Pituitary beta-endorphin, naloxone, and feeding in several experimental obesities

1981 ◽  
Vol 241 (3) ◽  
pp. R173-R184
Author(s):  
M. W. Gunion ◽  
R. H. Peters
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Food Access ◽  
Opiate Antagonist ◽  
Once Daily ◽  
Beta Endorphin ◽  
Normal Body Weight ◽  
Dose Dependent ◽  
Body Weight Dose

The role of beta-endorphin in the development of several obesity syndromes was examined. Adult female hooded rats received ventromedial hypothalamic lesions, dorsolateral tegmental lesions, parasagittal hypothalamic knife cuts, intraventricular 5,7-dihydroxytryptamine, ovariectomy, control surgery, or were deprived to 75% of normal body weight. Dose-dependent suppression of food intake by the opiate antagonist naloxone (0.5, 1.8, 6.8, or 25.0 mg/kg, ip) was measured during once-daily 4-h food access periods. No difference was found among the groups at any dose. Pituitary beta-endorphinlike immunoreactivity (BELI) was substantially decreased in knife-cut rats, but was unaltered by other treatments. Obesity had no effect on BELI. In another experiment, rats made obese by prolonged maintenance on palatable foods had elevated pituitary BELI levels. Feeding mechanisms involving opioid peptides do not appear to be of etiological significance in the syndromes examined.

scholarly journals Intestinal microbiota, obesity and prebiotics

2015 ◽  
Vol 64 (2) ◽  
pp. 93-100 ◽  
Author(s):  
R. BARCZYNSKA ◽  
K. BANDURSKA ◽  
K. SLIZEWSKA ◽  
M. LITWIN ◽  
M. SZALECKI ◽  
...  
Keyword(s):  
Body Weight ◽  
Gut Microbiota ◽  
Disease Risk ◽  
Global Scale ◽  
Weight One ◽  
Prevalence Of Obesity ◽  
Normal Body Weight ◽  
Healthy Body Weight ◽  
Treatment Of Obesity

Over the past few decades there has been a significant increase in the prevalence of obesity in both children and adults. Obesity is a disease that has reached epidemic levels on a global scale. The development of obesity is associated with both environmental and genetic factors. Recent studies indicate that intestinal microorganisms play an important function in maintaining normal body weight. One of the objectives in the gut microbiota research is to determine the role it plays and can it be a reliable biomarker of disease risk, including the predisposition to obesity. This article discusses (1) the role of prebiotics and gut microbiota in maintaining a healthy body weight and (2) potential influence on the gut microbiota in the prevention and treatment of obesity.

The role of pulses in satiety, food intake and body weight management

2017 ◽  
Vol 38 ◽  
pp. 612-623 ◽  
Author(s):  
Sandra Clark ◽  
Alison M. Duncan
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Weight Management

scholarly journals The role of nesfatin-1 in the regulation of food intake and body weight: recent developments and future endeavors

2013 ◽  
Vol 14 (11) ◽  
pp. 859-870 ◽  
Author(s):  
A. Stengel ◽  
M. Mori ◽  
Y. Taché
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Recent Developments

Endogenous opioids and ventilatory responses to hypercapnia in normal humans

1985 ◽  
Vol 58 (5) ◽  
pp. 1415-1420 ◽  
Author(s):  
S. E. Weinberger ◽  
R. A. Steinbrook ◽  
D. B. Carr ◽  
E. R. von Gal ◽  
J. E. Fisher ◽  
...  
Keyword(s):  
Opioid Peptides ◽  
Endogenous Opioids ◽  
Opiate Antagonist ◽  
Endogenous Opioid Peptides ◽  
Short Term ◽  
Endogenous Opioid ◽  
Beta Endorphin ◽  
Ventilatory Responses ◽  
Normal Humans

Though administration of opioid peptides depresses ventilation and ventilatory responsiveness, the role of endogenous opioid peptides in modulating ventilatory responsiveness is not clear. We studied the interaction of endogenous opioids and ventilatory responses in 12 adult male volunteers by relating hypercapnic responsiveness to plasma levels of immunoactive beta-endorphin and by administering the opiate antagonist naloxone. Ventilatory responsiveness to hypercapnia was not altered by pretreatment with naloxone, and this by itself suggests that endogenous opioids have no role in modulating this response. However, there was an inverse relationship between basal levels of immunoactive beta-endorphin in plasma and ventilatory responsiveness to CO2. Furthermore, plasma beta-endorphin levels rose after short-term hypercapnia but only when subjects had been pretreated with naloxone. We conclude that measurement of plasma endorphin levels suggests relationships between endogenous opioid peptides and ventilatory responses to CO2 that are not apparent in studies limited to assessing the effect of naloxone.

Role of the stria terminalis in food intake and body weight in rats

2006 ◽  
Vol 89 (2) ◽  
pp. 139-145 ◽  
Author(s):  
Bethany L. Rollins ◽  
Samuel G. Stines ◽  
Bruce M. King
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Stria Terminalis

Viewing the ventromedial hypothalamus from the adrenal gland

1984 ◽  
Vol 246 (1) ◽  
pp. R1-R12 ◽  
Author(s):  
M. F. Dallman
Keyword(s):  
Circadian Rhythm ◽  
Insulin Secretion ◽  
Food Intake ◽  
Adrenal Gland ◽  
Ventromedial Hypothalamus ◽  
Adrenocortical Function ◽  
Suprachiasmatic Nuclei ◽  
Inhibit Food Intake ◽  
Dose Dependent

The relationships among food intake, insulin secretion, and adrenocortical function are reviewed. It is hypothesized that a major role of structures in, or passing through, the ventromedial hypothalamus is to inhibit food intake, insulin secretion, and adrenocortical function during the day (in the nocturnally active rat) and that this activity is normally driven by elements within the suprachiasmatic nuclei. Lesions of the ventromedial hypothalamus of rats result in nonrhythmic food intake, hyperinsulinemia, nonrhythmic adrenocortical function, and obesity. Adrenalectomy prevents or reverses the effects of lesions of the ventromedial hypothalamus on food intake, insulin secretion, and obesity, and corticosteroid replacement restores them. Because the actions of corticosteroids are both time- and dose-dependent, it is proposed that the effects of the tonic levels of corticosteroids observed after lesions of the ventromedial hypothalamus are to augment the hyperphagia, hyperinsulinemia, and substrate flow into fat to a greater extent than would occur if there were a normal circadian rhythm in adrenocortical function.

N-methyl-d-aspartate receptor coagonist d-serine suppresses intake of high-preference food

2015 ◽  
Vol 309 (5) ◽  
pp. R561-R575 ◽  
Author(s):  
Tsutomu Sasaki ◽  
Yoshihiro Kinoshita ◽  
Sho Matsui ◽  
Shigeru Kakuta ◽  
Hiromi Yokota-Hashimoto ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Food Intake ◽  
Food Choice ◽  
Food Access ◽  
High Preference ◽  
Normal Chow ◽  
The One ◽  
Different Strains ◽  
Agouti Related Protein

d-Serine is abundant in the forebrain and physiologically important for modulating excitatory glutamatergic neurotransmission as a coagonist of synaptic N-methyl-d-aspartate (NMDA) receptor. NMDA signaling has been implicated in the control of food intake. However, the role of d-serine on appetite regulation is unknown. To clarify the effects of d-serine on appetite, we investigated the effect of oral d-serine ingestion on food intake in three different feeding paradigms (one-food access, two-food choice, and refeeding after 24-h fasting) using three different strains of male mice (C57Bl/6J, BKS, and ICR). The effect of d-serine was also tested in leptin signaling-deficient db/ db mice and sensory-deafferented (capsaicin-treated) mice. The expression of orexigenic neuropeptides [neuropeptide Y ( Npy) and agouti-related protein ( Agrp)] in the hypothalamus was compared in fast/refed experiments. Conditioned taste aversion for high-fat diet (HFD) was tested in the d-serine-treated mice. Under the one-food-access paradigm, some of the d-serine-treated mice showed starvation, but not when fed normal chow. HFD feeding with d-serine ingestion did not cause aversion. Under the two-food-choice paradigm, d-serine suppressed the intake of high-preference food but not normal chow. d-Serine also effectively suppressed HFD intake but not normal chow in db/ db mice and sensory-deafferented mice. In addition, d-serine suppressed normal chow intake after 24-h fasting despite higher orexigenic gene expression in the hypothalamus. d-Serine failed to suppress HFD intake in the presence of L-701,324, the selective and full antagonist at the glycine-binding site of the NMDA receptor. Therefore, d-serine suppresses the intake of high-preference food through coagonism toward NMDA receptors.

Sign in / Sign up

Export Citation Format

Share Document