Mandibular Growth Retardation in Growing Rats Chronically Exposed to Hypobaria

1987 ◽  
Vol 66 (1) ◽  
pp. 65-66 ◽  
Author(s):  
C.E. Bozzini ◽  
R.M. Alippi ◽  
A.C. Barcelo
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Growth Retardation ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
Tail Length ◽  
Experimental Period ◽  
Close Relation ◽  
Exposure Period ◽  
Mandibular Growth

Weanling male Wistar rats aged 21 days were divided into three groups: initial control, normobaric, and hypobaric (C, N, and H, respectively). C rats were killed three days after being weaned. H rats were placed into an altitude chamber and maintained at 456 mb (6100 m) for 14 days. N rats were maintained at sea-level conditions. Body weight, body and tail lengths, and food intake were recorded every day. Animals were killed at the end of the experimental period, and four linear dimensions of the dried mandible were measured. The amount of food eaten by the H rats during the entire exposure period was 54.6% of that consumed by N ones. Body weight gain in H rats was 32.7% of that seen in N rats. Body length was 49.0% and tail length was 56.6% of normal. All mandibular dimensions were significantly reduced in H rats when compared with N rats and were, in general, in close relation with the reduction observed in skeletal growth. Only one dimension was reduced out of proportion, which indicates some deformation of the mandible. The average daily caloric intake related to metabolic body weight (body weight0.75) of H rats was 60% of the N value. Efficiency of protein utilization for growth was not significantly different between both groups of rats. These results indicate that chronic exposure to hypobaria induces overall skeletal and mandibular growth retardation, which appears to be the result of a diminution in food intake because of decreased appetite.

scholarly journals Effects of pulsatile secretion of growth hormone (GH) on fat deposition in human GH transgenic rats

2002 ◽  
Vol 15 (2) ◽  
pp. 231-244 ◽  
Author(s):  
Yasufumi Furuhata ◽  
Masugi Nishihara ◽  
Michio Takahashi
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Weight Ratio ◽  
Tail Length ◽  
Transgenic Rats ◽  
Gh Treatment ◽  
Secretory Pattern

AbstractGrowth hormone (GH) is an endocrine regulator of glucose and lipid metabolism as well as body growth. GH levels are decreased and a unique pulsatile secretory pattern becomes obvious after puberty particularly in males. Coincidentally with this, males tend to deposit body fat. Experimental and clinical evidence has accumulated that obesity is associated with a decrease in GH levels. A strain of transgenic rats has been generated with severe obesity but normal nose-to-tail length, which has low circulating GH levels without pulsatility (human growth hormone (hGH) transgenic rats). The present review mainly focuses on recent and current work analysing the relationship between the occurrence of obesity and low GH levels and/or the absence of GH pulsatility in this transgenic animal model. This model has elevated blood glucose, non-esterified fatty acid, insulin and leptin levels associated with hyperphagia, suggesting that these rats also carry insulin- and leptin-resistant characteristics. hGH transgenic rats were subjected to a pair-feeding treatment to normalize food intake and chronic GH replacement to normalize GH levels. While the pair-feeding for 8 weeks successfully suppressed body-weight gain, the fat pad : body weight ratio remained very similar to freely-eating control hGH transgenic rats, which indicates the hyperphagia is not the sole contributor to the excess fat accumulation in this model. However, continuous elevation of peripheral hGH levels (approximately 2-fold) for 8 weeks by means of a slow-release vehicle resulted in a significant decrease in the fat mass : body weight ratios by 30 %. This GH treatment altered neither food intake nor body-weight gain. Thus, two characteristic phenotypes observed in the hGH transgenic rats, hyperphagia and obesity, seem to be closely related to GH levels and GH secretory pattern. This relationship might be working in the regulation of changes in seasonal body composition in wild animals.

Abstract 19336: Chronic Vagal Nerve Stimulation Causes Weight Loss by Reducing Food Intake and Feeding Efficiency in Mice

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Harald M Stauss ◽  
Daniel P Dias ◽  
Donald A Morgan ◽  
Kamal Rahmouni
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Oxygen Consumption ◽  
Weight Gain ◽  
Food Intake ◽  
Metabolic Rate ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
Vagal Nerve ◽  
Feeding Efficiency

Chronic electrical vagal nerve stimulation (VNS) has emerged as a new tool to treat human diseases including obesity. Indeed, chronic VNS has been shown to cause weight loss in humans and in experimental animal models. However, the mechanisms for VNS-induced weight loss are largely unknown. We hypothesized that an increase in metabolic rate together with reduced caloric intake and reduced feeding efficiency (body weight gain per calories consumed) contribute to chronic VNS-induced weight loss or reduced weight gain. To test this hypothesis, we developed a miniaturized microprocessor-operated nerve stimulator for chronic use in conscious mice. Effectiveness of the stimulator was verified by bradycardia at stimulation frequencies above 5 Hz (3V, 1mA, 1ms pulses). Male C57Bl/6 mice (16 weeks old, standard mouse chow diet) were instrumented with nerve stimulators (3V, 1mA, 1ms pulses at 5 Hz) on the right cervical vagal nerve and body weight, food intake and metabolic rate (indirect calorimetry) were determined at baseline and weekly thereafter. After the initial post-surgical weight loss, sham animals (n=9, stimulators off) regained pre-surgical body weight within 16 days (100.0±2.7%). In contrast, mice with chronic VNS (n=12) never reestablished pre-surgical body weight (94.5±0.9% on day 16, P<0.05 vs. sham). Caloric intake was significantly reduced in mice with chronic VNS compared to sham animals (74.7±2.4 vs. 84.6±4.2 kcal/week, P<0.05). Likewise, mice with chronic VNS showed significantly reduced feeding efficiency compared to sham mice (2.6±2.0 vs. 10.6±2.4 mg body weight gain per kcal consumed). Oxygen consumption tended to be elevated (2734±152 vs. 2490±124 mL/kg/h, P=0.23) during the first week, but not thereafter. In conclusion reduced food intake and lower feeding efficiency contribute to reduced weight gain in mice with chronic VNS. We speculate that an initial increase in metabolic rate (assessed by oxygen consumption) may be antagonized by compensatory mechanisms in response to chronic VNS.

EFFECT OF INCREASED METABOLISM AND OF HYPERPHAGIA ON DIETARY AMINO ACID IMBALANCE IN THE RAT

1967 ◽  
Vol 45 (6) ◽  
pp. 1011-1019 ◽  
Author(s):  
John R. Beaton
Keyword(s):  
Body Weight ◽  
Amino Acid ◽  
Food Intake ◽  
Cold Exposure ◽  
Body Weight Gain ◽  
Experimental Period ◽  
Exposure To Cold ◽  
Dietary Amino Acid ◽  
Subsequent Exposure ◽  
Amino Acid Imbalance

In male Wistar rats, the effects of cold exposure (6 °C) on dietary amino acid imbalances were investigated. In agreement with the previous observation of Klain et al., exposure to cold throughout the experimental period (28 days) prevented the decreased food intake and body weight gain observed at 24 °C in rats fed a 6% fibrin diet supplemented with 0.4% DL-methionine and 0.6% DL-phenylalanine. It was also observed that subsequent exposure to cold eliminated these effects of an existing- imbalance previously induced at: 24 °C. With a 10% fibrin diet supplemented with 0.6% DL-methionine and 0.9% DL-phenylalanine, no pronounced effect attributable to an amino acid imbalance was observed at 24 °C. It is concluded that exposure to cold prevents the deleterious effects of an amino acid imbalance superimposed on a 6% protein diet, and subsequent exposure to cold eliminates these effects of an existing imbalance, L-Thyroxine, injected daily at a level of 30 μg/100 g body weight, simulated cold exposure in that it caused an increased food intake in rats fed a 6% fibrin – unbalanced diet. In hypothalamic-hyperphagic rats, a deleterious effect of a 6% fibrin – imbalanced diet was apparent initially; after 10 days' feeding, lesioned rats fed a 6% fibrin diet ceased to gain weight whereas those fed the imbalanced diet continued to do so.

Feeding and temperature responses to intravenous leptin infusion are differential predictors of obesity in rats

2004 ◽  
Vol 286 (4) ◽  
pp. R756-R763 ◽  
Author(s):  
Marie-Pierre Ruffin ◽  
Tiziana Adage ◽  
Folkert Kuipers ◽  
Jan H. Strubbe ◽  
Anton J. W. Scheurink ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
High Energy ◽  
Leptin Resistance ◽  
Variable Effect ◽  
Male Wistar Rats ◽  
Plasma Leptin

Obesity is frequently associated with leptin resistance. The present study investigated whether leptin resistance in rats is present before obesity develops, and thus could underlie obesity induced by 16 wk exposure to a liquid, palatable, high-energy diet (HED). Before HED exposure, male Wistar rats (weighing between 330 and 360 g) received intravenous infusions of 20 μg leptin 2 h before dark (∼57 μg/kg rat). Relative to saline infusion, this caused a highly variable effect on food intake (ranging between -94 and +129%), with food intake suppression that appeared negatively correlated with HED-induced increases in body weight gain, caloric intake, adiposity, and plasma leptin levels. In contrast, leptin's thermogenic response was positively correlated to body weight gain linked to weights of viscera, but not to adiposity. Before HED exposure, leptin unexpectedly increased food intake in some rats (fi+, n = 8), whereas others displayed the normal reduction in food intake (fi-, n = 7). HED-exposed fi+ rats had higher plasma leptin levels, retroperitoneal fat pad weight, HED intake, and body weight gain than fi- and chow-fed rats. These parameters were also higher in HED-exposed fi- rats relative to chow rats, except for plasma leptin concentrations. It is concluded that leptin's reduced efficacy to suppress food intake could predict obesity on an HED. An unexpected orexigenic effect of leptin might potentially contribute to this as well.

scholarly journals Cannabinoid-1 receptor antagonists reduce caloric intake by decreasing palatable diet selection in a novel dessert protocol in female rats

2008 ◽  
Vol 295 (1) ◽  
pp. R67-R75 ◽  
Author(s):  
Clare M. Mathes ◽  
Marco Ferrara ◽  
Neil E. Rowland
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
Diet Selection ◽  
Female Rats ◽  
Sprague Dawley ◽  
Receptor Antagonists ◽  
Sprague Dawley Rats ◽  
Cb1 Receptor Antagonists

Although many feeding protocols induce obesity, few use multiple foods to analyze diet selection within a single group of animals. To this end, we describe a protocol using time-limited access to a dessert that induces hyperphagia and body weight gain while allowing simple analysis of diet selection. Female retired breeder Sprague-Dawley rats were provided with ad libitum access to standard moist chow (1.67 kcal/g) and daily 8-h nocturnal access to either a sugar gel (SG; 0.31 kcal/g) or sugar fat whip (SFW; 7.35 kcal/g) for 15 days, and food intake and body weight were measured daily. Rats given SFW reduced moist chow intake but not enough to compensate for the large amount of calories consumed from SFW, and thus gained weight. We use this SFW overconsumption protocol to investigate the hypothesis that cannabinoid (CB)1 receptor antagonists reduce caloric intake by selectively decreasing consumption of palatable foods. In two experiments, female retired breeder Sprague-Dawley rats were injected with either Rimonabant (1 mg/kg ip) or vehicle (equal parts polyethylene glycol and saline, 1 ml/kg ip) for 7 days, or one of three doses of AM251 (0.3, 1.0, or 3.0 mg/kg ip), or vehicle for 15 days; food intake and body weight were measured daily. Both Rimonabant and AM251 decreased 24-h caloric intake, but the reduction was specific to a decrease in SFW consumption. This supports the hypothesis that these CB1 receptor antagonists impact feeding by modulating the perception of palatability.

Abstract 512: Anorectic and Thermogenic Effects of Chronic Vagal Nerve Stimulation in Mice

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Daniel P Dias ◽  
Donald A Morgan ◽  
Harald M Stauss ◽  
Kamal Rahmouni
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Oxygen Consumption ◽  
Weight Gain ◽  
Food Intake ◽  
Metabolic Rate ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
Vagal Nerve ◽  
Feeding Efficiency

Electrical vagal nerve stimulation (VNS) has emerged as a new tool to treat human diseases including obesity. Indeed, chronic VNS has been shown to cause weight loss in humans and in experimental animal models. However, the mechanisms by which chronic VNS causes weight loss are largely unknown due in part to the unavailability of implantable nerve stimulators for mice excluding the use of genetically engineered mouse models to investigate these mechanisms. Identification such mechanisms promises to identify novel approaches for weight loss. Here, we report the development of a miniaturized microprocessor-operated nerve stimulator for chronic use in conscious mice. Effectiveness of the stimulator was verified by the bradycardia induced at stimulation frequencies above 5 Hz (3V, 1mA, 1ms pulses). Next, we used the stimulator to test whether changes in metabolic rate, caloric intake and feeding efficiency (body weight gain per calories consumed) contribute to chronic VNS-induced weight loss. Male C57Bl/6 mice (16 weeks old, on standard mouse chow diet) were instrumented with nerve stimulators (3V, 1mA, 1ms pulses at 5 Hz) on the right cervical vagal nerve and body weight, food intake and metabolic rate (indirect calorimetry) were determined at baseline and weekly thereafter. After the initial post-surgical weight loss, sham animals (n=9, stimulators off) regained pre-surgical body weight within 16 days (100.0±2.7%). In contrast, mice with chronic VNS (n=12) never re-established pre-surgical body weight (94.5±0.9% on day 16, P<0.05 vs. sham). Caloric intake was significantly reduced in mice with chronic VNS compared to sham group (74.7±2.4 vs. 84.6±4.2 kcal/week, P<0.05). Likewise, mice with chronic VNS showed significantly reduced feeding efficiency compared to sham mice (2.6±2.0 vs. 10.6±2.4 mg body weight gain per kcal consumed). Oxygen consumption tended to be elevated (2734±152 vs. 2490±124 mL/kg/h) during the first week, but not thereafter. In conclusion, reduced food intake and lower feeding efficiency contribute to VNS-induced weight loss in mice. We speculate that an initial increase in metabolic rate (assessed by oxygen consumption) may be antagonized by compensatory mechanisms triggered by chronic VNS.

scholarly journals The Effects of Feed Color on Broiler Performance between Day 1 and 21

Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1511
Author(s):  
Joseph P. Gulizia ◽  
Kevin M. Downs
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Treatment Effects ◽  
Body Weight Gain ◽  
Experimental Period ◽  
Feed Consumption ◽  
Feed Conversion ◽  
Broiler Performance ◽  
Average Body ◽  
Average Body Weight

Two trials were conducted to determine feed color effects on broiler performance. A completely randomized design was used. Trial 1 included four treatments: control (complete broiler starter diet), red, green, and blue; and Trial 2 included four treatments: control, orange, yellow, and purple. Each trial had 4 treatments with 4 replicates (60 birds/treatment) fed to 240 male Cobb 500 broilers during a 21 d grow out. Data were analyzed using the GLM procedure. In Trial 1, there were no treatment effects on average body weight, body weight gain, and feed consumption (p > 0.05). Adjusted feed conversion for control (1.23) was less than red (1.27; p = 0.001) and green (1.26; p = 0.009), with blue (1.25; p = 0.056) tending to be different during the experimental period. In Trial 2, there were no treatment effects on average body weight, feed consumption, and adjusted feed conversion during this study (p > 0.05). Body weight gain between d 1 to 14 for purple (490.78 g/bird) was more than orange (467 g/bird; p = 0.013) and yellow (461 g/bird; p= 0.004), with control (474 g/bird; p = 0.052) tending to be different. Results indicate that these feed colors had some, albeit limited, influence on broiler performance parameters.

scholarly journals Neonatal nutritional programming impairs adiponectin effects on energy homeostasis in adult life of male rats

2018 ◽  
Vol 315 (1) ◽  
pp. E29-E37 ◽  
Author(s):  
Mariana Peduti Halah ◽  
Paula Beatriz Marangon ◽  
Jose Antunes-Rodrigues ◽  
Lucila L. K. Elias
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
White Adipose Tissue ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
Adult Life ◽  
Male Rats ◽  
Nutritional Programming

Neonatal nutritional changes induce long-lasting effects on energy homeostasis. Adiponectin influences food intake and body weight. The aim of this study was to investigate the effects of neonatal nutritional programming on the central stimulation of adiponectin. Male Wistar rats were divided on postnatal (PN) day 3 in litters of 3 (small litter, SL), 10 (normal litter, NL), or 16 pups/dam (large litter, LL). We assessed body weight gain for 60 days, adiponectin concentration, and white adipose tissue weight. We examined the response of SL, NL, and LL rats on body weight gain, food intake, oxygen consumption (V̇o2), respiratory exchange ratio (RER), calorimetry, locomotor activity, phosphorylated-AMP-activated protein kinase (AMPK) expression in the hypothalamus, and uncoupling protein (UCP)-1 in the brown adipose tissue after central stimulus with adiponectin. After weaning, SL rats maintained higher body weight gain despite similar food intake compared with NL rats. LL rats showed lower body weight at weaning, with a catch up afterward and higher food intake. Both LL and SL groups had decreased plasma concentrations of adiponectin at PN60. SL rats had increased white adipose tissue. Central injection of adiponectin decreased body weight and food intake and increased V̇o2, RER, calorimetry, p-AMPK and UCP- 1 expression in NL rats, but it had no effect on SL and LL rats, compared with the respective vehicle groups. In conclusion, neonatal under- and overfeeding induced an increase in body weight gain in juvenile and early adult life. Unresponsiveness to central effects of adiponectin contributes to the imbalance of the energy homeostasis in adult life induced by neonatal nutritional programming.

Effects of the lipase inhibitor orlistat on intake and preference for dietary fat in rats

1996 ◽  
Vol 271 (1) ◽  
pp. R48-R54 ◽  
Author(s):  
K. Ackroff ◽  
A. Sclafani
Keyword(s):  
Body Weight ◽  
Dietary Fat ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
Female Rats ◽  
Control Group ◽  
Fat Intake ◽  
Fat Absorption ◽  
Drug Induced ◽  
Dietary Fat Intake

Orlistat (Ols), a potent inhibitor of pancreatic lipase, was added to the fat source (1 or 4 mg Ols/g fat) of a macronutrient self-selection diet fed to adult female rats. The rats responded to the drug-induced reduction in fat absorption by decreasing their dietary fat intake and increasing their protein and carbohydrate intake in a dose-related manner. Total caloric intake also increased, but body weight gain was inhibited compared with the nondrug control group. When Ols was removed from the diet, nutrient selection, caloric intake, and body weight returned to control levels. In additional short-term experiments (30 min/day), rats developed a preference for a plain fat diet over an Ols-fat diet (4 mg/g fat) and also for a cue flavor paired with plain fat over a flavor paired with Ols-fat. Yet, when not given the choice, the rats consumed nearly as much Ols-fat as plain fat diet. These results indicate that, by reducing fat absorption, Ols reduced the attractiveness of dietary fat, although it did not make the fat diet aversive. In clinical use, lipase inhibitors may be effective in reducing dietary fat intake by reducing both the consumption and absorption of fat.

Protein appetite is increased after central leptin-induced fat depletion

2007 ◽  
Vol 293 (4) ◽  
pp. R1468-R1473 ◽  
Author(s):  
Michael F. Wiater ◽  
Bryan D. Hudson ◽  
Yvette Virgin ◽  
Sue Ritter
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Body Fat ◽  
Caloric Intake ◽  
Sprague Dawley ◽  
Body Protein ◽  
Macronutrient Selection ◽  
Daily Diet ◽  
Nadir Point ◽  
And Control

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.

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