Phenobarbital Effects on Weight Gain and Circadian Cycling of Food Intake and Body Temperature

1980 ◽  
Vol 165 (3) ◽  
pp. 473-479 ◽  
Author(s):  
C. Peraino ◽  
C. F. Ehret ◽  
K. R. Groh ◽  
J. C. Meinert ◽  
G. D'Arcy-Gomez
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Body Temperature

The effect of different housing systems and feeding regimes on the performance and rectal temperature of sheep

1991 ◽  
Vol 53 (3) ◽  
pp. 331-337 ◽  
Author(s):  
K. Bøe ◽  
J. J. Nedkvitne ◽  
D. Austbø
Keyword(s):  
Weight Gain ◽  
Birth Weight ◽  
Food Intake ◽  
Body Temperature ◽  
Rectal Temperature ◽  
Average Birth Weight ◽  
Housing Systems ◽  
Feeding Regimes ◽  
Effect Of Treatment ◽  
The Mean

AbstractThe effect of insulated (IN) and uninsulated (UN) buildings on food intake, performance and body temperature of sheep was studied over 4 years. The lowest average monthly temperature was -13·1°C. In the UN the temperature was on average 6-6°C higher than outside but the temperature in the IN remained fairly constant and was close to 10°C. Summarized for all 4 years the roughage intake was proportionately 0·02 higher in the UN than in IN (P > 0·05). There was no effect of treatment on weight gain, but the weight of the fleece was higher in IN than in UN (1·74 kg v. 1·66 kg per sheep). The mean age at first oestrus was 222 days. There was no difference in the length of pregnancy and lambing percentage was 185% in both treatments. The average birth weight was higher for lambs born in UN than IN (5·10 v. 4·95 kg), but the weight at weaning was the same. On only one occasion was the rectal temperature lower for ewes in UN than IN before shearing (38·7°C v. 39·2°C). After shearing no effect of treatment was found except for the 1st year, but in year 2 there was an interaction between plane of nutrition and housing. Results clearly indicated that uninsulated buildings are well suited for sheep.

Adrenalectomy and food restriction in the genetically obese (ob/ob) mouse

1984 ◽  
Vol 246 (1) ◽  
pp. R20-R25 ◽  
Author(s):  
M. Saito ◽  
G. A. Bray
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Body Temperature ◽  
Phenotypic Expression ◽  
Tail Length ◽  
Liver Weight ◽  
The Body ◽  
Brain Weight ◽  
Spleen Weight ◽  
Muscle Weight

After adrenalectomy in obese mice the rate of weight gain parallels that in lean controls and falls progressively behind that in intact ob/ob mice. Food intake was reduced to normal, but the body temperature of adrenalectomized ob/ob mice was similar to that of intact ob/ob mice and remained below that of control lean mice. After exposure to an ambient temperature of 6 degrees C the body temperature in adrenalectomized ob/ob mice fell at the same rate as in intact ob/ob mice. The increase in tail length, brain weight, spleen weight, and muscle weight after adrenalectomy in ob/ob mice could not be duplicated by reducing the weight gain of ob/ob mice to that of the adrenalectomized mice. Similarly the induction of obesity with gold thioglucose significantly increased the weight of the gastrocnemius muscle and spleen rather than lowering it to levels found in ob/ob mice. Treatment of adrenalectomized ob/ob mice with cortisone acetate, but not with deoxycorticosterone acetate (DOCA), reduced muscle weight, spleen weight, brain weight, and the growth in tail length. Both cortisone and DOCA increased food intake, liver weight, growth rate, and the weight of the adipose tissue in ob/ob mice. These effects are significantly greater than observed in comparably treated lean animals and suggest that glucocorticoids of adrenal origin play an integral role in the phenotypic expression of genetic obesity. These data also indicate that the hypothermia is not a sufficient cause of the obesity in the ob/ob mice, since hypothermia persists in the adrenalectomized mice, but when food intake falls to normal there is no progression of the obesity.

scholarly journals A hindbrain dopaminergic neural circuit prevents weight gain by reinforcing food satiation

2021 ◽  
Vol 7 (22) ◽  
pp. eabf8719
Author(s):  
Yong Han ◽  
Guobin Xia ◽  
Yanlin He ◽  
Yang He ◽  
Monica Farias ◽  
...  
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Neural Circuit ◽  
Neural Circuitry ◽  
Dynamic Regulation ◽  
Satiety Response ◽  
Food Satiation ◽  
Lateral Parabrachial Nucleus ◽  
Genetic Deletion ◽  
Feeding Bout

The neural circuitry mechanism that underlies dopaminergic (DA) control of innate feeding behavior is largely uncharacterized. Here, we identified a subpopulation of DA neurons situated in the caudal ventral tegmental area (cVTA) directly innervating DRD1-expressing neurons within the lateral parabrachial nucleus (LPBN). This neural circuit potently suppresses food intake via enhanced satiation response. Notably, this cohort of DAcVTA neurons is activated immediately before the cessation of each feeding bout. Acute inhibition of these DA neurons before bout termination substantially suppresses satiety and prolongs the consummatory feeding. Activation of postsynaptic DRD1LPBN neurons inhibits feeding, whereas genetic deletion of Drd1 within the LPBN causes robust increase in food intake and subsequent weight gain. Furthermore, the DRD1LPBN signaling manifests the central mechanism in methylphenidate-induced hypophagia. In conclusion, our study illuminates a hindbrain DAergic circuit that controls feeding through dynamic regulation in satiety response and meal structure.

scholarly journals Role of Ventromedial Hypothalamus in Sucrose-Induced Obesity on Metabolic Parameters

2021 ◽  
pp. 097275312110057
Author(s):  
Archana Gaur ◽  
G.K. Pal ◽  
Pravati Pal
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Food Intake ◽  
Ventromedial Hypothalamus ◽  
Female Rats ◽  
Metabolic Parameters ◽  
Male Rats ◽  
Significant Weight Gain ◽  
The Metabolic Syndrome

Background: Obesity is because of excessive fat accumulation that affects health adversely in the form of various diseases such as diabetes, hypertension, cardiovascular diseases, and many other disorders. Our Indian diet is rich in carbohydrates, and hence the sucrose-induced obesity is an apt model to mimic this. Ventromedial hypothalamus (VMH) is linked to the regulation of food intake in animals as well as humans. Purpose: To understand the role of VMHin sucrose-induced obesity on metabolic parameters. Methods: A total of 24 adult rats were made obese by feeding them on a 32% sucrose solution for 10 weeks. The VMH nucleus was ablated in the experimental group and sham lesions were made in the control group. Food intake, body weight, and biochemical parameters were compared before and after the lesion. Results: Male rats had a significant weight gain along with hyperphagia, whereas female rats did not have a significant weight gain inspite of hyperphagia. Insulin resistance and dyslipidemia were seen in both the experimental and control groups. Conclusion: A sucrose diet produces obesity which is similar to the metabolic syndrome with insulin resistance and dyslipidemia, and a VMH lesion further exaggerates it. Males are more prone to this exaggeration.

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.

A comparison of the effects of infection with Eimeria maxima and dietary restriction on weight gain, plasma metabolites and liver glycogen in the immature fowl, Gallus domesticus

Parasitology ◽  
1982 ◽  
Vol 84 (2) ◽  
pp. 205-213 ◽  
Author(s):  
H. D. Chapman ◽  
D. L. Fernandes ◽  
T. F. Davison
Keyword(s):  
Growth Rate ◽  
Body Weight ◽  
Uric Acid ◽  
Weight Gain ◽  
Food Intake ◽  
Acute Phase ◽  
Plasma Glucose ◽  
Liver Glycogen ◽  
Plasma Metabolites ◽  
Eimeria Maxima

SUMMARYThe effects of Eimeria maxima or restricted pair-feeding on weight gain, plasma concentrations of protein, glucose, free fatty acids (FFA) and uric acid and liver glycogen were compared in immature fowl. Food intake/kg body weight and weight gain decreased during the acute phase of infection (days 5–7) while weight loss was prolonged for an extra day compared with pair-fed birds. During recovery, food intake/kg body weight of infected birds was greater than that of non-infected controls but there was no evidence for an increase in growth rate compared with controls when body weight was considered. Growth rate of pair-fed birds was greater than that of infected birds during recovery, indicating their better use of ingested food. Liver glycogen and plasma protein concentration were decreased during the acute phase of infection but the concentrations of plasma glucose, free fatty acid (FFA) and uric acid were not affected. In pair-fed birds liver glycogen was depleted, concentrations of plasma glucose and uric acid decreased and FFA increased, and these changes persisted for the remainder of the experiment. The findings are similar to those in birds whose food has been withheld and were probably due to the pattern of food intake imposed by the experimental protocol. It is concluded that the metabolic differences between infected and pair-fed birds are of doubtful significance.

Intestinal motility during acute Yersinia enterocolitica enteritis in rabbits

1989 ◽  
Vol 67 (6) ◽  
pp. 553-560 ◽  
Author(s):  
R. B. Scott ◽  
D. G. Gall ◽  
S. C. Diamant
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Motor Activity ◽  
Yersinia Enterocolitica ◽  
Phase Iii ◽  
Intestinal Lumen ◽  
Fecal Excretion ◽  
Cycle Period ◽  
Motility Index ◽  
And Control

To determine if Yersinia enterocolitica (YE) enteritis is associated with an alteration of intestinal myoelectric and motor activity, and with an increased rate of aboral transit, New Zealand white rabbits (500–900 g) were surgically prepared with ileal bipolar electrodes and a manometry catheter adjacent to the distal electrode. One week later animals were inoculated with 1010 organisms of YE in 10 mL NaHCO3 (infected group) or 10 mL NaHCO3 (sham-infected pair-fed and control groups). Daily food intake, weight gain, YE excretion, and stool pattern were noted. Intestinal myoelectric and motor activity over a 6- to 8- h period before and 3, 6, and 14 days after inoculation was compared in infected (I), pair-fed (PF), and control (C) groups. Intestinal transit was evaluated in I and C animals on days 3 and 6 after inoculation by measuring the distribution in the intestinal lumen of 51Cr 20 min after it was instilled directly into the jejunum. Infected animals exhibited diarrhea, fecal excretion of YE, and significantly decreased food intake, weight gain, and survival (11.4 ± 0.6 days). Infection was associated with a significant (p < 0.05) decrease in both the cycle period of the migrating myoelectric complex (MMC) and the total number of single, paired, and (or) clustered contractions per MMC, and a significant (p < 0.001) increase in duration of phase III of the MMC. There was no change in intestinal slow wave frequency (19 cycles/min), motility index per MMC, or the percentage of contractions that propagated in an orad (7%) or aboral (69%) direction or that appeared stationary (25%). The changes in myoelectric and motor activity were specific for YE infection (not related to decreased food intake and weight gain) and were associated with a significantly increased rate of aboral transit. Thus, the inflammatory enteritis induced by YE is associated with alterations of intestinal myoelectric and motor activity, and an increased rate of aboral transit.Key words: Yersinia enterocolitica, infection, intestine, motility, transit.

scholarly journals The Gut Microbiome Derived From Anorexia Nervosa Patients Impairs Weight Gain and Behavioral Performance in Female Mice

Endocrinology ◽  
2019 ◽  
Vol 160 (10) ◽  
pp. 2441-2452 ◽  
Author(s):  
Tomokazu Hata ◽  
Noriyuki Miyata ◽  
Shu Takakura ◽  
Kazufumi Yoshihara ◽  
Yasunari Asano ◽  
...  
Keyword(s):  
Body Weight ◽  
Anorexia Nervosa ◽  
Weight Gain ◽  
Food Intake ◽  
Brain Stem ◽  
Body Weight Gain ◽  
Field Tests ◽  
Compulsive Behavior ◽  
The Brain ◽  
Poor Weight Gain

Abstract Anorexia nervosa (AN) results in gut dysbiosis, but whether the dysbiosis contributes to AN-specific pathologies such as poor weight gain and neuropsychiatric abnormalities remains unclear. To address this, germ-free mice were reconstituted with the microbiota of four patients with restricting-type AN (gAN mice) and four healthy control individuals (gHC mice). The effects of gut microbes on weight gain and behavioral characteristics were examined. Fecal microbial profiles in recipient gnotobiotic mice were clustered with those of the human donors. Compared with gHC mice, gAN mice showed a decrease in body weight gain, concomitant with reduced food intake. Food efficiency ratio (body weight gain/food intake) was also significantly lower in gAN mice than in gHC mice, suggesting that decreased appetite as well as the capacity to convert ingested food to unit of body substance may contribute to poor weight gain. Both anxiety-related behavior measured by open-field tests and compulsive behavior measured by a marble-burying test were increased only in gAN mice but not in gHC mice. Serotonin levels in the brain stem of gAN mice were lower than those in the brain stem of gHC mice. Moreover, the genus Bacteroides showed the highest correlation with the number of buried marbles among all genera identified. Administration of Bacteroides vulgatus reversed compulsive behavior but failed to exert any substantial effect on body weight. Collectively, these results indicate that AN-specific dysbiosis may contribute to both poor weight gain and mental disorders in patients with AN.

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