Gastric bypass reduces fat intake and preference

Roux-en-Y gastric bypass is the most effective therapy for morbid obesity. This study investigated how gastric bypass affects intake of and preference for high-fat food in an experimental (rat) study and within a trial setting (human). Proportion of dietary fat in gastric bypass patients was significantly lower 6 yr after surgery compared with patients after vertical-banded gastroplasty ( P = 0.046). Gastric bypass reduced total fat and caloric intake ( P < 0.001) and increased standard low-fat chow consumption compared with sham controls ( P < 0.001) in rats. Compared with sham-operated rats, gastric bypass rats displayed much lower preferences for Intralipid concentrations > 0.5% in an ascending concentration series (0.005%, 0.01%, 0.05%, 0.1%, 0.5%, 1%, 5%) of two-bottle preference tests ( P = 0.005). This effect was demonstrated 10 and 200 days after surgery. However, there was no difference in appetitive or consummatory behavior in the brief access test between the two groups ( P = 0.71) using similar Intralipid concentrations (0.005% through 5%). Levels of glucagon-like peptide-1 (GLP-1) were increased after gastric bypass as expected. An oral gavage of 1 ml corn oil after saccharin ingestion in gastric bypass rats induced a conditioned taste aversion. These findings suggest that changes in fat preference may contribute to long-term maintained weight loss after gastric bypass. Postingestive effects of high-fat nutrients resulting in conditioned taste aversion may partially explain this observation; the role of GLP-1 in mediating postprandial responses after gastric bypass requires further investigation.

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High-fat diets rich in saturated fat protect against azoxymethane/dextran sulfate sodium-induced colon cancer

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00345.2015 ◽

2016 ◽

Vol 310 (11) ◽

pp. G906-G919 ◽

Cited By ~ 20

Author(s):

Reilly T. Enos ◽

Kandy T. Velázquez ◽

Jamie L. McClellan ◽

Taryn L. Cranford ◽

Mitzi Nagarkatti ◽

...

Keyword(s):

Colon Cancer ◽

Dose Response ◽

Dextran Sulfate ◽

Dextran Sulfate Sodium ◽

Caloric Intake ◽

Saturated Fat ◽

Intestinal Barrier ◽

Inverse Association ◽

High Fat ◽

Total Fat

High-fat-diet (HFD) consumption is associated with colon cancer risk. However, little is known about how the lipid composition of a HFD can influence prooncogenic processes. We examined the effects of three HFDs differing in the percentage of total calories from saturated fat (SF) (6, 12, and 24% of total caloric intake), but identical in total fat (40%), and a commercially available Western diet (26 and 41% saturated and total fat, respectively) on colon cancer development using the azoxymethane (AOM)/dextran sulfate sodium (DSS) murine model. A second dose-response experiment was performed using diets supplemented with the saturated-fatty-acid (SFA)-rich coconut oil. In experiment 1, we found an inverse association between SF content and tumor burden. Furthermore, increased SF content was associated with reduced inflammation, increased apoptosis, and decreased proliferation. The second dose-response experiment was performed to test whether this effect may be attributed to the SF content of the diets. Consistent with the initial experiment, we found that high SF content was protective, at least in male mice; there was a decrease in mortality in mice consuming the highest concentration of SFAs. To explore a potential mechanism for these findings, we examined colonic mucin 2 (Muc2) protein content and found that the HFDs with the highest SF content had the greatest concentration of Muc2. Our data suggest that high dietary SF is protective in the AOM/DSS model of colon cancer, which may be due, at least in part, to the ability of SF to maintain intestinal barrier integrity through increased colonic Muc2.

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Chronic high-fat feeding increases GIP and GLP-1 secretion without altering body weight

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00351.2013 ◽

2015 ◽

Vol 309 (10) ◽

pp. G807-G815 ◽

Cited By ~ 14

Author(s):

Fei Wang ◽

Stephanie M. Yoder ◽

Qing Yang ◽

Alison B. Kohan ◽

Tammy L. Kindel ◽

...

Keyword(s):

Body Weight ◽

Energy Intake ◽

Caloric Intake ◽

Sprague Dawley ◽

High Fat ◽

Sprague Dawley Rats ◽

Lymphatic Duct ◽

Secretion Profile ◽

Incretin Secretion ◽

Glucagon Like Peptide 1

The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), enhance postprandial insulin secretion, promote adipogenesis, and regulate gastrointestinal motility and food intake. To date, a consensus on how the incretin response is altered in obesity is lacking. We investigated the effects of chronic high-fat (HF) feeding on incretin secretion in the lymph fistula rat model. Male Sprague-Dawley rats (8 wk) were provided a semipurified AIN93M HF or low-fat (LF) diet ad libitum for 3 or 13 wk; a HF pair-fed (HF-PF) group was included as a control during the 3-wk feeding trial. Energy intake, body weight, and body composition were regularly monitored. At the culmination of the feeding period, an intestinal lymphatic duct cannula and duodenal infusion tube were installed. All animals were challenged with a 3-ml Ensure bolus (3.125 kcal/animal) to measure lymphatic incretin secretion. Despite a significantly higher energy intake, both the 3-wk and 13-wk HF-fed animals did not have an increase in body weight and only a slight increase in body fat compared with LF-fed rats. Following the duodenal Ensure challenge, the 3-wk and 13-wk HF-fed rats had significantly greater lymphatic GIP and GLP-1 secretion than the LF-fed animals. Additionally, the HF-PF group displayed a secretion profile similar to the HF-fed animals for GIP but a similar pattern to the LF-fed animals for GLP-1. The HF-PF data suggest that the increased GIP secretion is driven by the greater percentage of fat intake, whereas the increased GLP-1 secretion is driven by the excess caloric intake.

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PVN infusion of GLP-1-(7—36) amide suppresses feeding but does not induce aversion or alter locomotion in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.274.1.r23 ◽

1998 ◽

Vol 274 (1) ◽

pp. R23-R29 ◽

Cited By ~ 30

Author(s):

Lance R. McMahon ◽

Paul J. Wellman

Keyword(s):

Taste Aversion ◽

Paraventricular Nucleus ◽

Water Intake ◽

Conditioned Taste Aversion ◽

Locomotor Behavior ◽

Hypothalamic Paraventricular Nucleus ◽

Intracerebroventricular Infusion ◽

Food And Water Intake ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1

Intracerebroventricular infusion of glucagon-like peptide-1-(7—36) amide (GLP-1) reduces feeding in rats, an effect that could be localized to the hypothalamic paraventricular nucleus (PVN). Intracerebroventricular GLP-1, however, may also induce conditioned taste aversion (CTA), thereby putting into question the specificity of the action of GLP-1 on feeding. The present experiments evaluated the action of PVN GLP-1 (0, 100, or 200 ng) on induction of CTA, on locomotion, and finally, on feeding and drinking in rats. PVN infusion of GLP-1 (100 or 200 ng) did not support the induction of CTA and did not reliably alter locomotion, but did suppress feeding and drinking. The present study suggests that GLP-1 infusions into the PVN reduce food and water intake without producing illness or disrupting locomotor behavior. These data, in conjunction with reports of increased feeding following antagonism of central GLP-1 receptors, support the notion that endogenous GLP-1, perhaps within the PVN, functions to suppress feeding in the rat.

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Roux-en-Y gastric bypass in rats increases sucrose taste-related motivated behavior independent of pharmacological GLP-1-receptor modulation

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00214.2011 ◽

2012 ◽

Vol 302 (6) ◽

pp. R751-R767 ◽

Cited By ~ 41

Author(s):

C. M. Mathes ◽

M. Bueter ◽

K. R. Smith ◽

T. A. Lutz ◽

C. W. le Roux ◽

...

Keyword(s):

Gastric Bypass ◽

Sucrose Concentration ◽

Appetitive Behavior ◽

Receptor Modulation ◽

Motivated Behavior ◽

Bottle Test ◽

Vehicle Injection ◽

Glucagon Like Peptide 1 ◽

Access Test ◽

Concentration Series

Roux-en-Y gastric bypass (RYGB) surgery has been shown to decrease consummatory responsiveness of rats to high sucrose concentrations, and genetic deletion of glucagon-like peptide-1 receptors (GLP-1R) has been shown to decrease consummatory responsiveness of mice to low-sucrose concentrations. Here we assessed the effects of RYGB and pharmacological GLP-1R modulation on sucrose licking by chow-fed rats in a brief-access test that assessed consummatory and appetitive behaviors. Rats were tested while fasted presurgically and postsurgically and while nondeprived postsurgically and 5 h after intraperitoneal injections with the GLP-1R antagonist exendin-3(9–39) (30 μg/kg), agonist exendin-4 (1 μg/kg), and vehicle in 30-min sessions during which a sucrose concentration series (0.01–1.0 M) was presented in 10-s trials. Other rats were tested postsurgically or 15 min after peptide or vehicle injection while fasted and while nondeprived. Independent of food-deprivation state, sucrose experience, or GLP-1R modulation, RYGB rats took 1.5–3× as many trials as sham-operated rats, indicating increased appetitive behavior. Under nondeprived conditions, RYGB rats with presurgical sucrose experience licked more to sucrose relative to water compared with sham-operated rats. Exendin-4 and exendin-3(9–39) impacted 0.3 M sucrose intake in a one-bottle test, but never interacted with surgical group to affect brief-access responding. Unlike prior reports in both clearly obese and relatively leaner rats given RYGB and in GLP-1R knockout mice, we found that neither RYGB nor GLP-1R blockade decreased consummatory responsiveness to sucrose in our less obese chow-fed rats. Collectively, these results highlight the fact that changes in taste-driven motivated behavior to sucrose after RYGB and/or GLP-1R modulation are very model and measure dependent.

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The gastrointestinal tract “tastes” nutrients: evidence from the intestinal taste aversion paradigm

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00047.2004 ◽

2004 ◽

Vol 287 (5) ◽

pp. R1086-R1100 ◽

Cited By ~ 16

Author(s):

Andrea L. Tracy ◽

Robert J. Phillips ◽

Michael M. Chi ◽

Terry L. Powley ◽

T. L. Davidson

Keyword(s):

Gastrointestinal Tract ◽

Taste Aversion ◽

Conditioned Taste Aversion ◽

Corn Oil ◽

Preference Test ◽

Conditioned Stimuli ◽

Oral Consumption ◽

Behavioral Paradigm ◽

Combined Features ◽

Small Intestines

To develop and use a behavioral paradigm for assessments of what nutrient properties are detected by intestinal chemoreceptors, we combined features of the “electronic esophagus” preparation (Elizalde G and Sclafani A. Physiol Behav 47: 63–77, 1990) and the conditioned taste aversion protocol (Garcia J and Koelling RA. Psychon Sci 4: 123–124, 1966). In four experiments, separate groups of food-deprived rats with gastric ( experiments 1–4) or duodenal ( experiment 4) catheters were infused with either carbohydrates (maltodextrin) or fats (corn oil) into their stomachs or small intestines, either while they consumed nonnutritive flavored solutions ( experiments 1 and 2) or in the absence of any intake ( experiments 3 and 4). For some animals, one of the macronutrient infusions was paired with lithium chloride injections shown to support conventional conditioned aversions. After training, in various oral preference test trials, animals were given opportunities to taste and consume the nonnutritive solutions that had served as oropharyngeal conditioned stimuli as well as the nutrients that had been infused intragastrically, with or without poisoning, but never sampled by mouth. As previously established, preferences for the nonnutritive flavors were enhanced by association with intragastric infusions of macronutrients, with carbohydrates producing the greater preference. On first exposure to the two macronutrients for oral consumption, animals reduced their intake of the nutrient that had been previously poisoned when it was infused into the gastrointestinal tract. These results, along with additional controls, suggest that nutrient tastes detected in the intestines can be recognized centrally based on oropharyngeal gustatory stimulation.

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