Influence of Dietary Fat and Carbohydrate on Food Intake, Body Weight and Body Fat of Adult Dogs

1978 ◽  
Vol 157 (2) ◽  
pp. 278-281 ◽  
Author(s):  
D. R. Romsos ◽  
M. J. Hornshuh ◽  
G. A. Leveille
Keyword(s):  
Body Fat ◽  
2016 ◽  
Vol 311 (3) ◽  
pp. R618-R627 ◽  
Author(s):  
Eva-Lena Stenblom ◽  
Emil Egecioglu ◽  
Caroline Montelius ◽  
Deepti Ramachandran ◽  
Britta Bonn ◽  
...  

Thylakoids reduce body weight gain and body fat accumulation in rodents. This study investigated whether an enhanced oxidation of dietary fat-derived fatty acids in the intestine contributes to the thylakoid effects. Male Sprague-Dawley rats were fed a high-fat diet with ( n = 8) or without thylakoids ( n = 8) for 2 wk. Body weight, food intake, and body fat were measured, and intestinal mucosa was collected and analyzed. Quantitative real-time PCR was used to measure gene expression levels of key enzymes involved in fatty acid transport, fatty acid oxidation, and ketogenesis. Another set of thylakoid-treated ( n = 10) and control rats ( n = 10) went through indirect calorimetry. In the first experiment, thylakoid-treated rats ( n = 8) accumulated 25% less visceral fat than controls. Furthermore, fatty acid translocase ( Fat/Cd36), carnitine palmitoyltransferase 1a ( Cpt1a), and mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase 2 ( Hmgcs2) genes were upregulated in the jejunum of the thylakoid-treated group. In the second experiment, thylakoid-treated rats ( n = 10) gained 17.5% less weight compared with controls and their respiratory quotient was lower, 0.86 compared with 0.91. Thylakoid-intake resulted in decreased food intake and did not cause steatorrhea. These results suggest that thylakoids stimulated intestinal fatty acid oxidation and ketogenesis, resulting in an increased ability of the intestine to handle dietary fat. The increased fatty acid oxidation and the resulting reduction in food intake may contribute to the reduced fat accumulation in thylakoid-treated animals.


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.


1995 ◽  
Vol 268 (4) ◽  
pp. E546-E550 ◽  
Author(s):  
C. N. Boozer ◽  
G. Schoenbach ◽  
R. L. Atkinson

This study examined the effects of increasing levels of dietary fat fed isocalorically on body weight, body composition, and adipose distribution. Adult male rats were weight matched into four groups. One group that was fed a low-fat diet (12%) served as reference controls. The other three groups were fed diets of 24, 36, or 48% fat in amounts to equal the energy intake of the control group. After 6 wk, body weights of the four groups were not significantly different. Intrascapular brown fat did not differ between groups. Total body fat and adipose depot weights, however, increased in proportion to the level of fat in the diet. Total body fat and retroperitoneal and mesenteric depot weights of the 48% fat group were greater than controls (P < 0.05). Mesenteric fat in this group was also significantly increased over all other groups (P < 0.05). These results show that high-fat diets fed to adult animals cause increased body fat in the absence of significant changes in body weight and that mesenteric fat is increased disproportionately.


1981 ◽  
Vol 240 (1) ◽  
pp. E72-E78 ◽  
Author(s):  
M. R. Greenwood ◽  
M. P. Cleary ◽  
R. Gruen ◽  
D. Blase ◽  
J. S. Stern ◽  
...  

Young Zucker lean (Fa/-) and obese (fa/fa) female rats were fed the fatty acid synthesis inhibitor (-)-hydroxy-citrate as a dietary admixture for 39 days. In the lean rats, (-)-hydroxycitrate treatment decreased body weight, food intake, percent of body fat, and fat cell size. In the obese rat, food intake and body weight were reduced but the percent of body fat remained unchanged. Throughout the treatment period, obese rats maintained a fat cell size equivalent to their obese controls. Although a reduction in fat cell number in the obese rats occurred during the treatment period, marked hyperplasia was observed during the posttreatment period. The results of this study indicate that the obese rat, despite a substantial reduction in body weight produced by (-)-hydroxycitrate, still defends its obese body composition.


2001 ◽  
Vol 280 (2) ◽  
pp. R331-R337 ◽  
Author(s):  
Mihai Covasa ◽  
Jeremy K. Marcuson ◽  
Robert C. Ritter

Rats maintained on a high-fat (HF) diet exhibit reduced sensitivity to the satiation-producing effect of exogenous CCK. Because more CCK is released in response to HF meals than low-fat (LF) meals, we hypothesized that increased circulating CCK associated with ingestion of HF diets contributes to the development of decreased CCK sensitivity. To test this hypothesis, we implanted osmotic minipumps filled with either NaCl or CCK octapeptide into the peritoneal cavity. Subsequently, we examined the effect of intraperitoneal NaCl or CCK (0.5 μg/kg) injection on 30-min food intake. CCK significantly reduced 30-min food intake less in rats implanted with CCK-releasing minipumps compared with those with NaCl-releasing minipumps. Because dietary protein is a potent releaser of endogenous CCK, we hypothesized that rats adapted to a high-protein (HP) diet might also exhibit reduced sensitivity to exogenous CCK. Therefore, in a second experiment, we examined CCK-induced reduction of food intake in rats maintained on LF and rats maintained on HF or HP. Ingestion of LF stimulates very little endogenous CCK secretion, whereas both HF and HP markedly increase plasma CCK concentrations. Both doses of CCK reduced food intake significantly less in HF and HP rats compared with LF rats. There were no differences in 24-h food intake, body weight, or body fat composition among LF-, HF-, and HP-fed rats. These results are consistent with the hypothesis that sustained elevation of CCK either by infusion of exogenous CCK or by dietary-induced elevation of plasma CCK contributes to the development of reduced sensitivity to exogenous CCK.


2011 ◽  
Vol 300 (4) ◽  
pp. E735-E745 ◽  
Author(s):  
Matthew D. Bruss ◽  
Airlia C. S. Thompson ◽  
Ishita Aggarwal ◽  
Cyrus F. Khambatta ◽  
Marc K. Hellerstein

Calorie restriction (CR) reduces the rate of cell proliferation in mitotic tissues. It has been suggested that this reduction in cell proliferation may mediate CR-induced increases in longevity. However, the mechanisms that lead to CR-induced reductions in cell proliferation rates remain unclear. To evaluate the CR-induced physiological adaptations that may mediate reductions in cell proliferation rates, we altered housing temperature and access to voluntary running wheels to determine the effects of food intake, energy expenditure, percent body fat, and body weight on proliferation rates of keratinocytes, liver cells, mammary epithelial cells, and splenic T-cells in C57BL/6 mice. We found that ∼20% CR led to a reduction in cell proliferation rates in all cell types. However, lower cell proliferation rates were not observed with reductions in 1) food intake and energy expenditure in female mice housed at 27°C, 2) percent body fat in female mice provided running wheels, or 3) body weight in male mice provided running wheels compared with ad libitum-fed controls. In contrast, reductions in insulin-like growth factor I were associated with decreased cell proliferation rates. Taken together, these data suggest that CR-induced reductions in food intake, energy expenditure, percent body fat, and body weight do not account for the reductions in global cell proliferation rates observed in CR. In addition, these data are consistent with the hypothesis that reduced cell proliferation rates could be useful as a biomarker of interventions that increase longevity.


2009 ◽  
Vol 50 (10) ◽  
pp. 283-290 ◽  
Author(s):  
Barbara J. Rolls ◽  
David J. Shide
Keyword(s):  

2015 ◽  
Vol 114 (7) ◽  
pp. 1013-1025 ◽  
Author(s):  
Alison O. Booth ◽  
Catherine E. Huggins ◽  
Naiyana Wattanapenpaiboon ◽  
Caryl A. Nowson

This meta-analysis of randomised controlled trials assessed the effect of Ca on body weight and body composition through supplementation or increasing dairy food intake. Forty-one studies met the inclusion criteria (including fifty-one trial arms; thirty-one with dairy foods (n 2091), twenty with Ca supplements (n 2711). Ca intake was approximately 900 mg/d higher in the supplement groups compared with control. In the dairy group, Ca intake was approximately 1300 mg/d. Ca supplementation did not significantly affect body weight (mean change ( − 0·17, 95 % CI − 0·70, 0·37) kg) or body fat (mean change ( − 0·19, 95 % CI − 0·51, 0·13) kg) compared to control. Similarly, increased dairy food intake did not affect body weight ( − 0·06, 95 % CI − 0·54, 0·43) kg or body fat change ( − 0·36, 95 % CI − 0·80, 0·09) kg compared to control. Sub-analyses revealed that dairy supplementation resulted in no change in body weight (nineteen studies, n 1010) ( − 0·32, 95 % CI − 0·93, 0·30 kg, P= 0·31), but a greater reduction in body fat (thirteen studies, n 564) ( − 0·96, 95 % CI − 1·46, − 0·46 kg, P < 0·001) in the presence of energy restriction over a mean of 4 months compared to control. Increasing dietary Ca intake by 900 mg/d as supplements or increasing dairy intake to approximately 3 servings daily (approximately 1300 mg of Ca/d) is not an effective weight reduction strategy in adults. There is, however, an indication that approximately 3 servings of dairy may facilitate fat loss on weight reduction diets in the short term.


1975 ◽  
Vol 48 (5) ◽  
pp. 431-440 ◽  
Author(s):  
C. J. Edmonds ◽  
B. M. Jasani ◽  
T. Smith

1. Total body potassium was estimated by 40K measurement with a high-sensitivity whole-body counter in normal individuals over a wide age range and in patients who were obese or were grossly wasted as a result of various conditions which restricted food intake. 2. Potassium concentration (mmol/kg body weight) fell with increasing age over 30 years in both normal males and females, but when individuals of different age groups were matched for height, a significant fall in total body potassium with increasing age was observed only in males. Total body potassium of females was about 75% that of males of similar height when young, the sex difference decreasing with ageing. In the normal population, total body potassium was significantly correlated with height and with weight; regression equations for various relationships are given. 3. Fat-free mass was estimated from total body potassium, values of 65 and 56 mmol of potassium/kg fat-free mass being used for males and females respectively. Body fat estimated by this method correlated well with skinfold measurements over a wide range of body weight but in malnourished individuals having inadequate food intake there was considerable discrepancy and present formulae for estimating fat-free mass from total body potassium appear unsatisfactory in malnutrition. Considerable differences between expected and observed values of total body potassium were found in muscular individuals and in normal individuals who were thin but whose body weight was relatively constant. 4. The patients with malnutrition were low both in body fat as estimated by skinfold thickness and in total body potassium estimated on the basis of height. Plasma potassium was, however, normal and potassium supplements did not increase the total body potassium. 5. Total body potassium of obese individuals was not significantly different from that of normal weight individuals on the basis of height. Total body potassium fell on weight reduction with a very low energy diet of 1260 kJ (300 kcal.) daily but changed little with a 3300 kJ (800 kcal.) diet over several months' observation. 6. For overweight, obese individuals, total body potassium was best predicted from the individual's height. For those whose body weight was less than expected, the use of weight gave the best prediction but the error was considerable when the weight deviation was large.


1993 ◽  
Vol 264 (1) ◽  
pp. R35-R40 ◽  
Author(s):  
G. W. Reed ◽  
G. Cox ◽  
F. Yakubu ◽  
L. Ding ◽  
J. O. Hill

We examined the effects of weight cycling, produced by bouts of weight loss and regain, on body weight, body composition, dietary fat intake, and energy efficiency. Three groups of adult female Wistar rats were followed for 116 days: control rats (n = 10) were allowed ad libitum access to three mixed diets with protein as a constant proportion of energy and fat provided at 10, 30, and 50% of energy; cycled rats (n = 10) had four bouts of food restriction (50% of baseline intake for 10 days) and refeeding (18-20 days of ad libitum access to the 3 mixed diets); maturity controls (n = 10) were treated identically to controls during the first two cycles and identical to cyclers during the final two weight cycles. At the end of the experiment, we could identify no negative effects of weight cycling on any of the measures taken, and in fact body weight and percentage body fat were lower in cyclers than controls. Dietary fat intake was not altered by weight cycling. In summary, weight cycling did not promote body weight or body fat gain.


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