scholarly journals Reduction of Food Intake and Weight Gain by the ob Protein Requires a Specific Secondary Structure and Is Reversible

1996 ◽  
Vol 2 (1) ◽  
pp. 50-58 ◽  
Author(s):  
Klaus Giese ◽  
Wendy J. Fantl ◽  
Charles Vitt ◽  
James C. Stephans ◽  
Lawrence Cousens ◽  
...  
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Secondary Structure ◽  
Ob Protein

Effect of acute food deprivation on lactational infertility in rats is reduced by leptin administration

1998 ◽  
Vol 274 (6) ◽  
pp. R1653-R1658 ◽  
Author(s):  
Barbara Woodside ◽  
Alfonso Abizaid ◽  
Shelina Jafferali
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Food Deprivation ◽  
Maternal Weight Gain ◽  
Maternal Weight ◽  
Ad Libitum ◽  
Ob Protein

The goals of these experiments were to determine whether lactational anestrus would be prolonged by a 48-h fast at days 13 and 14 postpartum (pp) and, if so, to determine whether this effect could be reversed by treatment with the Ob protein leptin. We found that food deprivation on days 13 and 14 pp prolonged lactational infertility by 7 days and that the nutritional experience of both the dam and her litter contributed to this effect. Leptin administration (2.5 mg ⋅ kg−1 ⋅ day−1) during food deprivation was sufficient to reduce the length of lactational infertility compared with vehicle-treated food-deprived rats ( P < 0.05). Similar leptin treatment in ad libitum-fed animals reduced food intake ( P < 0.05) and litter growth ( P < 0.05) but had no statistically significant effect on maternal weight gain or length of lactational infertility. Food-deprived lactating animals had lower circulating leptin levels than ad libitum-fed lactating animals on day 15 pp ( P < 0.05), as determined by RIA. Levels in nonlactating rats were higher than in either lactating group ( P < 0.05).

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.

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

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.

scholarly journals Effects of a high-fat-diet supplemented with probiotics and ω3-fatty acids on appetite regulatory neuropeptides and neurotransmitters in a pig model

2020 ◽  
Vol 11 (4) ◽  
pp. 347-359
Author(s):  
D. Valent ◽  
L. Arroyo ◽  
E. Fàbrega ◽  
M. Font-i-Furnols ◽  
M. Rodríguez-Palmero ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Animal Model ◽  
Weight Gain ◽  
Food Intake ◽  
High Fat Diet ◽  
Control Diet ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
High Fat ◽  
Brain Functions

The pig is a valuable animal model to study obesity in humans due to the physiological similarity between humans and pigs in terms of digestive and associated metabolic processes. The dietary use of vegetal protein, probiotics and omega-3 fatty acids is recommended to control weight gain and to fight obesity-associated metabolic disorders. Likewise, there are recent reports on their beneficial effects on brain functions. The hypothalamus is the central part of the brain that regulates food intake by means of the production of food intake-regulatory hypothalamic neuropeptides, as neuropeptide Y (NPY), orexin A and pro-opiomelanocortin (POMC), and neurotransmitters, such as dopamine and serotonin. Other mesolimbic areas, such as the hippocampus, are also involved in the control of food intake. In this study, the effect of a high fat diet (HFD) alone or supplemented with these additives on brain neuropeptides and neurotransmitters was assessed in forty-three young pigs fed for 10 weeks with a control diet (T1), a high fat diet (HFD, T2), and HFD with vegetal protein supplemented with Bifidobacterium breve CECT8242 alone (T3) or in combination with omega-3 fatty acids (T4). A HFD provoked changes in regulatory neuropeptides and 3,4-dihydroxyphenylacetic acid (DOPAC) in the hypothalamus and alterations mostly in the dopaminergic system in the ventral hippocampus. Supplementation of the HFD with B. breve CECT8242, especially in combination with omega-3 fatty acids, was able to partially reverse the effects of HFD. Correlations between productive and neurochemical parameters supported these findings. These results confirm that pigs are an appropriate animal model alternative to rodents for the study of the effects of HFD on weight gain and obesity. Furthermore, they indicate the potential benefits of probiotics and omega-3 fatty acids on brain function.

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