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Department of Nutrition, University of California, Davis, CA 95616
We investigated the influence of luminal fat, including intestinal exposure time to fat, on food intake and body weight (BW) gain under conditions that resemble normal feeding. Male Wistar rats were divided into three groups: two groups received 30 mL Intralipid® and one group received 30 mL saline, in addition to having access to a nonfat diet. The saline-infused and one of the fat-infused groups were schedule fed (SF), i.e., allowed to eat for 7 h of the dark cycle; the other fat-infused group had diet available for 24 h. The three groups of rats were subdivided further by rate of infusion, i.e., 0.13 mL/min or 1.0 mL/min for a total of 6 groups. Rats infused with fat had lower BW gain than saline controls, except when diet was available for 24 h and rate of fat infusion was 1.0 mL/min (BW gain was similar to saline group). Daily energy intake corresponded to BW gain data. Pancreata and intestinal mucosa were examined (after 2 wk of treatment) for hypertrophic changes that may be related to specific factors stimulated by luminal fat; these may also be involved in the control of food intake. Rats infused with fat had heavier pancreata than saline-infused rats, and infusion of fat at 0.13 mL/min resulted in heavier pancreata than infusion at the faster rate. DNA and protein analysis indicated that hypertrophy rather than hyperplasia was responsible for this effect. Thus, prolonged fat exposure to intraluminal receptors resulted in reduced total daily energy intake, suppressed BW gain and heavier pancreata. The combined data support a connection among intraluminal fat, negative feedback signals that inhibit food intake and factor(s) associated with pancreatic stimulation.
KEY WORDS: fat satiety food intake rats infusion
1 The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.
2 Supported by a predoctoral fellowship from Nestlé Inc., Lansanne, Switzerland.
3 To whom correspondence should be addressed.
Manuscript received 3 January 1996. Revision accepted 1 August 1996.
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