scholarly journals Minireview: From Anorexia to Obesity—The Yin and Yang of Body Weight Control

Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 3749-3756 ◽  
Author(s):  
Jeffrey M. Zigman ◽  
Joel K. Elmquist
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Body Weight ◽  
Food Intake ◽  
Weight Control ◽  
Public Health Goal ◽  
Control Food ◽  
Control Body ◽  
Body Weight Control ◽  
Control Food Intake

Abstract Over the past decade, there has been a tremendous increase in the understanding of the molecular and neural mechanisms that control food intake and body weight. Yet eating disorders and cachexia are still common, and obesity cases are rising at alarming rates. Thus, despite recent progress, an increased understanding of the molecular and neural substrates that control body weight homeostasis is a major public health goal. In this review, we discuss the mechanisms by which metabolic signals interact with key behavioral, neuroendocrine, and autonomic regulatory regions of the central nervous system. Additionally, we offer a model in which hormones such as leptin and ghrelin interact with similar central nervous system circuits and engage them in such a way as to maintain an appropriate and tight regulation of body weight and food intake. Our model predicts that overstimulation or understimulation of these central pathways can result in obesity, anorexia, or cachexia.

Insulin: its relationship to the central nervous system and to the control of food intake and body weight

1985 ◽  
Vol 42 (5) ◽  
pp. 1063-1071 ◽  
Author(s):  
S C Woods ◽  
D Porte ◽  
E Bobbioni ◽  
E Ionescu ◽  
J F Sauter ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Body Weight ◽  
Food Intake ◽  
The Central Nervous System

scholarly journals TOXIC EFFECTS OF LARGE DOSE OF QUASSIN IN NORMAL AND DEPRIVED MICROFLORA RAT GROUPS

2021 ◽  
Vol 22 (1) ◽  
pp. 67-83
Author(s):  
Duraid A.Abbas ◽  
O.M.S. Al—Shaha,
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Water Intake ◽  
Daily Food ◽  
Daily Water Intake ◽  
Control Food ◽  
Liver And Kidney ◽  
Daily Water ◽  
Control Food Intake ◽  
Intake Water

Eighteen rats were divided into three equal groups. The first group was closed orally with quassin, the second group was dosed with quassin after the gut flora were suppressed by difierent antibiotics, and the third group was served as a control. Food intake, water intake, and change in body weight were measured daily before dosing, during two weeks of dosing, and during one week after stopping dosing. Two eats from each group were killed at the end of each week, and stomach, liver, and kidney were collected for histopathologic examination. The results show a significant decline in daily food intake and daily change in body weight, and a significant increase in daily water intake in both dosed groups during the dosing period. Microscopic lesions were seen in the kidneys of both dosed rats group killed at the end of first and second week

scholarly journals Food intake, energy balance and body weight control

1997 ◽  
Vol 51 (12) ◽  
pp. 846-855 ◽  
Author(s):  
E Doucet ◽  
A Tremblay
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Weight Control ◽  
Body Weight Control

Cannabinoid receptor 1 antagonist treatment induces glucagon release and shows an additive therapeutic effect with GLP-1 agonist in diet-induced obese mice

2014 ◽  
Vol 92 (12) ◽  
pp. 975-983 ◽  
Author(s):  
Kartikkumar Navinchandra Patel ◽  
Amit Arvind Joharapurkar ◽  
Vishal Patel ◽  
Samadhan Govind Kshirsagar ◽  
Rajesh Bahekar ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Body Weight ◽  
Food Intake ◽  
Cannabinoid Receptor ◽  
Forced Swim Test ◽  
Conditioned Aversion ◽  
Serum Glucose ◽  
Body Weight Reduction ◽  
Glucagon Like Peptide 1

Cannabinoid 1 (CB1) receptor antagonists reduce body weight and improve insulin sensitivity. Preclinical data indicates that an acute dose of CB1 antagonist rimonabant causes an increase in blood glucose. A stable analog of glucagon-like peptide 1 (GLP-1), exendin-4 improves glucose-stimulated insulin secretion in pancreas, and reduces appetite through activation of GLP-1 receptors in the central nervous system and liver. We hypothesized that the insulin secretagogue effect of GLP-1 agonist exendin-4 may synergize with the insulin-sensitizing action of rimonabant. Intraperitoneal as well as intracerebroventricular administration of rimonabant increased serum glucose upon glucose challenge in overnight fasted, diet-induced obese C57 mice, with concomitant rise in serum glucagon levels. Exendin-4 reversed the acute hyperglycemia induced by rimonabant. The combination of exendin-4 and rimonabant showed an additive effect in the food intake, and sustained body weight reduction upon repeated dosing. The acute efficacy of both the compounds was additive for inducing nausea-like symptoms in conditioned aversion test in mice, whereas exendin-4 treatment antagonized the effect of rimonabant on forced swim test upon chronic dosing. Thus, the addition of exendin-4 to rimonabant produces greater reduction in food intake owing to increased aversion, but reduces the other central nervous system side effects of rimonabant. The hyperglucagonemia induced by rimonabant is partially responsible for enhancing the antiobesity effect of exendin-4.

scholarly journals Central and peripheral control of food intake

2017 ◽  
Vol 51 (1) ◽  
pp. 52-70 ◽  
Author(s):  
M. M. I. Abdalla
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Current Knowledge ◽  
The Body ◽  
Therapeutic Implications ◽  
New Therapeutic Approaches ◽  
Control Food ◽  
Adiposity Signals ◽  
Control Food Intake

Abstract The maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. The obesity has an evil effect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity.

scholarly journals Amylin Acts in the Central Nervous System to Increase Sympathetic Nerve Activity

Endocrinology ◽  
2013 ◽  
Vol 154 (7) ◽  
pp. 2481-2488 ◽  
Author(s):  
Caroline Fernandes-Santos ◽  
Zhongming Zhang ◽  
Donald A. Morgan ◽  
Deng-Fu Guo ◽  
Andrew F. Russo ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Body Weight ◽  
Food Intake ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Peripheral Tissues ◽  
Brown Adipose ◽  
The Central Nervous System

Abstract The pancreatic hormone amylin acts in the central nervous system (CNS) to decrease food intake and body weight. We hypothesized that amylin action in the CNS promotes energy expenditure by increasing the activity of the sympathetic nervous system. In mice, ip administration of amylin significantly increased c-Fos immunoreactivity in hypothalamic and brainstem nuclei. In addition, mice treated with intracerebroventricular (icv) amylin (0.1 and 0.2 nmol) exhibited a dose-related decrease in food intake and body weight, measured 4 and 24 hours after treatment. The icv injection of amylin also increased body temperature in mice. Using direct multifiber sympathetic nerve recording, we found that icv amylin elicited a significant and dose-dependent increase in sympathetic nerve activity (SNA) subserving thermogenic brown adipose tissue (BAT). Of note, icv injection of amylin also evoked a significant and dose-related increase in lumbar and renal SNA. Importantly, icv pretreatment with the amylin receptor antagonist AC187 (20 nmol) abolished the BAT SNA response induced by icv amylin, indicating that the sympathetic effects of amylin are receptor-mediated. Conversely, icv amylin-induced BAT SNA response was enhanced in mice overexpressing the amylin receptor subunit, RAMP1 (receptor-activity modifying protein 1), in the CNS. Our data demonstrate that CNS action of amylin regulates sympathetic nerve outflow to peripheral tissues involved in energy balance and cardiovascular function.

scholarly journals Peripheral and Central GLP-1 Receptor Populations Mediate the Anorectic Effects of Peripherally Administered GLP-1 Receptor Agonists, Liraglutide and Exendin-4

Endocrinology ◽  
2011 ◽  
Vol 152 (8) ◽  
pp. 3103-3112 ◽  
Author(s):  
Scott E. Kanoski ◽  
Samantha M. Fortin ◽  
Myrtha Arnold ◽  
Harvey J. Grill ◽  
Matthew R. Hayes
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Body Weight ◽  
Food Intake ◽  
Vagal Afferents ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Long Acting ◽  
Higher Doses ◽  
Cns Delivery

The long-acting glucagon-like peptide-1 receptor (GLP-1R) agonists, exendin-4 and liraglutide, suppress food intake and body weight. The mediating site(s) of action for the anorectic effects produced by peripheral administration of these GLP-1R agonists are not known. Experiments addressed whether food intake suppression after ip delivery of exendin-4 and liraglutide is mediated exclusively by peripheral GLP-1R or also involves direct central nervous system (CNS) GLP-1R activation. Results showed that CNS delivery [third intracerebroventricular (3rd ICV)] of the GLP-1R antagonist exendin-(9–39) (100 μg), attenuated the intake suppression by ip liraglutide (10 μg) and exendin-4 (3 μg), particularly at 6 h and 24 h. Control experiments show that these findings appear to be based neither on the GLP-1R antagonist acting as a nonspecific competing orexigenic signal nor on blockade of peripheral GLP-1R via efflux of exendin-(9–39) to the periphery. To assess the contribution of GLP-1R expressed on subdiaphragmatic vagal afferents to the anorectic effects of liraglutide and exendin-4, food intake was compared in rats with complete subdiaphragmatic vagal deafferentation and surgical controls after ip delivery of the agonists. Both liraglutide and exendin-4 suppressed food intake at 3 h, 6 h, and 24 h for controls; for subdiaphragmatic vagal deafferentation rats higher doses of the GLP-1R agonists were needed for significant food intake suppression, which was observed at 6 h and 24 h after liraglutide and at 24 h after exendin-4. Conclusion: Food intake suppression after peripheral administration of exendin-4 and liraglutide is mediated by activation of GLP-1R expressed on vagal afferents as well as direct CNS GLP-1R activation.

Safety Assessment ofLactobacillus fermentumCECT5716, a probiotic strain isolated from human milk

2009 ◽  
Vol 76 (2) ◽  
pp. 216-221 ◽  
Author(s):  
Federico Lara-Villoslada ◽  
Saleta Sierra ◽  
María Paz Díaz-Ropero ◽  
Juan Miguel Rodríguez ◽  
Jordi Xaus ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Oral Administration ◽  
Human Milk ◽  
Bacterial Translocation ◽  
Probiotic Strain ◽  
Oxidative Markers ◽  
Control Food ◽  
Stress Oxidative ◽  
Control Food Intake

Lactobacillus fermentumCECT5716, a probiotic strain isolated from human milk, was characterized in a previous study. The objective of this study was to evaluate its sensitivity to antibiotics and its potential toxicity and translocation ability after oral administration to mice. For this puropose, 40 Balb/C mice were divided in two groups (n=20 per group). One group was treated orally with 1010colony forming units (cfu)/mouse/day ofLb. fermentumCECT5716 during 28 d. The other group only received the excipient and was used as control. Food intake, body weight, bacterial translocation and different biochemical and haematological parameters were analysed. Oral administration ofLb. fermentumCECT5716 to mice had no adverse effects on mice. There were no significant differences in body weight or food intake between control and probiotic-treated mice. No bacteraemia was observed and there was no treatment-associated bacterial translocation to liver or spleen. Stress oxidative markers were not different in control and probiotic-treated mice. These results suggest that the strainLb. fermentumCECT5716 is non-pathogenic for mice even in doses 10,000 times higher (expressed per kg of body weight) than those normally consumed by humans.

scholarly journals Fibroblast Growth Factor-19 Action in the Brain Reduces Food Intake and Body Weight and Improves Glucose Tolerance in Male Rats

Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 9-15 ◽  
Author(s):  
Karen K. Ryan ◽  
Rohit Kohli ◽  
Ruth Gutierrez-Aguilar ◽  
Shrawan G. Gaitonde ◽  
Stephen C. Woods ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Body Weight ◽  
Growth Factor ◽  
Food Intake ◽  
Glucose Tolerance ◽  
Fibroblast Growth ◽  
Fgf Receptor ◽  
The Central Nervous System ◽  
Fibroblast Growth Factor 19

Fibroblast growth factor-19 (FGF19) and its rodent ortholog, FGF15, are hormones produced in the distal small intestine and secreted into the circulation after a meal. In addition to controlling the enterohepatic circulation of bile acids, FGF15/19 also regulates systemic lipid and glucose metabolism. In these experiments we investigated the hypothesis that, like other gut-derived postprandial hormones, FGF15/19 can act in the central nervous system to elicit its metabolic effects. We found that FGF-receptors 1 and 4 are present in rat hypothalamus, and that their expression was reduced by up to 60% in high-fat fed rats relative to lean controls. Consistent with a potential role for brain FGF15/19 signaling to regulate energy and glucose homeostasis, and with a previous report that intracerebroventricular (i.c.v.) administration of FGF19 increases energy expenditure, we report that acute i.c.v. FGF19 reduces 24-h food intake and body weight, and acutely improves glucose tolerance. Conversely, i.c.v. administration of an FGF-receptor inhibitor increases food intake and impairs glucose tolerance, suggesting a physiological role for brain FGF receptor signaling. Together, these findings identify the central nervous system as a potentially important target for the beneficial effects of FGF19 in the treatment of obesity and diabetes.

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