Substrate oxidation and availability during acute exercise in non-obese, obese, and post-obese sedentary females.

OBJECTIVE: This study compared fat oxidation rates during an acute bout of cycle ergometry exercise (E) typical of progressive fat oxidation in healthy, but sedentary, women of different obesity histories. DESIGN: Five never-obese (NO) (mean age=25+/-3 (s.e.)y, mean body fat=25.0+/-2.8 (s.e.)%), five obese (O) (26+/-3 y, 44. 4+/-1.7%), and five post-obese (PO) (22+/-1 y, 32.2+/-3.0%) women cycled for 60 min at 60-65% peak VO2. To identify the specific effects of E, a control trial consisting of 60 min of seated rest (R) was also performed. E and R trials were counterbalanced one month apart in the follicular phase and conducted following a 3 d normalized, eucaloric diet. MEASUREMENTS: Dual energy X-ray absorptiometry (DEXA) was used to determine body composition, and all were weight stable for at least eight weeks prior to experimentation. During both trials breath by breath measurements of VO2 and RER were used to determine substrate oxidation and energy expenditure. Blood samples were collected for hormone and metabolite analysis before, and every 15 min during exercise or rest. RESULTS: All three groups showed a similar and progressive shift toward fat oxidation as exercise progressed. No group differences were observed for E energy expenditure or fat oxidation. Glycerol (P<0.0001) and free fatty acids (P<0.0001) increased similarly in all three groups, but PO maintained the highest free fatty acid level during exercise (group effect; P<0.01). E and R decreased (P<0.001 for both) insulin levels across groups, with lowest levels noted in PO and highest in O. Plasma epinephrine (P<0.0001) and norepinephrine (P<0.001) increased similarly during E in all three groups. Plasma growth hormone (GH) levels rose (P<0.05) during E, with a pronounced increase observed in PO. CONCLUSION: We conclude that exercise of equal relative intensity elicited similar fat oxidation rates among NO, O, and PO women, despite group differences in free fatty acid availability. The PO women's persistently lower insulin and higher plasma GH levels may have enhanced free fatty acid availability.

Perception of sweetness intensity determines women's hedonic and other perceptual responsiveness to chocolate food.

This study tested 63 women for hedonic and other perceptual responsiveness to a chocolate food. Subjects tasted four chocolate puddings varying in sugar (high and low) and fat (high and low) content and rated them for pleasantness, caloric density, fillingness and flavor intensities. Results emphasised the importance of sweetness intensity in determining women's responses to the chocolate puddings. Women's perception of sweetness intensity was accurate to sugar content and results consistently indicated that their hedonic responses to the chocolate puddings were based on the perceived sweetness. Women's perception of the caloric density of the puddings was based on their perception of the fat content of the puddings; however, interpretation of that finding must be qualified because the subjects' perception of fat content was inaccurate. The women's perception of sweetness intensity accounted for 31% of the variability in fat perception. Women's perception of the intensity of chocolate flavor was also significantly associated with perceived sweetness of the puddings. These data suggest that the women's accurate perception of the sugar content of the chocolate puddings played a primary role in determining their hedonic and other perceptual responses.

Reliability and validity of a macronutrient self-selection paradigm and a food preference questionnaire.

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.

Association of dietary restraint and disinhibition with eating behavior, body mass, and hunger.

This study investigated the association of dietary restraint and disinhibition with self-reported and actual eating behavior, body mass, and hunger. A sample of 124 women were categorized into one of four groups based upon high and low scores on measures of Dietary Restraint and Disinhibition using the Three Factor Eating Questionnaire. Half of the participants in each group consumed a high sugar/high fat chocolate pudding as a dietary preload. All participants were given a meal comprised of a standard macaroni and beef product. The interaction of Dietary Restraint and Disinhibition was related to differences in body mass. The Dietary Restraint factor was related to self-reported pathological eating behavior and influenced both perceived hunger and subjective hunger ratings. However, actual eating behavior measured by calories consumed and rate of intake was unrelated to the Dietary Restraint factor. Disinhibition was associated with excessive eating, an increased rate of eating, self-reports of eating disorder symptomatology, and perceived hunger. Hence, actual eating behavior was significantly influenced by the ingestive motivational factor, Disinhibition, but not by the cognitive factor, Dietary Restraint. These data also suggest that the Disinhibition construct is measuring overeating rather than disinhibited eating which implies the disruption of Dietary Restraint.

Body temperature and wheel running predict survival times in rats exposed to activity-stress.

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.

Control of food intake. A physiologically complex, motivated behavioral system.

This article has examined the control of food intake as a physiologically complex, motivated behavioral system. During the past four decades, considerable progress has been made in understanding putative signals for hunger, satiation, and satiety, although hunger signals have proven to be more difficult to identify. The putative physiologic controls of food intake include positive and negative sensory feedback; gastric and intestinal distension; the effects of nutrients, nutrient reserves, and metabolism in producing signals to the liver or brain; and peptides and hormones released in the gastrointestinal tract or the brain. However, food intake is not influenced solely by physiologic signals for hunger, satiation, and satiety. To comprehend feeding behavior more thoroughly, current physiologic models must be extended to include modulating factors such as feeding-associated responses adapted through learning processes and the influence of circadian rhythms, which can be dominating over hunger, satiation, and satiety signals.

Effects of amygdaloid lesions on gastric erosion formation during exposure to activity-stress.

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.

Vagally mediated feeding responses to phloridzin infusion in the rabbit.

Rabbits were infused with the plant glycoside, phloridzin, which blocks absorption of glucose across a number of bodily tissues. Feeding was dramatically increased in the first 0.5 h following phloridzin infusion into either the duodenum or the hepatic-portal vein of intact rabbits. Food intake covaried inversely with glycemic levels after phloridzin infusion into the hepatic-portal vein, but rabbits did not show a systematic relationship between blood glucose levels and food intake following duodenal infusion of phloridzin. When administered into the general circulation via the jugular vein, phloridzin did not elicit feeding. Finally, vagotomized rabbits did not show the hyperphagic response to phloridzin that was observed in intact rabbits. It was concluded that the feeding response to phloridzin is vagally mediated and appears to be induced by glucose transport inhibition at some peripheral site.

The metabolic bases for "paradoxical" and normal feeding.

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).

Sugar-induced hyperphagia: is hyperinsulinemia, hypoglycemia, or any other factor a "necessary" condition?

Results of a number of studies have suggested that hyperinsulinemia and resultant hypoglycemia are part of a sequence of responses that can lead to hunger and to sugar-induced hyperphagia. However, it is argued in the present paper that neither hyperinsulinemia, hypoglycemia, nor any other factor per se is solely responsible for the hyperphagic effect of sugar or any other feeding effect. Also, the present paper emphasizes the need for caution in attempting to evaluate the role of a given factor in sugar-induced hyperphagia, or any other feeding effect, by eliminating the factor of interest. I have reviewed evidence indicating that the elimination of preabsorptive insulin, which may mediate sugar-induced hyperphagia, actually potentiates other factors that may mediate the same effect.

Amygdaloid lesions attenuate neurogenic gastric mucosal erosions but do not alter gastric secretory changes induced by intracisternal bombesin.

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.

Gastric mucosal damage induced by lateral hypothalamic lesions in rats: the potential contribution of bile.

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.

Sugar infusion can enhance feeding.

An investigation was made of the role of glucose in the regulation of hunger and satiety in the rabbit. Glucose, when infused intraduodenally at a low rate (1 milliliter per minute), produced a decrease in food intake. However, when glucose was infused into the duodenum at a high rate (3 milliliters per minute), the rabbits nearly doubled their food intake during the first half-hour after infusion. It is hypothesized that the rapid arrival and glucose in the duodenum may produce hunger.

Amygdaloid lesions impair ingestive responses to 2-deoxy-D-glucose but not insulin.

Bilateral lesions of the amygdala in male rats impaired the feeding response to 2-deoxy-D-glucose (2-DG; 100, 200, and 400 mg/kg). During the first 3 h postinjection, control rats displayed a dose-related increase in both food and water consumption. Rats with amygdaloid lesions did not respond to 2-DG until the 3rd h postinjection, when only the two largest doses significantly increased food consumption. Their water intake remained unaffected throughout the 3-h postinjection period. During the 4th-24th h post-2-DG administration, both groups displayed a dose-related suppression of food and water intake. Following insulin (10 U/kg), amygdaloid and control animals were indistinguishable: both groups showed a significant short-term increase in food and water intake followed by a reduction in intakes during the 4th-24th h. Central visceral pathways that are important for the ingestive responses to 2-DG may be interrupted by amygdaloid lesions. However, pathways responsible for the ingestive behavior induced by insulin appear unaffected by damage to the amygdala.

Multivariate analysis of meal patterning in intact and vagotomized rabbits.

Meal patterns of female rabbits were measured throughout a 12:12 hr light/dark cycle and subjected to a multivariate-univariate analysis. Increased food intake occurring during the first 6 hr of dark was attributed to increased meal frequency and feeding rate, while that found during the last 6 hr of dark was attributed to increased meal duration and meal size. Meal patterning was also nonhomogeneous between the 6-hr periods in the light portion of the cycle. Experiment 2 demonstrated the times of day when feeding patterns of vagotomized animals are different from those of intact animals and, further, delineated the relevant variables that are altered by vagotomy. Immediately following light offset, vagotomized animals were distinguished from intact animals by sloer feeding rate and decreased food intake. Immediately following light onset, vagotomized animals were distinguished from intact animals by decreased feeding frequency, increased meal duration, and increased satiety ratio. During the 6 hr immediately preceding light onset or offset, none of the variables could discriminate the feeding patterns of intact animals from those of vagotomized animals.

Pancreatic glucagon, food deprivation and feeding in intact and vagotomized rabbits.

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.