scholarly journals Liraglutide suppression of caloric intake competes with the intake-promoting effects of a palatable cafeteria diet, but does not impact food or macronutrient selection.

2017 ◽  
Vol 177 ◽  
pp. 4-12 ◽  
Author(s):  
Kellie M. Hyde ◽  
Ginger D. Blonde ◽  
Carel W. le Roux ◽  
Alan C. Spector
2007 ◽  
Vol 293 (4) ◽  
pp. R1468-R1473 ◽  
Author(s):  
Michael F. Wiater ◽  
Bryan D. Hudson ◽  
Yvette Virgin ◽  
Sue Ritter

Leptin reduces body fat selectively, sparing body protein. Accordingly, during chronic leptin administration, food intake is suppressed, and body weight is reduced until body fat is depleted. Body weight then stabilizes at this fat-depleted nadir, while food intake returns to normal caloric levels, presumably in defense of energy and nutritional homeostasis. This model of leptin treatment offers the opportunity to examine controls of food intake that are independent of leptin's actions, and provides a window for examining the nature of feeding controls in a “fatless” animal. Here we evaluate macronutrient selection during this fat-depleted phase of leptin treatment. Adult, male Sprague-Dawley rats were maintained on standard pelleted rodent chow and given daily lateral ventricular injections of leptin or vehicle solution until body weight reached the nadir point and food intake returned to normal levels. Injections were then continued for 8 days, during which rats self-selected their daily diet from separate sources of carbohydrate, protein, and fat. Macronutrient choice differed profoundly in leptin and control rats. Leptin rats exhibited a dramatic increase in protein intake, whereas controls exhibited a strong carbohydrate preference. Fat intake did not differ between groups at any time during the 8-day test. Despite these dramatic differences in macronutrient selection, total daily caloric intake did not differ between groups except on day 2. Thus controls of food intake related to ongoing metabolic and nutritional requirements may supersede the negative feedback signals related to body fat stores.


2001 ◽  
Vol 122 (15) ◽  
pp. 1825-1839 ◽  
Author(s):  
Stéphane Boghossian ◽  
Didier Jourdan ◽  
Matthieu Dacher ◽  
Josette Alliot

1986 ◽  
Vol 64 (7) ◽  
pp. 976-982 ◽  
Author(s):  
Jacques LeBlanc ◽  
Diane Lupien ◽  
Pierre Diamond ◽  
Marcos Macari ◽  
Denis Richard

Complete energy balance studies were made on groups of overfed (A) and underfed (B) Wistar rats. In experiment A one group was fed cafeteria diet ad libitum (the intake was 29% larger than the control), two other groups were fed the same diet but in restricted quantities (18 and 9% above control), and a fourth group, fed a stock diet, served as control. In experiment B, caloric intake was restricted by 12 and 31% in two groups fed cafeteria diet, and by 21 and 34% in two other groups fed stock diet. The experiments lasted 41 days and during that period the protein gain was comparable between the control and the cafeteria-29% group (643.4 ± 33.3 vs. 578.1 ± 25.0) but the fat gain was significantly different between the two groups (863.2 ± 81.6 vs. 1663.2 ± 99.8 kJ). When energy expenditure (EE) (metabolizable energy less storage added to the cost of storage) is expressed as a percentage of metabolizable energy (ME) intake no significant difference was found among the groups. The average value was [Formula: see text]. This finding would not support the presence of dietary-induced thermogenesis in animals overfed on the cafeteria diet. However, since the obligatory cost associated with storing energy would not explain the higher EE of the overfed groups, it is suggested that the level of ME intake exerts continuous proportional regulatory action on EE and, as a result, energy is spared by underfeeding and it is wasted by overfeeding. Rats fed the cafeteria diet, independent of whether they are overfed or restricted were shown to increase both brown adipose tissue (BAT) protein content and thermogenic capacity in response to norepinephrine. For that reason it is suggested that it is not the caloric content of the diet which affects BAT but instead other factors such as fat content or palatability of the food. The results also suggest that BAT is not directly implicated in the regulatory responses associated with various intakes of food. Indeed in the underfed experiment, although the capacity of the BAT was enhanced in the cafeteria groups, the EE was not different from that of the animals fed the stock diet.


1982 ◽  
Vol 52 (3) ◽  
pp. 556-561 ◽  
Author(s):  
J. Leblanc ◽  
J. Dussault ◽  
D. Lupien ◽  
D. Richard

Male and female rats were fed standard laboratory chow or a highly palatable diet (cafeteria diet) for 10 wk. The cafeteria diet caused an increase in caloric intake and in body weight, and it induced thermogenesis that was associated with elevated plasma triiodothyronine (T3) levels, increased brown adipose tissue size, and enhanced metabolic response to norepinephrine. For a comparable caloric intake, body-weight gain was significantly greater in female than in male rats possibly because of difference in thermogenesis as suggested by the response to norepinephrine. Exercise training (swimming 2 h/day for 10 wk) reduced food intake and body-weight gain and failed to increase norepinephrine-induced thermogenesis in rats fed laboratory chow. In animals fed the cafeteria diet, food intake and body-weight gain were also reduced by exercise training, which at the same time diminished the diet-induced thermogenesis as evidenced by the diminution of 1) brown fat hypertrophy, 2) the elevation of plasma T3, and 3) the hyperthermic response to injected norepinephrine. It is suggested that the thyroid hormone and catecholamines through their actions on the brown adipose tissue are the important regulatory of thermogenesis. Exercise training would reduce the diet-induced thermogenesis by preventing increased T3 production. Enhanced thermogenesis may be considered an adaptive reaction as it serves to reduce fat deposition in animals fed cafeteria diet and to promote nonshivering heat production in the cold. On the other hand, exercise training reduces thermogenesis and thus prevents energy wasting.


1998 ◽  
Vol 275 (2) ◽  
pp. R485-R493 ◽  
Author(s):  
Bruce M. King ◽  
Kirk N. Rossiter ◽  
Samuel G. Stines ◽  
Gelana M. Zaharan ◽  
Jack T. Cook ◽  
...  

Lesions of the most posterodorsal aspects of the amygdala in female rats result in hyperphagia and moderate obesity. In the present study, rats with amygdaloid lesions did not increase their daily food intake when their powdered diet was diluted with 25 or 50% nonnutritive bulk. Control animals adjusted their food intake appropriately. In a second study, rats with lesions ate less food (lab chow pellets) than controls when allowed to eat for only 1 h/day for 10 days. In experiment 3, rats were offered a three-choice macronutrient diet. Whereas four of six control animals preferred the high-fat diet, all eight of the rats with amygdaloid lesions displayed a distinct preference for the high-carbohydrate diet, including those that had preferred the high-fat diet before surgery. These results, along with the previous finding that identical lesions result in hyperinsulinemia, indicate that the amygdala is involved in both the homeostatic regulation of food (caloric) intake and the selection of macronutrients.


1984 ◽  
Vol 247 (3) ◽  
pp. R449-R455 ◽  
Author(s):  
A. C. Swann

This study examined the effects of diet and treatment with noradrenergic receptor antagonists on weight gain and indices of Na+-K+-adenosine triphosphatase (ATPase) activity in the rat. When rats were fed a palatable cafeteria diet, their caloric consumption increased by about 80%, but they did not gain weight significantly. Ouabain binding and K+-p-nitrophenylphosphatase (NPPase) activity were increased in brown adipose tissue and soleus. These indices remained elevated after the rats were returned to a regular diet. When rats were fasted for 3 days, they lost weight, and the indices of Na+-K+-ATPase activity were markedly reduced in brown adipose tissue and soleus. After refeeding the fasted rats gained weight three times more rapidly than nonfasted rats with similar food intake. Indices of Na+-K+-ATPase activity remained as low as they had been when the rats were fasting. There was a consistent negative correlation between weight gain per calorie eaten and brown adipose tissue NPPase activity. Changes in Na+-K+-ATPase could therefore be involved in the effects of overfeeding and fasting on metabolic efficiency. Desmethylimipramine binding was increased by cafeteria diet and decreased by fasting, consistent with changes in sympathetic nervous system activity. Treatment with prazosin, an alpha 1-noradrenergic receptor antagonist, reduced Na+-K+-ATPase in either control or cafeteria diet-fed rats but did not alter the effect of cafeteria diet feeding. By contrast, treatment with propranolol, a beta-receptor antagonist, prevented the increase in Na+-K+-ATPase during cafeteria diet feeding.(ABSTRACT TRUNCATED AT 250 WORDS)


Author(s):  
D.C. Dominguez ◽  
J.T. Ellzey

Peroxisomes which participate in 1ipid metabolism have been shown to be altered in several metabolic disorders and toxic conditions. In alcoholic liver disease, the single lesion most frequently found is lipid accumu1ation in hepatocytes. However, the mechanisms for this 1ipid accumu1ation are not clear. The occurrence of modifications of liver peroxisomes due to excess alcohol consumption has not been subjected to a controlled study. We utilized a combination of cytochemica1 and morphometrictechniques to study the size and number of liver peroxisomes in rats fed an alcohol-supplemented diet compared to those of matched-paired control animals.Male Sprague-Daw1ey rats (400-500 g) received a liquid diet. The experimental group (N = 5/group) was fed a diet containing 30% ethanol-derived calories (EDC) and the control group was fed an isocaloric diet to 30% EDC. A pair feeding procedure was employed to control for caloric intake. Small pieces of liver randomly selected, were fixed in 2.3% -glutaraldehyde in 0.1 M sodium cacodylate buffer, pH 7.2, incubated in a DAB medium and postfixed with. 2% aqueous osmium tetroxide. EM photographs were taken from sections of 3 tissue blocks from each sample (7,200X) with a Zeiss EM10-A (60 kV). With the use of a point counting method and a digital planimeter the volume density (Vv) and numerical density (Nv) were determined.


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