 (GLP-1). Unsaturated fats also appear to suppress ghrelin release, further impacting appetite regulation.
Area of Science:
- Animal Science
- Nutritional Physiology
- Endocrinology
Background:
- Dietary unsaturated fats are known to reduce energy intake in lactating dairy cows.
- The physiological mechanisms underlying this effect remain poorly understood.
Purpose of the Study:
- To investigate the role of gut peptides, specifically cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1), and ghrelin, in mediating the reduced feed intake response to unsaturated fats in dairy cattle.
Main Methods:
- A replicated 4x4 Latin square experiment was conducted with lactating dairy cows.
- Three dietary treatments were administered: control, saturated fat (SAT), and unsaturated fat (UNS).
- Periprandial plasma concentrations of CCK, GLP-1, and ghrelin were measured via radioimmunoassay.
Main Results:
- Unsaturated fat (UNS) diets increased duodenal unsaturated fatty acid flow and plasma CCK concentrations compared to control and SAT diets.
- UNS diets also elevated plasma GLP-1 concentrations relative to the control diet.
- Both SAT and UNS diets tended to suppress the prandial ghrelin surge observed in the control group.
Conclusions:
- Increased secretion of CCK and GLP-1 likely contributes to the suppression of feed intake induced by dietary unsaturated fats in dairy cows.
- Dietary fat, particularly unsaturated fat, may also inhibit ghrelin release prior to anticipated meals, further influencing appetite regulation.
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