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 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

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 Obesity and Appetite Control

2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Keisuke Suzuki ◽  
Channa N. Jayasena ◽  
Stephen R. Bloom
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Appetite Control ◽  
Control Food ◽  
Adiposity Signals ◽  
Term Energy ◽  
Glucagon Like Peptide 1 ◽  
Control Food Intake

Obesity is one of the major challenges to human health worldwide; however, there are currently no effective pharmacological interventions for obesity. Recent studies have improved our understanding of energy homeostasis by identifying sophisticated neurohumoral networks which convey signals between the brain and gut in order to control food intake. The hypothalamus is a key region which possesses reciprocal connections between the higher cortical centres such as reward-related limbic pathways, and the brainstem. Furthermore, the hypothalamus integrates a number of peripheral signals which modulate food intake and energy expenditure. Gut hormones, such as peptide YY, pancreatic polypeptide, glucagon-like peptide-1, oxyntomodulin, and ghrelin, are modulated by acute food ingestion. In contrast, adiposity signals such as leptin and insulin are implicated in both short- and long-term energy homeostasis. In this paper, we focus on the role of gut hormones and their related neuronal networks (the gut-brain axis) in appetite control, and their potentials as novel therapies for obesity.

scholarly journals Autonomic Nervous System in the Control of Energy Balance and Body Weight: Personal Contributions

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
G. Messina ◽  
V. De Luca ◽  
An. Viggiano ◽  
A. Ascione ◽  
T. Iannaccone ◽  
...  
Keyword(s):  
Nervous System ◽  
Body Weight ◽  
Autonomic Nervous System ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Sympathetic Activity ◽  
The Body ◽  
World Health ◽  
Autonomic Nervous

The prevalence of obesity is increasing in the industrialized world, so that the World Health Organization considers obesity as a “pandemia” in rich populations. The autonomic nervous system plays a crucial role in the control of energy balance and body weight. This review summarizes our own data and perspectives, emphasizing the influence exerted by autonomic nervous system on energy expenditure and food intake, which are able to determine the body weight. Activation of the sympathetic discharge causes an increase in energy expenditure and a decrease in food intake, while reduction of food intake and body weight loss determines a reduction of the sympathetic activity. On the other hand, pathophysiological mechanisms of the obesity involve alterations of the sympathetic nervous system in accordance with the “Mona Lisa Hypothesis,” an acronym for “most obesities known are low in sympathetic activity.” Furthermore, the parasympathetic influences on the energy expenditure are analyzed in this review, showing that an increase in parasympathetic activity can induce a paradoxical enhancement of energy consumption.

scholarly journals Melanocortin 4 receptor signals at the neuronal primary cilium to control food intake and body weight

2021 ◽  
Vol 131 (9) ◽  
Author(s):  
Yi Wang ◽  
Adelaide Bernard ◽  
Fanny Comblain ◽  
Xinyu Yue ◽  
Christophe Paillart ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Primary Cilium ◽  
Melanocortin 4 Receptor ◽  
Control Food ◽  
Control Food Intake

Pharmacological actions of the peptide hormone amylin in the long-term regulation of food intake, food preference, and body weight

2007 ◽  
Vol 293 (5) ◽  
pp. R1855-R1863 ◽  
Author(s):  
Christine Mack ◽  
Julie Wilson ◽  
Jennifer Athanacio ◽  
James Reynolds ◽  
Kevin Laugero ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Locomotor Activity ◽  
Food Intake ◽  
Energy Expenditure ◽  
Food Preference ◽  
Body Weight Gain ◽  
The Body ◽  
High Fat

The ability of amylin to reduce acute food intake in rodents is well established. Longer-term administration in rats (up to 24 days) shows a concomitant reduction in body weight, suggesting energy intake plays a significant role in mediating amylin-induced weight loss. The current set of experiments further explores the long-term effects of amylin (4–11 wk) on food preference, energy expenditure, and body weight and composition. Furthermore, we describe the acute effect of amylin on locomotor activity and kaolin consumption to test for possible nonhomeostatic mechanisms that could affect food intake. Four-week subcutaneous amylin infusion of high-fat fed rats (3–300 μg·kg−1·day−1) dose dependently reduced food intake and body weight gain (ED50for body weight gain = 16.5 μg·kg−1·day−1). The effect of amylin on body weight gain was durable for up to 11 wks and was associated with a specific loss of fat mass and increased metabolic rate. The body weight of rats withdrawn from amylin (100 μg·kg−1·day−1) after 4 wks of infusion returned to control levels 2 wks after treatment cessation, but did not rebound above control levels. When self-selecting calories from a low- or high-fat diet during 11 wks of infusion, amylin-treated rats (300 μg·kg−1·day−1) consistently chose a larger percentage of calories from the low-fat diet vs. controls. Amylin acutely had no effect on locomotor activity or kaolin consumption at doses that decreased food intake. These results demonstrate pharmacological actions of amylin in long-term body weight regulation in part through appetitive-related mechanisms and possibly via changes in food preference and energy expenditure.

scholarly journals Increased Energy Expenditure Contributes More to the Body Weight-Reducing Effect of Rimonabant than Reduced Food Intake in Candy-Fed Wistar Rats

Endocrinology ◽  
2008 ◽  
Vol 149 (5) ◽  
pp. 2557-2566 ◽  
Author(s):  
Andreas W. Herling ◽  
Susanne Kilp ◽  
Ralf Elvert ◽  
Guido Haschke ◽  
Werner Kramer
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Indirect Calorimetry ◽  
Wistar Rats ◽  
Fat Oxidation ◽  
The Body ◽  
Metabolizable Energy ◽  
Male Rats ◽  
Fat Stores

The CB1 receptor antagonist, rimonabant, affects the endocannabinoid system and causes a sustained reduction in body weight (BW) despite the transient nature of the reduction in food intake. Therefore, in a multiple-dose study, female candy-fed Wistar rats were treated with rimonabant (10 mg/kg) and matched with pair-fed rats to distinguish between hypophagic action and hypothesized effects on energy expenditure. Within the first week of treatment, rimonabant reduced BW nearly to levels of standard rat chow-fed rats. Evaluation of energy balance (energy expenditure measured by indirect calorimetry in relation to metabolizable energy intake calculated by bomb calorimetry) revealed that increased energy expenditure based on increased fat oxidation contributed more to sustained BW reduction than reduced food intake. A mere food reduction through pair feeding did not result in comparable effects because animals reduced their energy expenditure to save energy stores. Because fat oxidation measured by indirect calorimetry increased immediately after dosing in the postprandial state, the acute effect of rimonabant on lipolysis was investigated in postprandial male rats. Rimonabant elevated free fatty acids postprandially, demonstrating an inherent pharmacological activity of rimonabant to induce lipolysis and not secondarily postabsorptively due to reduced food intake. We conclude that the weight-reducing effect of rimonabant was due to continuously elevated energy expenditure based on increased fat oxidation driven by lipolysis from fat tissue as long as fat stores were elevated. When the amount of endogenous fat stores declined, rimonabant-induced increased energy expenditure was maintained by a re-increase in food intake.

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.

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