Cincinnati Obesity Research Center, Genome Research Institute, University of Cincinnati, Cincinnati, Ohio 45237, USA.
Gastroenterology. 2010 May;138(5):1997-2005. doi: 10.1053/j.gastro.2010.01.044. Epub 2010 Feb 1.
BACKGROUND & AIMS: Cholecystokinin (CCK) is a satiation peptide released during meals in response to lipid intake; it regulates pancreatic digestive enzymes that are required for absorption of nutrients. We proposed that mice with a disruption in the CCK gene (CCK knockout [CCK-KO] mice) that were fed a diet of 20% butter fat would have altered fat metabolism.
We used quantitative magnetic resonance imaging to determine body composition and monitored food intake of CCK-KO mice using an automated measurement system. Intestinal fat absorption and energy expenditure were determined using a noninvasive assessment of intestinal fat absorption and an open circuit calorimeter, respectively.
After consuming a high-fat diet for 10 weeks, CCK-KO mice had reduced body weight gain and body fat mass and enlarged adipocytes, despite the same level of food intake as wild-type mice. CCK-KO mice also had defects in fat absorption, especially of long-chain saturated fatty acids, but pancreatic triglyceride lipase did not appear to have a role in the fat malabsorption. Energy expenditure was higher in CCK-KO than wild-type mice, and CCK-KO mice had greater oxidation of carbohydrates while on the high-fat diet. Plasma leptin levels in the CCK-KO mice fed the high-fat diet were markedly lower than in wild-type mice, although levels of insulin, gastric-inhibitory polypeptide, and glucagon-like peptide-1 were normal.
CCK is involved in regulating the metabolic rate and is important for lipid absorption and control of body weight in mice placed on a high-fat diet.
胆囊收缩素（CCK）是一种在进食过程中响应脂质摄入而释放的饱腹感肽；它调节胰腺消化酶，这些酶是吸收营养物质所必需的。我们提出，CCK 基因缺失（CCK 敲除 [CCK-KO] 小鼠）的小鼠在喂食 20%黄油脂肪的饮食时，脂肪代谢会发生改变。
我们使用定量磁共振成像来确定身体成分，并使用自动测量系统监测 CCK-KO 小鼠的食物摄入量。通过非侵入性的肠道脂肪吸收评估和开路量热计分别确定肠道脂肪吸收和能量消耗。
在食用高脂肪饮食 10 周后，尽管 CCK-KO 小鼠的食物摄入量与野生型小鼠相同，但体重增加和体脂肪量减少，脂肪细胞增大。CCK-KO 小鼠的脂肪吸收也存在缺陷，特别是长链饱和脂肪酸，但胰腺三酰基甘油脂肪酶似乎不是脂肪吸收不良的原因。与野生型小鼠相比，CCK-KO 小鼠的能量消耗更高，并且在高脂肪饮食时，碳水化合物的氧化更多。尽管胰岛素、胃抑制肽和胰高血糖素样肽-1水平正常，但喂食高脂肪饮食的 CCK-KO 小鼠的血浆瘦素水平明显低于野生型小鼠。
CCK 参与调节代谢率，对于高脂肪饮食喂养的小鼠的脂质吸收和体重控制很重要。
