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Postcessation weight gain is of concern to many female cigarette smokers. A multidisciplinary treatment combining psychological, dietary, and exercise components followed a 2-week smoking cessation program. Participants were randomly assigned to receive six follow-up relapse prevention sessions (in a group format or in an individually tailored format) directed by trained representatives from clinical psychology, dietary counseling, and exercise physiology. As predicted, abstinence rates were significantly higher among the individually tailored follow-up participants than among those assigned to the group follow-up condition at 3 and 6 months posttreatment. Differences between conditions in postcessation weight gain were not significant. However, the postcessation weight gain that did occur was significantly associated with subsequent smoking relapse in the group follow-up condition only.

Our laboratory has developed a macronutrient self-selection paradigm (MSSP) designed to vary fat content significantly and systematically with sugar, complex carbohydrates, and protein content in a battery of foods in which fat is commonly consumed in the American diet. We have also developed a food preference questionnaire (FPQ) according to an identical design but using a list of foods mutually exclusive of those presented for selection and intake in the MSSP. Men were tested twice on both instruments, with a 4-week interval between tests. It was determined that the MSSP has strong test-retest reliability for overall fat (r = 0.91) and other macronutrient intake and total caloric intake. In addition, hunger and fullness ratings were reproducible, and fat preferences (r = 0.99) and hedonic responses to foods listed on the FPQ were highly consistent across trials. This study also demonstrated that the MSSP is a valid instrument with respect to the men's reports of habitual intake of fat (r = 0.80) and total carbohydrates on the Block food questionnaire (FQ). In addition, men's fat preferences on the FPQ were validated with respect to overall fat (r = 0.86) and total caloric intake in the MSSP and fat intake (r = 0.83) reported on the Block FQ. The MSSP also has the capability to detect a wide range of fat intake (3.06-50.35% among the present subjects), indicating that this instrument can identify individuals who differ markedly in fat intake or could detect changes in fat preference within subjects. In addition, this paradigm detected a large range of sugar and total caloric intake. It is anticipated that the use of these laboratory tools can enhance our understanding of the relationship between dietary fat intake and obesity.

The relationship between restricted feeding, core body temperature (Tb), wheel running, survival, and gastric erosion formation was examined in female rats exposed to activity-stress. Core body temperature and gross motor activity were telemetrically monitored in four groups of rats that had free access to running wheels and in one group that was not allowed to run on the wheels. Twenty-four hours prior to the onset of hypothermia and predicted mortality, different groups were left undisturbed, warmed with a heat lamp, denied access to running wheels, or euthanized. Length of survival in wheel-running rats varied from 2 to 12 days. During the first day of food deprivation, premorbid changes in the variability of Tb during the diurnal period and the mean number of wheel revolutions during the nocturnal period were strongly predictive of length of survival. Warming rats with a heat lamp or preventing rats from ever running on the wheel increased the length of survival and attenuated gastric erosion formation. Only rats that were warmed had a greater likelihood of survival. Gastric pathology was also reduced in rats that were euthanized prior to becoming moribund. Rats that were left undisturbed or locked from the running wheel over the last 24 h of testing became moribund and had extensive gastric mucosal damage. These results indicate that thermoregulatory disturbances induced by restricted feeding and not wheel running alone are critical in determining survival and the degree of gastric mucosal injury in rats exposed to activity-stress. Results further suggest that predisposing factors may put some rats at risk for the development of activity-stress-induced mortality.

To examine the role of the amygdala in the production of gastric ulcers induced by activity-stress, electrolytic lesions were placed in the centromedial (CENT) and medial (MED) amygdaloid nuclei, as well as in the intra-amygdaloid division of the bed nucleus of the stria terminalis (BNST). As compared to sham-operated controls (CONT), gastric ulceration was attenuated in rats with CENT lesions and exacerbated in rats with lesions located in the BNST or MED. Wheel running did not differ significantly between control animals and lesioned rats, but did differ within lesioned groups. Rats with MED lesions ran more than rats with CENT or BNST lesions. Results support the view that the integrity of the centromedial amygdala is critical for the maintenance of the viscera and demonstrate that neurogenic factors contribute to the development of gastric erosions during exposure to activity-stress.

Hexoses infused slowly into the duodenum or hepatic-portal vein reduce feeding. However, hexoses can increase food intake following rapid infusion via either of these two routes. Insulin responses and resultant glycemic changes differ following fast and slow duodenal glucose infusion. This is unlikely to be the primary explanation, because fructose affects feeding but is not a secretagogue of insulin under our testing conditions. In follow-up studies, we infused glucose or fructose into the hepatic-portal vein at the fast or the slow rate, and measured 14C incorporation into liver mitochondria and glycogen, and tritiated water uptake into hepatic lipids. Fast infusion of glucose or fructose increased lipid formation, reducing mitochondrial uptake and glycogen formation, and was associated with hunger enhancement. Slow hexose infusion was associated with substrate uptake into mitochondria and glycogen, with reduced uptake into hepatic fat. These findings all are consistent with the previously observed positive correlation seen between mitochondrial oxidation and satiety (28).

Septal destruction and ovariectomy each influenced food intake and body weight differentially. Animals sustaining septal damage ingested significantly more food than the other groups, and septal hyperphagia persisted for as long as 109 days. Ovarian hyperphagia did not occur under conditions of constant illumination. Septal destruction exerted essentially no effect on body weight, while ovariectomy substantially increased body weight. Sequential surgical manipulations provided further evidence that the ovaries and the septum influence food intake and body weight via independent mechanisms. Results indicated that the septal and ovarian effects on water intake are not mediated via independent mechanisms. Septal and ovarian hyperdipsia were found to be very robust effects occurring regardless of the lighting regimen. It was further demonstrated that ovarian hyperdipsia is not secondary to food intake but rather is primary hyperdipsia.

The present study was conducted to investigate the potential contribution of bile to gastric mucosal damage induced by lesions of the lateral hypothalamic area in rats. In two separate experiments it was found that (1) lateral hypothalamic lesions did not alter the rate of bile flow in the acute preparation, but (2) bile duct ligation significantly reduced the incidence of gastric mucosal damage. Based on these and previous findings it is suggested that the reflux of bile interacts with the weakened gastric mucosal barrier to elicit ulceration.

Thirty New-Zealand female rabbits were implanted with hepatic-portal cannulas and six simultaneously underwent bilateral subdiaphragmatic vagotomy. When recovered, all animals received pancreatic glucagon infused at 1.0 cc/min for a total dosage of 12 microgram in 3.0 cc of isotonic saline. On alternate days, isotonic saline alone was infused as a control. Twelve intact and six vagotomized animals received infusions terminating food deprivations of 4, 8, and 24 hr while the remaining animals received the infusions only when free feeding. The feeding behavior of all animals was measured at 0.5, 1 and 2 hr postinfusion. Glucagon significantly suppressed feeding relative to saline only in 0- and 4-hr-food-deprived intact rabbits. Longer deprivations followed by glucagon did not produce suppression, and glucagon was completely ineffective in suppressing feeding in vagotomized animals. Although glucagon infusion in 4-hr food-deprived intact rabbits produced 38% suppression of food intake during the first hr postadministration, glycogen analysis revealed no significant reduction under the behavioral testing paradigm. These results indicate that glucagon can suppress food intake without depletion of liver glycogen. It is suggested that glucagon is not a satiety signal but can probably suppress feeding through initiating glycogenolysis.

Bilateral lesions of the lateral hypothalamus in rats produce glandular gastric mucosal damage. The results of the first experiment demonstrated that the severity of the neurogenic gastric erosions is attenuated by prior lesions of the centromedial amygdala. In a second experiment it was shown that fasting gastric acidity is significantly reduced following chronic amygdaloid lesions and this may be the mechanism involved in the protective nature of the amygdaloid lesions against gastric mucosal damage. In addition, it was found that gastric secretory changes induced by intracisternal injection of bombesin are unaffected by amygdaloid damage. The present results are consistent with the view that the centromedial amygdaloid region may influence gastric functions by modulating the activity of the preoptic-anterolateral hypothalamic areas or by directly influencing lower brain stem autonomic control areas.